Page Summary Flashcards by Alyssa Rivera

Which nerve is responsible for the larynx?

Vagus

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2 nerves for motor of larynx?

External superior laryngeal and recurrent laryngeal

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Where is external superior laryngeal nerve responsible for with motor?

Cricothyroid

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Stimulation of which nerve causes laryngospasm?

Superior laryngeal nerve

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Which 2 nerves are responsible for sensory of larynx?

Internal superior laryngeal and recurrent laryngeal

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Where is internal superior laryngeal nerve responsible for with sensory?

Above vocal cords and cords

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Where is recurrent laryngeal nerve responsible for with sensory?

Below vocal cords

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Posterior cricoarytenoid movement?

Abduct
“You take it out back”

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Lateral cricoarytenoid movement?

Adduct
“You bring it in from the side”

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Cricothyroid does — to vocal cords

Tenses

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Thyroarytenoid does — to vocal cords.

Relaxes

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Which 2 nerves are responsible for pharynx?

Spinal accessory and glossopharyngeal

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Which nerve controls motor in pharynx?

Spinal accessory

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Which nerve controls sensory in pharynx?

Glossopharyngeal

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Laryngeal cartilages from superior to inferior (6)

Epiglottis
Thyroid
Cuneiform
Corniculate
Arytenoids
Cricoid

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Normal P50 value?

26-27mmHg

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8 causes of left shift in oxyhemoglobin dissociation curve?

Decrease PCO2
Decrease H+
Increase pH
Decrease temp
Increase CO poisoning (carboxyhemoglobin)
Fetal hemoglobin
Methemoglobin (prilocaine, benzocaine, nitroprusside)
Smoking

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6 causes of right shift in oxyhemoglobin dissociation curve?

Increase PCO2
Increase H+
Decrease pH
Increase temp
Increase 2-3 DPG
Sickle cell anemia

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Right shift — O2 from blood

Unloads

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Right shift of oxyhemoglobin dissociation curve=

Release

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Left shift — O2 affinity

Increases

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Left shift of oxyhemoglobin dissociation curve=

Locked

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PaCO2 affects oxyhemoglobin dissociation curve

Bohr effect

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PaO2 affects CO2 dissociation curve

Haldane affect

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Cl- exchange for HCO3- in RBC’s

Hamburger shift

What is the hamburger shift?

HCO3- out, Cl- in ; non pulmonary

90% SaO2 =

60mmHg

70% SaO2 =

40 mmHg

Dissolved O2 =

.003 x PaO2

O2 bound to Hb =

1.34 x Hb x SaO2

Total O2 Content (CaO2) =

(1.34 x Hb x SaO2) + (.003 x PaO2)

O2 consumption ~

3-4 ml/kg/min ; 250ml/min

Dissolved CO2 =

.003 x PaCO2

CO2 produced and eliminated @

200ml/min ; 2.4-3.2ml/kg/min

CO2 is — more soluble than O2

20x

Anatomical dead space =

2ml/kg

Alveolar ventilation (VA) =

(TV - DS) x RR

PaO2 on O2 =

FiO2 x 5

PaO2 on RA =

102 - age/3

PAO2 on O2 =

FiO2 x 6

PAO2 on RA =

100 - (.4 x age)

PAO2 proper equation =

[FiO2 x (Patm - PH2O) - (PACO2/RQ)]

Pulmonary ventilation (VT) =

RR and TV

Net Filtration pressure =

Kf [(Pc-Pi) - (Oc-Oi)] x SA

Normal net filtration pressure

Ficks law of diffusion proportional to

(Change in P x SA x diff. Coefficient) / membrane thickness

Poiseuille’s law =

R = 8nl/pie(r^4)

Tidal volume ml

500

Inspiratory reserve volume ml

3000

Expiratory reserve volume ml

1000

Residual volume ml

1200

Which PFT cannot be measure by spirometry?

Residual volume

Inspiratory capacity equation

TV + IRV

Inspiratory capacity ml

3500

Vital capacity equation

TV + IRV + ERV

Vital capacity ml

4500

Functional residual capacity equation

ERV + RV

Functional residual volume ml

2200

Total lung capacity equation

TV+ IRV + ERV + RV

Total lung capacity ml

5700

Total CO2 content of arterial blood

48 mlCO2/100ml blood

Total CO2 content of venous blood

52 mlCO2/100ml blood

Normal CO2 arterial-venous difference

4 mlCO2/100ml blood

2 primary respiratory centers

Dorsal respiratory group (DRG) pacemaker and ventral respiratory group

Which location of the brainstem can the primary respiratory centers be found?

Medulla

Dorsal respiratory group pacemaker is in charge of which muscles?

Phrenic and external intercostals

Ventral respiratory group is in charge of which muscles?

Internal intercostal

Secondary respiratory centers can be found where in the brainstem?

Pons

What 2 things make up the secondary respiratory center?

Apneustic center and pneumotaxic center

Apneustic center is in charge of what?

Deep and prolonged respiration

Pneumotaxic center is in charge of what?

Shuts off respiration (hering-Bering 1.5L)

Central chemoreceptors in medulla respond to what?

Increase H+, PCO2 in CSF

Peripheral chemoreceptors respond to what?

Decrease O2 <60 mmHg

Carotid body response to what?

Increase CO2

Aortic arch responds to what?

Increase H+

Which nerve is in charge of carotid?

Glossopharyngeal

Which nerve is in charge of aortic and stretch receptors?

Vagus

—: Partial pressure of CO2 in CSF

LeChatelier’s Principle

Vagus nerve, prevents overstretching (TV 1.5L)

Hering-Breuer reflex

Inspiration HR and intrathoracic pressure response?

Increase HR Decrease intrathoracic pressure

Dead space vent and perfusion

Well vent/poor perfusion

Shunt perfusion and vent

Well perfusion/ poor vent

4 things to increase dead space?

1. Age 2. PP vent 3. PE 4. Lung disease

Compliance equation =

Change V / change P

Un-anesthetized V and Q in lateral decubitus?

Non dependent: decrease V and Q Dependent: increase V and Q

Anesthetized V and Q in lateral decubitus?

Non dependent: increase V and decrease Q Dependent: decrease V and increase Q

Jackson-Reese is which mapleson?

Jackson-Reese minimum — L/min (2.5-3xMV)

Bain circuit is which mapleson circuit?

Bain circuit minimum flow for CV and SV?

CV: 70 ml/kg SV: 100-300 ml/kg

Normal A-a gradient on RA

5-15mmHg

Normal FEV1

Normal FVC

Normal FEV1/FVC

FEV25-75

4.7 L/sec

Asthma, bronchitis, emphysema: FEV1, FVC, and FEV1/FVC

FEV1: decrease (<2.5L) FVC: normal FEV1/FVC: decrease (<.7)

What is the best test to access early stages of COPD?

FEV 25-75

Obstruction is — to get out

Hard

Restrictive is — to get in

Hard

Pulmonary fibrosis, pneumothorax, scoliosis FEV1, FVC, and FEV1/FVC?

FEV1: decrease FVC: decrease FEV1/FVC: normal to high

Moderate risk FEV1 and FEV1/FVC?

FEV1: <2L FEV1/FVC: <50%

High risk FEV1, FVC, and FEV1/FVC?

FEV1: <1L FVC: <1.5L or 20 ml/kg FEV1/FVC: <35%

CO has — greater affinity for Hb than O2

200-250x

4 ways CO2 is carried in blood:

1. Physically dissolved (5%) 2. Carbonic Acid (<1%) 3. Bicarbonate ion (HCO3-, 90%) 4. Protein bound (5%)

Responsible for converting CO2 to HCO3-

Carbonic anhydrase

Central chemoreceptors response to —

Systemic CO2 & H+ in the CSF

Peripheral chemoreceptors respond mostly to —

Decrease PaO2

— is the primary stimulus for ventilatory response

PaCO2

Mast cells can cause — through histamine release

Bronchoconstriction

6 anatomical characteristics of a difficult intubation?

1. Short,muscular neck 2. Receding mandible 3. Protruding maxillary incisors 4. Unable to visualize uvula 5. Limited TMJ (<40mm) 6. Limited cervical mobility

Permanent dilation of a bronchus or group of small bronchi, airway resistance increase, compliance increases

COPD

Copious sputum, increase Hct, “blue bloater”

Bronchitis

Cough with exertion, scant sputum, “pink puffer”

Emphysema

COPD post op FEV1/FVC and preop CO2:

FEV1/FVC: <.5 CO2: >50mmHg

#1 symptom to asthma?

Wheezing

Asthma acid-base:

Hypoxia and hypocarbia with alkalosis

2 most common reasons for pulmonary edema:

Increase pulmonary hydrostatic pressure Increase in permeability of alveolar capillary membrane

Pulmonary edema colloid osmotic pressure and hydrostatic pressure:

Colloid osmotic pressure: 28mmHg Hydrostatic pressure: 6-8mmHg

What is the #1 manifestation of ARDS?

Hypoxia

ARDS causes a which kind of shunt?

Right to left

Which syndrome has a increased risk of aspiration?

Mendelson’s syndrome

Earliest and most reliable sign of aspiration?

Hypoxemia

4 causes of pulmonary restrictive disease?

1. Acute intrinsic (ARDS, aspiration, or CHF) 2. Chronic intrinsic (sarcoidosis, drug induce) 3. Chronic extrinsic (obesity, ascites, pregnant; “big bellies”) 4. Disorders of the pleura or mediastinum

Intrinsic restrictive lung disease Restrictive ♥ myopathy ↑ Ca++ Splenomegaly Hepatic granulomas Optic and facial nerve involvement

Sarcoidosis

Hypotension, Hypoxemia, Tachycardia, increase CVP, increase PIP, Absence of unilateral breath sounds, Tracheal shift, Asymmetric chest wall movement

S/S of tension pneumothorax

Transtracheal Jet Vent location?

Cricothyroid membrane

Barotrauma & pneumothorax, Mediastinal air (emphysema), Arterial perforation, DAMAGE TO TRACHEAL MUCOSA, Sub Q emphysema, Exhalation difficulty, Esophageal puncture, THICKENED SECRETIONS

Complications of transtrachael jet ventilation

Vent modes for — ventilation: IMV, SIMV, MMV, PSV & HFJV

spontaneous ventilation

Vent modes for — ventilation: CMV, AC, and PCV

Not supporting spontaneous

— is a phosphodiesterase inhibitor (PDEIII). Phosphodiesterase breaks down cAMP. When phosphodiesterase is inhibited, cAMP accumulates and bronchodilation occurs. It also improves diaphragmatic contractility. — cause release of NE from sym postganglionic neurons – avoid w/ halothane, adenosine receptors

Aminophylline ; Xanthines

— and— are both methylated xanthines.

Caffeine and Theophylline

— receptor stimulation activates adenylate cyclase which converts ATP to cAMP resulting in bronchodilation

Beta-2

— is a mast cell stabilizer that prevents the release of histamine, bradykinin. It prevents bronchospasm in asthmatics, but is not effective once bronchospasm develops. CHRONIC

Cromolyn sodium

—, a quaternary ammonium compound, is an antimuscarinic used to augment bronchodilation produced by beta-2 agonists. Blockade of the muscarinic receptor leads to a decrease of IP3 so less calcium is released form intracellular vesicles. Smooth muscle tone is reduced.

Ipratroprium

— is a non-xanthine central respiratory stimulant. It increases tidal volume and to a lesser extent respiratory rate. It is not good for newborns because it is dissolved in benzyl alcohol. It acts through peripheral chemoreceptors to stimulate central chemoreceptors.

Doxapram

ETT equation

Age/4 + 4 (uncuffed) (-) 0.5 cuffed

ETT length equation

12 + age/2

<6.5kg LMA

<20kg LMA

20-30kg LMA

2.5

>30kg LMA

Normal adult LMA

Large adult/men LMA

Crazy large LMA

Sterilization temperatures:

275F & 135C

Aspiration steps:

1. head down (#1) 2. disconnect circuit 3. Suction 4. examine w/ bronchoscope 5. x-ray 6. abx (debatable) 7. physiotherapy

What is a cleaner used?

Endozime

Differences in Neonatal Respiratory System: — Lung compliance — Chest wall compliance — FRC O2 consumption — ml/kg/min

Decrease, increase, decrease, 7

Neonatal decrease lung compliance 2nd to less —

Alveoli

Neonatal increase chest wall compliance shows — ribs

Floppy

Neonatal has decrease FRC to ~ — ml/kg

Thyro-mental distance

> 6.5 cm = ~3 fingerbreadths

Auto regulation: Cerebral Perfusion Pressure = MAP — mmHg Coronary Perfusion Pressure = MAP — mmHg Renal Perfusion Pressure = MAP — mmHg

50-150 60-160 80-180

Four types of abnormal Cardiac wall motion:

1. Hypokinesis (less than normal wall motion) 2. Hyperkinesia (greater than normal wall motion) 3. Akinesis (absence of wall motion) 4. Dyskinesis (paradoxical outward motion)

Atrial contraction wave on CVP:

A wave on CVP

Ventricular contraction, tricuspid valve elevation wave on CVP:

C wave on CVP

Tricuspid closed, systolic atrial filling wave on CVP:

V wave on CVP

Ventricular systole, atrial relax, displace tricuspid valve wave on CVP:

X wave on CVP

Diastole, early ventricular filling, open tricuspid wave on CVP:

Y wave on CVP

RIJ or LIJ preferred and why?

RIJ because LIJ has the thoracic duct

CVP waveform: tricuspid stenosis, pulmonary stenosis, pulmonary HTN, ↓ right ventricular compliance

Large A waves

CVP waveform: tricuspid regurg, r vent papillary muscle ischemia, pericarditis, cardiac tamponade

Large V waves

Multiorifice catheter — below SVC

2cm

Single orifice catheter — above SVC

3cm

— interspace above level of 3rd rib

T4-T5

Right ventricular failure, tamponade, tricuspid stenosis, tricuspid regurgitation, pericarditis, pulmonary hypertension, chronic left ventricular failure, and hypervolemia : — CVP

Increased CVP

Increase CVP PEEP

may read high- need to d/c from vent 10-15 seconds

Where are the venous baroreceptors located?

RA and great veins

—: stretch of RA = increase HR with inspiration via vagus nerve

Bainbridge reflex

Where are the arterial baroreceptors located?

Aortic arch and carotid sinus

Which arterial barorecpetor: Vagus nerve afferent, stretch

Aortic arch

Which arterial barorecpetor: Glossopharyngeal (hering’s) nerve afferent

Carotid sinus

Action potentials (efferent) via —and — sympathetic cardio accelerators.

vagus and T1-T4

Swan-ganz catheter max ballon air

1.5ml

Swan-ganz catheter: RA pressure

1-8

Swan-ganz catheter: RV pressure

15-25/1-8

Swan-ganz catheter: PA pressure

15-25/8-15

Swan-ganz catheter: PCWP pressure

6-12

Swan-ganz catheter: LA pressure

2-12

Swan-ganz catheter: LV pressure

100-140/0-12

Swan-ganz catheter: RA depth

Swan-ganz catheter: RV depth

Swan-ganz catheter: PA depth

Swan-ganz catheter: PCWP depth

45-50

— is never higher than PADP

PAWP

When can PAWP be higher than PADP (3)

1. MS 2. Increase alveolar pressure 3. Pulmonary venous obstruction

CVP and PCWP from pt status: hypovolemia

CVP: low PCWP: low

CVP and PCWP from pt status: left ventricular failure

CVP: normal or high PCWP: high

CVP and PCWP from pt status: Right ventricular failure

CVP: high PCWP: normal

CVP and PCWP from pt status: PE

CVP: high PCWP: normal

CVP and PCWP from pt status: chronic pulmonary HTN

CVP: high PCWP: normal

CVP and PCWP from pt status: cardiac tamponade

CVP: high PCWP: high

— = Pressure problem = same size SV

Concentric Hypertrophy

— = Volume problem = Larger SV

Eccentric Hypertrophy

Arterial wave number: anacrotic limb: contractility & SVR(ease of LV emptying)

Arterial wave number: dicrotic limb: blood flow to periphery

Arterial wave number: dicrotic notch: aortic valve closure, coronary artery perfusion

Pulse pressure greatest in — d/t ↑SBP & ↓DBP

pediatrics

High a line transducer = — BP Low a line transducer = — BP

Low ; high

Invasive BP is — mmHg higher than non-invasice

Sitting position = transducer a line @ —

ear

Ventricular action potential: 0= 1= 2= 3= 4=

0= Na influx 1= Cl-in, K+out 2= Ca+ influx 3= K+ EF flux 4= Na-K pump

SA node action potential: 0= 3= 4=

0= Ca+ and Na+ influx (mostly Ca+) 3= K+ efflux 4= Na-K pump

SV equation

(CO x 1000)/HR

CI equation

CO/BSA

SI equation

CI/HR

SVR equation

(MAP-CVP/CO) 80

PVR equation

(MPAP-PCWP/CO) 80

CoPP equation

AoDBP-PCWP

MAP equation

(DBP x 2 + SBP) / 3

SV value

60-90 ml/min

CI value

2.5-3.5 L/min

SI valve

40-60

SVR valve

900-1500 dyn

PVR value

50-150 dyn

CoPP valve

60-160

MAP value

80-120

RBBB QRS V1 and V6

MARROW V1: m shape; broad R wave V6: w shape; broad S wave

LBBB QRS V1 and V6

WILLIAM V1: W shape; no R wave, wide negative S wave V6: M shape; no Q wave, wide notched R wave

II, III, aVF lead location

Inferior, posterior

I, aVL, V5-V6 lead location

Lateral

V1-V4 lead location

Anterior, septal

RCA supples blood to where

Inferior, posterior

Left circumflex supples blood where

Lateral

LAD supplies blood where

Anterior, septal

Obstruction of the — or — = SA & AV nodal dysrhythmias -sinus arrest, sinus pause, type I AV block, nodal rhythms, & complete heart

RCA or circumflex

Obstruction of the — = Wide complex rhythms- bundle branch block, complete heart block, mobitz type II block, idioventricular rhythms.

LAD

ECG electrodes have what type of voltage

Micro

Which lead: anterior axillary line at the level of 5th intercostal space

Small positive wave following T wave

U wave

Which wave is associated w/ ↓ K, ↑ Ca, quinidine, digitalis, epinephrine, intracranial hemorrhage, or papillary muscle dysfunction

U wave

Increase Preload = increase SV, same ED vol =

Give fluids

Decrease Preload = decrease SV, same ED vol =

NTG, Lasix, tamponade

Increase Afterload = increase SVR, decrease SV, increase BP, increase ED vol =

phenylephrine

Decrease Afterload = decrease SVR, increase SV, decrease BP, decrease ED vol =

Sodium nitroprusside (SNP)

Increase Contractility = increase SV, decrease ED vol, increase BP =

Digoxin, Ca++

Decrease Contractility = decrease SV, increase ED vol, decrease BP =

CHF

CO to liver

27%

CO to kidney

22%

CO to heart

5% (225ml)

CO to CNS

15% (750ml)

CO to lungs

100%

Aortic and mitral stenosis HR and SVR: use what

SSS (slow, sinus, SVR); HR: low; SVR: high Phenylephrine

Aortic and mitral regurgitation preload, SVR, and HR: come common cause

FFF (fast, forward, full); increase preload; decrease SVR; increase HR Rheumatic fever

IHSS (HOCM) volume and SVR: use what?

Keep full, increase SVR Phenylephrine

Tetralogy of Fallot SVR: and use what?

Increase SVR Phenylephrine

PVR — with acidosis and hypercarbia

Increases

Increase PVR causes what kind of shunt?

Right to left shunt

SVR — with acidosis and hypercarbia

Decrease

Sepsis: PCWP, CO, and SVR

PCWP decrease, CO increase, SVR decrease

What 3 things is with becks triad?

Muffled heart sounds, JVD, hypotension

Becks triad is most common with what?

Cardiac tamponade

Inhibitors of HMG-CoA recluctase

Statins

2 side effects of statins

1. Liver dysfunction 2. Sever myopathy

Protamine dose

1 mg/100 U heparin

Heparin for bypass

300 U/kg

Initial dose of FFP

10-15 ml/kg

What to give for an antithrombin III deficiency?

FFP

Mnemonic for cranial nerves

Oh Oh Oh To Touch And Feel A Girls Vagina - So Heavenly

CN 1: name and function

Olfactory and smell

CN 2: name and function

Optic and vision

CN 3: name and function

Occulomotor and adduction of eye (medial), pupil size

CN 4: name and function

Trochlear and eye movements

CN 5: name and function

Trigeminal and chewing, mastication, facial sensory

CN 6: name and function

Abducens and abduction of eye (lateral)

CN 7: name and function

Facial and facial muscles, taste (anterior 1/3 tongue)

CN 8: name and function

Acoustic and balance (vestibular), hearing (cochlear)

CN 9: name and function

Glossopharyngeal and taste (posterior 2/3 tongue), carotid & sinus afferent

CN 10: name and function

Vagus and parasympathetic efferent, decrease HR

CN 11: name and function

Spinal accessory and motor control of larynx & pharynx

CN 12: name and function

Hypoglossal and tongue muscles

CBF amount

750 ml/min, 50 ml/100g/min, 15% of CO

CBF equation

CPP/CVR

CPP equation

MAP-ICP

Cerebral glucose consumption

5 mg/100g/min

Blood flow and vessel diameter to non ischemic and ischemic for cerebral steal:

Non ischemic: BF increase & diameter increase Ischemic: BF decrease & diameter maxed dilate

Blood flow and vessel diameter to non ischemic and ischemic for inverse cerebral steal:

Non ischemic: BF decrease & diameter decrease Ischemic: BF increase & diameter max dilated

2 things that cause cerebral steal?

Hypoventilation and vasodilators (nitro)

What causes inverse cerebral steal?

Hyperventilation

CN: Superior rectus- supraaduction “look up”

CN: Inferior rectus- infradduction “look down”

CN: Medial rectus- adduction “look in”

CN: Lateral rectus- abduction “look out”

CN: Supeiror oblique- look in & down

CN: Inferior oblique- look out and up

— pathway = Trigeminal nerve- V

Afferent

— pathway = Vagus nerve - X

Efferent

Oculocardiac relfex ECG manifestation: 3

↓ HR, Junctional Rhythm, PVC’s

Oculocardiac reflex triggered by:

traction on extraocular muscles- MEDIAL RECTUS, ocular manipulation, manual pressure on globe

Oculocardiac reflex Tx/Blockade:

antimuscarinic meds, retrobulbar block, IA

What 2 nerves are associated with oculocardiac reflex?

Trigeminal (5) and vagus (10)

Normal ICP

5-15

Focal ischemia ICP

25-55

Global ischemia ICP

>55

IC volume: Brain matter & intracellular H2O

80%

IC volume: blood

12%

IC volume: CSF

ICP waveforms: plateau waves, found in pts with increase ICP

A waves

What 3 s/s of Cushing’s triad ?

Bradycardia Hypertension Irregular respirations

8 treatments for increase ICP:

1. Dehydrate brain w/ Mannitol (0.25-1g/kg) or Lasix 2. Give steroids- slowest but may restore BBB 3. Hyperventilate PaCO2 25-30 mmHg (1/2 life 6hr) 4. Restrict fluids 5. Elevate HOB to 30degrees 6. Administer cerebral vasoconstrictor (pentathol, etomidate) 7. Control BP 8.Cool pt to 34C for cerebral protection

—: above cerebellum= flexion upper & extension lower

Decordicate

—: at brainstem = extension arms & legs, arched body

Decerebrate

— = Frontal lobe — = Temporal lobe — = Brainstem & cerebellum

Anterior Middle Posterior

Time to Close of Fontanelles: Anterior, Posterior, Anterolateral, Posterolateral

18 mos. 2 mos 2 mos 2 years

Specific gravity of CSF =

1.003-1.009

Hyperbaric fluid =

D10

Isobaric fluid =

CSF

Hypobaric fluid =

NS/sterile H2O

CSF forms @ — in the choroid plexus

21 ml/hr or 500-700 ml/day

— is located specifically in temporal horn of each lateral ventricle, the posterior portion of the third ventricle, and the roof of the fourth ventricle.

Choroid plexus

CSF is reabsorbed mostly in the — (4/5), but also in spinal villi & lymphatics.

arachnoid villi

Total volume of CSF =

150 ml

CSF Pressure: —

10 & 20cm H2O

— is the most common site of CSF obstruction

Aqueduct of Sylvius

4 factors governing passage across BBB:

Size - smaller crosses easier Charge- (ions do not cross- Na, K, Mag) Lipid solubility- Cross Degree of protein binding

Do Water & Gases cross BBB?

Yes

Do H2O soluble drugs & Proteins cross BBB?

What 2 areas have no BBB?

Chemoreceptor trigger zone (CRTZ) and area surrounding the posterior pituitary

4 electrolyte disorders that decrease Seizure threshold:↑Sz activity

1. Hypocalcemia 2. Hypomagnesemia 3. Hyponatremia 4. Hypernatremia

(2)Conditions & (3)Meds Likely to↓Sz Threshold:

Hypoglycemia Alkalosis Demerol is opioid most likely to cause seizures Aminophylline & ketamine together

2 causes of Acute Spinal Shock:

1. Hypotension due to sympathetic blockade 2. bradycardia due to blockade of cardiac accelerators

Autonomic Hyperreflexia spinal location =

T5 or T6

When do Cerebral Vasospasm occur:

4-12 days post op

S/S of cerebral vasospasm: 3

worsening headache, confusion, HTN

Triple H Therapy For treatment of cerebral vasospasm and med=

1. Hypervolemia = CVP > 10 mm Hg, PCWP = 12-20 2. Hypertension = SBP 160-200 mm Hg 3. Hemodilution = Hct 33% -Medication - Nimodipine

Wake-up test monitors the anterior (ventral) spinal cord, which is supplied by the —. These are — tracts.

anterior spinal arteries ; motor

In Parkinson’s avoid: (4)

Reglan Compazine Droperidal All meds that↓Dopamine

VAE steps: 9

1. Notify surgeon so they can flood the field or pack 2. Turn off N2O 3. Administer 100% O2 4. Aspirate central venous catheter to remove air 5.↑CVP (Valsalva maneuver) 6. CV drugs to support circulation 7. Bilateral jugular vein compression 8. PEEP 9. Position- left lateral decub w/ 15 degree head down tilt

CSF pathway: (10)

1. Choroid plexus 2. Lateral ventricle 3. Foramen Monroe 4. 3rd ventricle 5. Aqueduct of Sylvius 6. 4th ventricle 7. Foramen luschka & foramen magendie 8. Subarachnoid space 9. Brain 10. Arachnoid Villi

4 main sources for circle of Willis:

1. R internal carotid 2. L internal carotid 3. Basilar artery 4. Vertebral artery

Slack Brain maneuvers= (4)

Mannitol/ Diuretics Hyperventilation PaCO2 = 25-30mmHg Hypertonic Saline Head up position

1-4 Hz- greatest amplitude- sleeping adult, abn in wake

Delta

4-8 Hz- Amplitude- higher than alpha & beta, but lower than delta

Theta

9-14 Hz- higher in amplitude, alert but relaxed- eyes close

Alpha

15-40 Hz- low amplitude, frontal head, business activity; Variations seen w/ benzo & propofol – mu wave

Beta

Amplitude of EEG:

Delta >Theta >Alpha >Beta

Frequency of EEG:

Beta > Alpha > Theta > Delta

high-order activity like problem solving (> 25yo)

Gamma

beta wave variant- seen over motor areas- amplitude 1⁄2 of beta

awake patient that is staring, reading or looking @ objects

Lambda

GA: — high frequency in Beta waves — low frequency in delta & theta waves

↓ ; ↑

Surgical stimulation or light anesthesia: — high frequency, low voltage activity

↑

Cerebral compromise & deep anesthesia: — frequency, — voltage activity

low ; high

Isoelectric at — MAC

1.5-2.0

Sevo & Enflurane: can accentuate — activity

epileptic

Barbiturates, etomidate, and propofol = — suppression

burst

Ketamine, opioids and etomidate- — produce a Δ in latency & amplitude

do not

— – Afferent – Dorsal Horn ; S.A.D. Posterior

Sensory

— – Efferent – Ventral Horn ; S.A.D. Anterior

Motor

MMEP: Peripheral- —, Central- —

popliteal ; anterior

Preganglionic SNS – —

Intermediolateral Horn

SSEP Monitoring (posterior spinal arteries) -Touch, pressure, vibration -Dorsal (posterior) cord – Cuneatus & Gracilis tracts -Ascend ipsilateral side -Decussate @ brainstem to contralateral thalamus & sensory cortex -Goes to RAS where it percolates to sensory cortex -Somewhat sensitive -Tibial – electrodes midline scalp, Ulnar- electrodes lateral

Dorsal-Lemniscal (sensory)

— very sensitive to SSEP monitoring

Visual evoked potential- CN II

— barely sensitive (altered most by temp) to SSEP monitoring

BAEP – CN VIII

Ketamine, etomidate, & opioids, barbs, propofol = — Δ in latency or amplitude in SSEP

— – Myelinated, Fast “first” Pain & temp Rexed’s lamina I & V, dorsal horn Neurotransmitter - glutamate

A-sigma Fibers

— – Unmyelinated, Slow “dull” Pain & temp Rexed’s lamina II (substantia gelatinosa) & III, dors Neurotransmitter – substance P Interneurons go from II & III to V Epidural steroids

C Fibers

Ascending Pain (—): Lateral Spinothalamic Tract (neopalatine)

Anterolateral

5 factors that alter the latency and/or amplitude of SSEP:

1. Decrease Cerebral perfusion secondary to hypotension, decrease PaCO2, increase ICP 2. Cerebral hypoxia 3. Hypothermia (MOST) 4. Hyperthermia 5. Hemodilution; Hct < 15%

Descending Pain (—): Dorsolateral Funiculus – modulates pain

Dorsolateral

Originate in the periventricular and periaqueductal gray areas and terminate on enkephalin-releasing interneurons in Rexed’s lamina II (substantia gelatinosa). This inhibits the release of —. (Presynaptic inhibition)

substance P

—: physiologic pain, carried by A-delta-sharp, prickly & C fibers-dull

Nociceptive

—-sharp & well localized

Somatic

—-diffuse, dull & vague

Visceral

—: Caused by abnormal processing of painful stimuli. This pain may occur after injury to neural tissue secondary to systemic disease, infection, trauma, ischemia, deficiencies in metabolism or nutrition, or exposure to environmental toxins or neurotoxin medications.

Neuropathic

— tract- most important spinal tract for pain

Lateral spinothalamic (neo)

—: perception of an ordinarily non-painful stimulus as pain

Allodynia

— is a combined disorder consisting of hyperesthesia, allodynia, and hyperalgesia

Hyperpathia

Sub P, Bradykinins & serotonin released → arachononic acid released = —, —, and—

thromboxane, prostaglandins & leukotrines

Preganglionic Parasympathetic Nerves originate (craniosacral):

Cranial nerves III, VII, IX, & X (3,7,9,10) Sacral segments S2-S4

—: (LA, ketamine, opiods, benzos) [- Charge/ Cl-, SO4-]

Weak Base

—: (Thiopental, other barbit, [+ Charge/ Na+, Mg++]

Weak Acids

— = H2O soluble

Ionized

— – lipid soluble (crosses BBB)

Non-Ionized

— = lipid solubility

Potency

— = protein binding & solubility

Duration

— = pKa

Speed of Onset

Fetus pH < maternal pH = —

↑ ion trapping

Blood flow highest to lowest- loss of LA d/t vascular reabsorb (9)

Intravenous Tracheal Intercostal Caudal Paracervical Epidural Brachial Plexus Spinal Subcutaneous

Mnemonic of LA reabsorption

In Time I Can Please Everyone But Susie & Sally

Mnemonic of brachial plexus:

Robert Taylor Drinks Cold Beer

Brachial plexus order:

Root, trunk, division, cord, branch

— block: -for forearm & wrist, safest, miss the muscultaneous 30-40ml, -musculocutaneous = 3-5 mL of LA into coracobrachialis muscle.

Axillary

— block = -greatest risk of pneumo, most compact 40ml -Less likely to miss the peripheral or proximal branches

Supraclavicular

— block = -shoulder surgery, miss of ulnar nerve & targets TRUNKS, no hand 40 ml -High incidence of ipsilateral hemidiaphragmatic paresis

Interscalene

— and — location = interscalene and Supraclavicular

Shoulder & humerus

— Block: -C1 (motor), C2, C3, and C4 = 4ml -some plastic surgery procedures, carotid endarterectomy tracheostomy and thyroidectomy. -Complications: hiccups, Horner’s, hoarse

Cervial Plexus

Horners Syndrome= -blockage of stellate ganglion @ — -Least likely w/ — block

C7 ; axillary

S/S of —: 1.Ptosis (droopy eye lid) 2. Miosis (pupil constriction) 3. Facial & Arm flushing (d/t vasodilatation) 4. ↑ Skin Tem 5. Anhydrosis (lack of sweating on face) 6. Nasal Congestion

Horners Syndrome

— block: -Minimum tourniquet time = 15-20 mins or 20-40 -Lidocaine 0.5% or Prilocaine 0. 5% -40 – 50ml -No bupivacaine- ♥ tox or chloroprocaine- thrombophlebitis -Contraindicated: severe crush injuries, uncontrolled hypertension, Raynaud's disease PVD, Homozygous sickle cell

Bier Block

Nerves that Flex the Forearm: — and —

Musculocutaneous & Radial

-Extension @ elbow, supination of FA, extension of wrist & fingers -Damage = inability to ABDUCT thumb & wrist drop

Radial Nerve

-Pronation of FA, flexion of wrist -To thumb, index finger, middle finger & lateral ring finger -Innervates the medial aspects of FA: Pronator teres, Flexor carpi radialis, Palmaris longus, Flexor digitorum superficialis -Damage = inability to ADDUCT thumb & Ape Hand

median nerve

-Flexion of wrist, adduction of all fingers -The little finger & medial ring finger (C8) In the forearm: Flexor carpi ulnaris, Medial 1⁄2 of flexor digitorum profundus -And in the hand: Palmaris brevis muscle, Abductor digiti minimi, Flexor digiti minimi -Damage = Claw hand -Innervates the adductor pollicis of the thumb

ulnar nerve

Flexion @ elbow

Musculocutaneous

Nerves of Lower extremity:

1. Femoral - saphenous 2. Sciatic - common peroneal to deep peroneal & superficial peroneal & tibial to sural

— = anteromedial foot, medial anterior calf and the dorsum of the foot

Saphenous

—= toe extension & sensation to medial 1⁄2

Deep peroneal nerve

— = sensation superficially to dorsum of foot & all 5 toes

Superficial peronal nerve

— – sensation to heel, medial sole & lateral sole

posterior tibial

— – sensation to lateral foot

Sural

— of foot= medial plantar & lateral plantar - tibial nerve

Flexion

— of foot – peroneal nerve

Extension

Superficial leg nerves :

saphenous, superficial peroneal, sural “S’s”

— Nerve: L2, L3, L4 Anterior thigh & knee Anterior muscles of the thigh

Femoral

Femoral nerve location mnemonic:

NAVEL (nerve, artery, vein, empty space, and lymphatics

Provides sensation to the medial aspect of the thigh and motor innervation to the adductor muscles located in the medial thigh

Obturator nerve

— surgeries: Femoral, Sciatic, Lateral Femoral, cutaneous obturator

On or above knee

L4, L5, and S1-S3 -innervates the muscles of the back of the thigh (biceps femoris, semitendinosis, semimembranosus, and adductor magnus). -As it continues, it innervates the muscles of the lower leg and foot

Sciatic nerve

Popiteal Block = — nerve

sciatic

Nerve injury: Face mask ventilation

CN 5 & 7 (facial & tongue numbness)

Nerve injury: LMA

SLN or RLN

Nerve injury: Intubation

RLN, SLN, CN 10, CN 12

Is the most commonly injured peripheral nerve in patients undergoing anesthesia More common in those with BMI > 38 & men

Ulnar nerve

Placement of shoulder braces = acromion

Brachial Plexus

Damaged = loss of the ability to supinate the extended forearm, wrist drop, abduct thumb, extend the metacarphophalaneal joints

Radial Nerve

Most commonly injured nerve of lower extremity Most common injured nerve during lateral position 3 issues: Loss of dorsiflexion of the foot is consistent with injury to the Foot drop and inability to evert foot

Common Peroneal nerve

Protect w/ pillow under knees Injured when patient rotated to semi supine (hips)

Sciatic

Inside of knee (litho with strap medially) Numbness & tingling along medial aspect of the calves

Saphenous

Femoral Decreased sensation — thigh

LATERAL

Complications of — block: Stimulation of the oculocardiac reflex, retrobulbar hemorrhage, circumorbital hematoma, penetration of the globe, optic nerve trauma, optic nerve sheath injection, extraocular muscle injury, intra-arterial injection

retrobulbar

— : Blocking of RLN through cricothyroid membrane w/4% lido Absorbed across mucous membranes (sim to sublingual)

Transtracheal

Isobaric =

CSF

Hyperbaric =

Dextrose solution

Hypobaric =

Sterile H2O

— in the epidural space communicates with the azygous system- important during times of engorgement which can cause engorgement of the vessels during instances of increased abdominal pressure

Batson's plexus

Sacrococcygeal membrane (injected into epidural space)

Caudal

Caudal Anatomical landmarks:

2 sacral cornua, the coccyx, and the posterior superior iliac spines

Caudal Dose Bupivacaine: — mg/kg Infant test dose = — mcg/kg epinephrine Max dose is — mg/kg

0.5-1.0 ; 0.5 ; 3 mg

Cutting needles:

Quinke, Pitkin

Non-Cutting needles:

Whitacre, Spotte, Greene

SAB needle — ga

27ga (normal), 25ga (used with 18ga introducer), 22ga (elderly & obese)

Epidural needle

17ga Toughy

Passage of Needle for spinal (8)

Skin Subcutanous tissue Supraspinous ligament Interspinous ligament Ligamentum flavum Epidural Space Dura Subarachnoid

What will you not pass through on a para median approach for a spinal?

Supraspinous and interspinous ligament; rather paraspinous muscle

Dermatome Landmarks —- Completely Motor —- Clavicle —- Nipples —- Xiphoid —- umbilicus —-Tibia —-Perineium

C1- Completely Motor C4- Clavicle T4- Nipples T6- Xiphoid T10- umbilicus L4-L5-Tibia S2-S5-Perineium

The tip of the 12th rib corresponds with —

The origin of the scapular spine corresponds with —

The most protuberant cervical vertebra is at the level of —

The tip of the scapula corresponds with —

level of the posterior superior iliac spine —

Hydrophilic: — Slow onset & prolonged DOA Intrathecal 0 early respiratory depression + late resp depression d/t rostral spread (6-12 hrs) Epidural + early respiratory depression after 2 hours + late resp depression d/t rostral spread (6-12 hrs)

Morphine

Lipophilic: — Fast onset & short DOA Intrathecal + early resp depression (2 hrs) 0 late respiratory depression Epidural + early resp depression (2 hrs) 0 late respiratory depression

Fentanyl, Sufentanil, Alfentanil

4 common side effects of intrathecal opiods:

1. Pruritus (most common) 2. Urinary retention 3. N & V 4. Respiratory depression

4 common side effects of epidural opioids:

1. urinary retention (bup/morphine) 2. pruritus (morphine) 3. weakness of hands 4. HoTn

— = Stellate Ganglion- if blocked = Horner’s syndrome

C8-T1

S/S of — include: ipsilateral miosis, ptosis, enopthalamos, flushing,↑skin temp, anhydrosis, nasal congestion

Horner’s syndrome

— = numbness @ little & ring finger

— = numbness @ middle fingers

— = numbness @ thumb & index finger

Progression of spinal blockade:

Autonomic>sensory>motor

Sensitivity to nerves with spinal block:

large mylenated > smaller mylenated > unmylenated

Fibers that are blocked with spinal:

Type B > Type Aδ = Type C > Aβ > Aα C type = more resistant to blockade than A & B fibers

SAB additives that prolong the duration w/o resulting significant ♥ changes

Epinephrine 0.2 to 0.3 mg Clonidine 75 to 100 mcg phenylephrine 2 to 5 mg

Procedure and level of block: TURP, hip arthroplasty, testicles, hysteroscopy

T10

Procedures & Level of Block: ESWL

T4-6

Procedures & Level of Block: Urinary bladder

S2-S4

Procedures & Level of Block: Lower abdominal

Procedures & Level of Block: Kidney

T10-L1

Procedures & Level of Block: Uterine and cysto

T8-T10

Procedures & Level of Block: C section

Procedures & Level of Block: Tourniquet

Procedures & Level of Block: Upper abdominal

—: transient radicular irritation, pain in the lower back or buttocks that may radiate to one or both legs after a spinal anesthetic

TNS

Absolute Contraindications to Regional Anesthesia: (8)

1.Infection @ site 2. Coagulopathy 3. Marked hypovolemia 4. True allergy to LA 5. Pt. refusal/inability to cooperate 6. Severe Stenosis 7. ↑ ICP 8. Abruption placentae

Relative contraindications to regional anesthesia (8)

1. Preexisting neurological dz 2. Back disorder (Ankylosis) 3. Heart Disease 4. Surgery above umbilicus 5. Failure to obtain free flow 6. Sepsis 7. Mobitz type I or II 8. 3rd degree w/o paceer

IV heparin; –need normal — before regional -Hold —hr after placement -Cathetars removed —/hr AFTER last heparin dose -Heparinization — hr after catheter removal

PTT ; 1 ; 2-4 ; 1

LMWH -first dose — hrs post op (2x daily dosing) -—hs post op (daily dose) -First dose — hours after catheter removal

24; 6-8 ; 2

Warfin- stop — days before surgery & INR —

4 ; < 1.5

Fibrinolytic or thrombolytic – — days

Ticlodipine – — days

Clopidorgrel- — days

GPIIb/IIIA – hold for — weeks post operative

↑potency of LA =↑—,↑DOA,↑affinity for Na channels,↑tendency of cardiac toxicity

protein binding

— local anesthetics are eliminated by plasma pseudocholinesterase except cocaine, which is eliminated by hepatic metabolism.

Ester

Metabolism of esters: greatest to least (3)

chloroprocaine > procaine > Tetracaine

Ester LA↑likely hood of allergic reactions d/t —

para-aminobenzoic acid

— local anesthetics are metabolized by hepatic metabolism.

Amide

Metabolism of amide LAs: greatest to least (5)

prilocaine >etidocaine > lido > Mepivicaine >Bup

— is the least toxic amide LA.

Prilocaine

Prilocaine is metabolized to —. It is an oxidizing agent capable of converting hemoglobin to methemoglobin

orthotoluidine

— is highly lipid soluble and dissociation form sodium channels are slow. Cardiac toxicity is high.

Bupivacaine

Mepivicaine, etidocaine, & bupivacaine = no enhancement w/ —

epi

—: an active metabolite of Lidocaine that contributes to toxicity even when lidocaine plasma levels are low

Monoethylglycinexylidide

Volatile anesthetics, propranolol, and cimetidine decrease hepatic clearance of —. (They inhibit Cytochrome P-450)

amides

Avoid Beta-blockers with amide LAs: & also…4

Labetalol & Propranolol ; Digitalis & Ca++ channel blockers

— is used to treat cardiac toxicity by amides.

Bretyllium

Max dose epi Subcutaneous or Submucosal infiltration: — mcg/kg for adults

2-3

Max Dose Epinephrine Subcutaneous or Submucosal infiltration: — mcg/kg for children

Max doses for chloroprocaine, cocaine, procaine, tetracaine:

12, 3, 12, 3

Duration for chloroprocaine:

.5-1 hr

Duration for tetracaine:

1.5-6hrs

Max dose with bupivicaine, lidocaine, mepivicaine, prilocaine, ropivicaine:

3, 4.5 (7 with epi), 4.5 (7 with epi), 8, 3

Cardiac Toxicity s/s of LA:

Hypoxia, hypercarbia, and acidosis

TNS: Transient Neurological Symptoms -with — LA spinals -Tx: —d/t sensory nature

Lidocaine ; NSAIDs

Lipid Rescue for LAST: — — ml/kg and then an infusion — ml/kg/min for 30-60 mins

20% Intralipid ; 1.2 to 2 ; 0.25

Benzocaine: Ester, Weak — May cause —

ACID ; methemoglobinia

Bld:Gas and Oil:Gas for N2O=

.47 and 1.4

Bld:Gas and Oil:Gas for sevo=

.65 and 53.4

Bld:Gas and Oil:Gas for iso=

1.4 and 90.8

Bld:Gas and Oil:Gas for des=

.42 and 18.7

Bld:Gas and Oil:Gas for Halo=

2.3 and 224

Vapor pressure for sevo=

170

Vapor pressure for iso=

239

Vapor pressure for des=

669

Vapor pressure for halo=

243

MAC for N2O=

104

MAC for sevo=

2.1

MAC for iso=

1.15

MAC for des=

6.3

MAC for halo=

.74

FA/FI for N2O=

.99

FA/FI for sevo=

.85

FA/FI for iso=

.73

FA/FI for des=

.91

FA/FI for halo=

.58

Increase potency = increase lipid solubility = — MAC

decrease

Oil/gas: measurement of —

solubility

Blood Solubility = — of uptake

speed

Inhalation agents: Increase solubility = — speed of inhalation induction Decrease solubility = — speed of inhalation induction

decrease ; increase

— = increase CBF, decrease CMR — = increase CBF, increase CMR — = decrease CBF, decrease CMR

Volatile ; Ketamine/N2O ; IV anesth

Vapor pressure of liquid dependent on SOLEY on —

temperature

Percentage of volatiles metabolized: Halothane —% Sevoflurane —% Isoflurane —% Desflurane —%

15-20, 2, .2, .02

CV side effects: sux

Decrease HR and histamine

CV side effects: mivacurium & atracurium

Histamine

CV side effects: d-tubocurarine & metocurine

Histamine, increase HR, decrease BP, ganglionic blockade

CV side effects: pancuronium & gallamine

Increase HR and increase BP

Sux elimination=

Metabolism

Atracurium, mivacurium, cisatracurium elimination:

Hoffman elimination

Vec and roc elimination:

Biliary primary, renal and metabolism secondary (vec has 20% in renal)

Brain uptake of anesthetics depends on: 4

1. Blood solubility 2. Cardiac output 3. Alveolar ventilation 4. Inspired concentration

Three ways to increase speed of equilibrium:

1. Increase Inspired anesthetic concentration 2. Second gas effect 3. Increase Alveolar ventilation

Two most important factors for increase alveolar partial pressure:

1. Inspired concentration 2. Blood solubility

Partial pressures of gas during induction: 4

Inspired>Alveolar>Arterial blood>Brain Note! This order is reversed during emergence when gas is turned off.

The — Theory explains that the anesthetic potency of anesthetic agents directly correlates with their lipid solubilities

Meyer-Overton

— of anesthetic at one atmosphere that produces immobility in 50% of patients exposed to a noxious stimulus. It is inversely proportional to potency.

MAC is the “Minimum Alveolar Concentration”

MAC ~ ED50 of —.

non-inhalational drugs

— MAC ~ ED95

1.3

There is approximately 1% — in MAC for every 1% of N2O delivery.

decrease

Highest Mac age is —

6mos-12mos

Seven factors that decrease MAC:

1. Increasing age 2. Hypothermia 3. CNS depressants 4. Acute ethanol intoxication 5. Alpha-2 agonists (Clonidine) 6. Pregnancy 7. Decrease Levels of CNS neurotransmitters

Five factors that increase MAC:

1. Hyperthermia 2. Hypernatremia 3. Increase Levels of CNS neurotransmitters 4. Young 5. Chronic alcohol use

Volatile anesthetics are metabolized in the — by — in hepatic microsomes.

liver ; cytochrome P-450

An oxidative trifluoroacetyl metabolite of — is thought to be responsible for acute hepatotoxicity in susceptible individuals. Reductive liver metabolism occurs with this volatile agent in the presence of hypoxia.

Halothane

— is the preservative in Halothane

Thymol

— is the most clinically important metabolite of Enflurane.

Fluoride

Inorganic — and — are common metabolites of Halothane and Enflurane.

fluoride and chloride

— is the only inhalational agent without a halogen.

N2O

Acceptable levels in the OR: N2O & Volatile together: N2O = — ppm Volatile = — ppm

25 ; 0.5

Acceptable levels in the OR: Volatile alone: Volatile = — ppm

N2O is metabolized to N2 in the intestine by — metabolism.

reductive anaerobic

Five contraindications to the use of N2O:

1. Venous air embolism 2. Ear surgery (middle ear) 3. Closed pneumothorax 4. Potential pneumocephalus 5. Bowel obstruction

Four adverse side-effect of N2O:

1. Aplastic anemia 2. Congenital anomalies 3. Spontaneous abortion 4. CNS toxicity

↓ methionine synthetase- — = no N2O

B12 deficiency

N2O — BP and CO when added to high dose opioids.

decreases

N2O — PVR and PA blood pressure due to mild sympathomimetic effects.

increase

— will support fire, but is neither flammable nor explosive.

N2O

N2O — CBF and — CMRO2

Increase and increase

Three renal changes associated with volatile anesthetics:

1. Decrease RBF 2. Decrease GFR 3. Decrease UO

— least potentiates NDMRs.

Halothane

— and — most decrease SVR, — has little effect on SVR.

Isoflurane and Desflurane ; Halothane

— and — produce the greatest myocardial depression.

Halothane and Enflurane

— and — most depress the baroreceptor reflex.

Halothane and Sevoflurane

— depresses the temperature-regulating center in the hypothalamus.

Isoflurane

Isoflurane, Desflurane, and Sevoflurane — cerebral metabolic rate.

decrease

N2O alone — cerebral blood flow & ICP.

increases

— and — most depress ventilation. — least depresses ventilation.

Enflurane and Desflurane ; Halothane

— is most degraded by soda lime and — least.

Sevoflurane ; Desflurane

— facilitates CSF absorption = favorable effect on CSF

Isoflurane

Point at which the plasma concentration of a drug is in equilibrium with all other tissues is the body

Steady-state

—: affinity and efficacy

Agonist

—: affinity for a receptor but lacks efficacy (cannot produce conformation Δ)

Antagonist

—: can be overcome by ↑ concentrations of agonist

Competitive

—: antagonism can’t be overcome by ↑ concern

Non-Competitive

—: bind with the receptor and has some efficacy, but it cannot elicit the maximal tissue response

Partial Agonist

—: but results in the opposite reaction of an agonist

Inverse Agonist

Constant AMOUNT of drug over a constant time ASA, phenytoin, ASA

Zero Order Kinetics

Constant FRACTION eliminated per time

First Order Kinetics

Dose response curve: —: determined by the binding affinity of receptors for the drugs as well as the efficiency of coupling of binding to response

Potency

Dose response curve: —: relationship between dose and effect

Slope

Dose response curve: —: maximum drug effect

Efficacy

—: Alter the molecular structure of a drug by modifying an existing functional group of a drug.

Phase I biotransformation

Phase I biotransformation: 3 functions

1. Oxidation 2. Reduction 3. Hydrolysis

Cytochrome P450 participates in most — and some —

oxidation ; reduction

—: Consists of a coupling or conjugation of a variety of endogenous compounds to polar chemical groups of the drug.

Phase II biotransformation

Biotransformation often makes drugs more — soluble and — for excretion in the urine or bile.

water ; inactive

Six groups of drugs metabolized by Cytochrome P450:

1. Barbiturates 2. Opioids 3. Benzodiazepines 4. Amide LA’s 5. Tricyclic antidepressants 6. Antihistamines

— Index = LD50/ED50

Therapeutic

— is the dose of drug that is effective in 50% of patients.

ED50

— dose that produce toxic effect in 50% of animals

TD50

— death to 50%

LD50

— = time taken for the plasma concentration to fall by one-half.

Elimination half-time (T 1⁄2)

T 1⁄2 is directly related to — and inversely related to —.

Vd ; Clearance (Cl)

Elimination half time equation =

Cl = Vd/ T 1⁄2

↑ Vd= ↑ T1/2

Fast CL=short T1/2

Small Vd=↓ T1/2

Slow CL= Long T1/2

—: Molecules that relay signals from receptors on the cell surface to target molecules inside the cell

Second messengers

Second messengers: 4

cAMP, cGMP, IP3, Ca++

Proteins Albumin = —

acid

Proteins Alpha-1 acid glycoprotein & Beta-globulins = —

Base

— is the major inhibitory transmitter of the CNS. It opens — ion channels. It hyperpolarizes neurons inhibiting action potential production.

GABA ; Cl-

—, —, —, and — work primarily on the GABA receptor.

Barbiturates, benzodiazepines, propofol, and etomidate

Opens Cl- channel- hyperpolarization

GABA receptor

Current research also indicates that inhaled anesthetics also work on — receptors.

GABA

— Prolong the attachment of GABA to its receptor. They work in the reticular activating system (RAS).

Barbiturates

— (acid) is 72-86% bound to albumin. It reduces the sensitivity of the central respiratory center to CO2. It’s onset is within 10-15 seconds. It’s elimination half-time is 11.6 hours. Metabolized by redistribution dependent on CO.

Sodium Thiopental

Sodium Thiopental: — CMRO2 & — CBF

Decrease and decrease

Sodium Thiopental: — steal

Inverse

Sodium Thiopental: reconstitute with — (no — bc precipitate)

Sterile saline ; LR

Sodium Thiopental: can cause this to pain

Hyperalgesia

S/S of intra-arterial Thiopental injection: 3

1. Arterial vasospasm with intense pain down the arm 2. Blanching of the skin with loss of distal pulses 3. Eventual cyanosis and possibly gangrene

Intra-arterial Thiopental injection is treated with —.

Phenoxybenzamine (Dibenzyline)

pH of Barbiturates is > —, pH of — is often cited.

9.0 ; 10-11

— are contraindicated in status asthmaticus and porphyria.

Barbiturates

— is associated with a higher incidence of hiccups than other non-opioid induction drugs.

Methohexital

Benzos: acid or base

Base

Benzos: Sedative: effects: the — amnesia: — and — anxiolytic effects: —, —, & —

cortex ; forebrain and hippocampus ; amygdala, hippocampus, & limbic system.

Benzos: — swallowing reflex & upper airway reflexes — CMRO2 & — CBF

↓; ↓; ↓

—- competitive antagonist of benzos

Flumazenil

Propofol: acid or base

Weak acid

Propofol: compound is —

2,6 diisoprorylphenol

Propofol: Liver metabolism —% & lung metabolism —%

70 ; 30

—: caution with soybean and egg allergy

Propofol

Etomidate: acid or base

Base

—: Maintains CV stability the best.

Etomidate

Etomidate: Directly depresses the —.

adrenal cortex

Etomidate: — cerebral blood flow, ICP, & CMRO2

Decrease

Venous thrombosis and phlebitis are most likely after —, —, & —.

etomidate, diazepam, & lorazepam

4 potential problems during recovery from etomidate:

1. Suppression of adrenocortical response to stress 2. N & V 3. Decrease Plasma cortisol concentration 4. Depressed immune response

Ketamine: acid or base

Base

Ketamine: Causes dissociation between the — and — systems by antagonistic actions on the — receptors.

thalamocortical and limbic ; NMDA

Ketamine: Dysphoria is cause by misperception and/or misinterpretation of auditory and visual stimuli by stimulating the — receptor, antagonizing the — receptor, and stimulating the — receptor.

kappa ; muscarinic ; sigma

Ketamine: ♥ Effects: — MAP, CI, PAP, CVP, HR

↑

Ketamine produces — airways

Bronchodilitation

Ketamine — airway secretions- give glyco

↑

Ketamine — emergence delirium in kids & higher bioavailability in kids

↓

Ketamine provides — for pain

Analgesia

Opioids: acid or base

Base

Opioids: shortest elimination 1/2 half (6)

Remi < alfent < morphine

Opioids: potency (6)

Sufent > remi > fent > alfent > morphine > meperidine

—: Less is protein bound in the neonate secondary to decrease in alpha-1 acid glycoprotein

Morphine

— Metabolite: morphine-6-glucuronide- prolonged in RF & crosses BBB by mass action

Morphine

Meperidine (Demerol): — myocardial contractility and — HR

decrease ; increase

Meperidine (Demerol): — shivering - — receptors

↓ ; Kappa

Meperidine (Demerol): — sz threshold (— having a sz) d/t —

↓ ; ↑ ; Normeperidine

Meperidine (Demerol): should be avoided with — & —

MAO inhibitors & Imipramine

Adverse S/S of — & — combined: 1. Hyperpyrexia 2. HTN 3. Hypotension 4. Respiratory depression 5. Skeletal muscle rigidity 6. Seizures 7. Coma ♥ Effects: ↓ HR,↓SVR,↓ venous return,↓ BP

MAO inhibitors & Demerol

Most clinically used opioids are relatively selective for — receptors.

Spinal analgesia is mediated primarily by — receptors, but also by kappa and delta receptors. Besides the substania gelatinosa (Rexed’s lamina II), the periaqueductal and periventricular gray areas are important sites of spinal analgesia.

Mu-2

Supraspinal analgesia is primarily mediated by — receptors, but also by kappa and delta receptors.

Mu-1

— receptors produce: 1. Euphoria 2. Miosis 3. Bradycardia 4. Hypothermia 5. Urinary retention 6. Pruritus

Mu-1

low abuse potential & Supraspinal analgesia common with — receptors.

Mu-1

- receptors produce: 1. Respiratory depression 2. Marked constipation 3. Physical dependence

Mu-2

high abuse potential & Spinal analgesia common with — receptors.

Mu-2

— receptors produce: 1. Sedation 2. Dysphoria

Kappa

4 Ventilatory effects of opioids:

1. Decrease Breathing rate 2. Decrease Minute ventilation 3. Decrease Response to CO2, secondary brainstem depression 4. Increase Arterial CO2 tension

—, —, & — can reverse opioid-induced sphincter of Oddi spasm.

Naloxone, Nitroglycerine, and Glucagon

— is eliminated faster than all other opioids (except Remifentanil) because it has a small —. The elimination 1⁄2 time is 10-30 minutes.

Alfentanil ; Vd

— is metabolized by blood and tissue nonspecific esterases.

Remifentanil

Can remifentanil be used for neuroaxial? And if not, why?

DO NOT use in neuroaxial - Has glycine buffer

Agonist-antagonist opioids —: provide analgesia —: reverse respiratory depression

Kappa ; Mu

Agonist-antagonist opioids: 3

Naltrexone, naloxone, nalbuphine

Muscle Paralyzation order: 5

Eye muscles → extremities→trunk→abd muscles→ diaphragm. Recovery is restored in reverse order

Facial muscle = — paralytic

diaphragm

— = readiness for intubation

Abductor pollis

Recovery from NMB = — nerve

ulnar nerve

MOA NMB:

Site of action is the motor end plate- nicotinic receptors

ALL MR resemble —

acetylcholine

Four NDMRs that release histamine:

1. d-Tubocurarine 2. Metocurarine 3. Atracurium 4. Mivacurium

— is metabolized by plasma cholinesterase. 25% spontaneous recovery is reached in 13 minutes in adults and 7 minutes in children.

Mivacurium

Method of anesthetizing a limb by IV injection while blood flow to extremity is occluded by a tourniquet

Bier Block

Bier Block: Minimum: — mins (don’t release before- local in systemic) Max: — min (usually d/t tourniquet pain)

15-20 ; 40-65

— is eliminated by ester hydrolysis and Hoffman elimination

Atracurium

— is only eliminated by Hoffman elimination.

Cisatracurium

Hoffman elimination is — & —dependent.

temperature and pH

Hoffman elimination: The rate of metabolism is slowed by — & — temperature.

acidosis or decrease temperature

— is a lipid-soluble metabolite of atracurium that can cause CNS stimulation in high concentrations.

Laudanosine

Four MRs that use renal excretion least:

1. Succinylcholine 2. Atracurium 3. Cisatracurium 4. Mivacurium

Three NDMRs not significantly excreted by kidneys:

1. Atracurium 2. Cisatracurium 3. Mivacurium

— is primarily eliminated by renal (70%) and secondarily by biliary (20%).

Pipecurium

What 5 things can augment NMB:

1. Hypermagnesium 2. Hypocalcemia 3. Hypokalemia 4. VA : des > sevoflurane > iso > N2O/fentanyl 5. Hypothermia

Eleven possible complications of Succinylcholine administration:

1. Hyperkalemia 2. Bradycardia (@ ♥ SA Node) 3. Increase HR and/or BP 4. Skeletal muscle myalgia 5. Allergic reaction 6. Triggering of MH 7. Sustained masseter muscle contraction 8. Myoglobinuria 9. Increase IOP (NOT prevented with defasculating dose) 10. Increase Intragastric Pressure (prevented with defasiculating dose) 11. Increase ICP (prevented with defasiculating dose)

Increase IOP (— prevented with defasculating dose) Increase Intragastric Pressure (— prevented with defasiculating dose) Increase ICP (— prevented with defasiculating dose)

NOT ; is ; is

Nine conditions that accentuate succinylcholine-induced hyperkalemia:

1. Unhealed third-degree burns 2. Denervation of skeletal muscle 3. Severe skeletal muscle trauma 4. Upper motor neuron injury (head injury, Parkinson’s, CVA) 5. Muscular dystrophy 6. Renal Failure w/ hyperkalemia 7. Severe Sepsis 8. Duchennes 9. Guillian Barre

11 clinical manifestations of MH:

1. Hypercarbia 2. Tachycardia 3. Tachypnea 4. Hyperthermia 5. Hypertension 6. Cardiac dysrhythmias 7. Acidosis (metabolic) 8. Hyperkalemia 9. Skeletal muscle rigidity 10. Myoglobinuria 11. Hypoxemia

The earliest sign of MH is —

increase ETCO2

Temperature may increase — C every — minutes

1-2 ; 5

— and — agents are triggering agents of MH.

Succinylcholine and volatile

— rigidity is an early sign of MH.

Masseter muscle

CPK > — confirms the diagnosis after masseter muscle rigidity following halothane and succinylcholine administration.

20,000

— contracture test is the standard diagnostic test for MH, but it has too many false positives.

Halothane-caffeine

Eight actions for initial management of MH:

1. Discontinue inhaled agents & Sux 2. Hyperventilate with 100% O2 3. Administer Dantrolene 4. Treat acidosis with NaHCO3 (1-2 mmoles/kg) 5. Decrease Body temp to 38C 6. Replace anesthesia circuit and CO2 absorber 7. Monitor ETCO2 & ABGs 8. Treat hyperkalemia and dysrhythmias if necessary

—: binds to the ryanodine-1 channel and inhibits the calcium channel in the sarcoplasmic reticulum. Decreasing the release of Ca++ from the sarcoplasmic reticulum in skeletal muscle and causes skeletal muscle to relax.

Dantrolene

Dantrolene: The initial dose is — mg/kg followed by — mg/kg boluses to a maximum dose of — mg/kg. The therapeutic blood level is 2.5 mcg/ml.

2.5 ; 1-2 ; 10

Vials of Dantrolene contain — mg and each is mixed with — ml of sterile distilled H2O.

20 ; 60

How often should dantrolene be repeated?

It should be repeated every 10-15 hours for three days.

Five dantrolene complications include:

1. Reoccurrence 2. DIC 3. Myoglobinuric renal failure 4. Skeletal muscle weakness 5. Electrolyte abnormalities

— is the best method to decrease Temp with MH.

Gastric lavage

—, 15 mg/kg is the best antiarrhythmic for MH.

Procainamide

The mortality rate of MH is —%

—: can mimic MH, but the onset and recovery are different. Patients treated with antipsychotic drugs such as Haldol, prolixin, or thorazine are susceptible to it.

Neuroleptic malignant syndrome

— is the cardinal sign for neuroleptic malignant syndrome.

Fever

Anticholinergic: —, - most ↑ HR

Atropine

Anticholinergic: —- most sedative

Scopolamine

Anticholinergic: — - does not cross BBB d/t being a quaternary

Glycopyrrolate

—: Combine reversibly w/ muscarinic cholinergic receptors prevent acetylcholine from binding to the receptor.

Anticholinergic

Anticholinergic: Sedative effect

Scopolamine > atropine > glycopyrrolate

Anticholinergic: Antisialogogues effect:

Scopolamine > glycol > atropine

Anticholinergic: HR:

Atropine > glycopyrrolate >scopolamine

Do not use scopolamine in —

GLAUCOMA

Anticholinergic: Bronchodilatory effects:

Ipratropium

Anticholinergics: gastric effects: — gastric secretions, — peristalsis and intestinal motility, — gastric emptying time, & — lower esophageal sphincter tone

↓ ; ↓ ; ↑ ;↓

—: Scopolamine & atropine both cross the blood-brain barrier and block muscarinic cholinergic receptors in the CNS, producing restlessness, hallucinations, somnolence, and potentially, unconsciousness.

Central anticholinergic syndrome

Central anticholinergic syndrome both caused by — and —.

Scopolamine & atropine

Central anticholinergic syndrome: Predisposed patients: —, —, and —

Tricyclic antidepressants (like amitriptyline), antipsychotics, and antihistamines (antimuscarinic characteristics)

Central anticholinergic syndrome: treatment:

physostigmine

Xanthines: 2

Aminophylline & theophylline

—: drug that cause release of norepinephrine from sympathetic postganglionic neurons and should be avoided with Halothane.

Xanthines

Halothane should be avoided with patients intoxicated with cocaine or using imipramine, because they both block reuptake of —.

norepinephrine

Calcium channel blockers and volatile agents act —

synergistically

Chemotherapy Medications and Site of Toxicity: Bleomyocin – —

Lungs

Chemotherapy Medications and Site of Toxicity: Cisplatin- —

Kidneys

Chemotherapy Medications and Site of Toxicity: doxorubicin -—

Heart

Chemotherapy Medications and Site of Toxicity: cyclophophains, streptozocin, Methotrexate-—

Liver

Calcium Channel Blockers work: Phase —, plateau phase of ventricular action potential Phase — of the pacemaker action potential

2 ; 4

4 Drugs to avoid with MAO inhibitors:

1. Tricyclic antidepressants (imipramine) 2. Opioids (especially Demerol) 3. Indirect acting sympathomimetics (ephedrine) 4. Fluoxetine

—: -Enhances myocardial contractility, decrease HR, & slows impulse propagation through the AV node. -Used to treat CHF & SVT

Digoxin: (Digitalis)

Digoxin: (Digitalis) MOA & phase

-Inhibits the Na+-K+ pump causing increasing intracellular Ca++ accumulation. -Work by decreasing Phase 4 depolarization of the SA node

— should be avoided because it creates a relative hypokalemia. Hypokalemia causes binding of digitalis to myocardial cells, resulting in an excessive drug effect.

Hyperventilation

Digoxin (digitalis): Eliminated primarily by the —, 35% daily

kidneys

—, —, & — increase the likelihood of digitalis toxicity.

Hypokalemia, hypercalcemia, and hypomagnesemia

Three side effects of tricyclic antidepressants: (Amitriptyline)

1. Anticholinergic effects (dry mouth, blurred vision, tachycardia) 2. Orthostatic hypotension 3. Sedation

Tricyclic antidepressants interact with: 5

1. Anticholinergics (atropine, scopolamine) 2. Sympathomimetics (ephedrine) 3. Inhaled anesthetics (increase dysrhythmias) 4. Antihypertensives (rebound HTN) 5. Opioids (increase analgesia & respiratory depression)

Anaphylactic Reaction: (Type I hypersensitivity reaction) Antibody — is produced in response to an antigen (foreign protein). Upon a second exposure to the antigen, it on the surface of mast cells and basophils triggers the release of mediators including histamine. This causes bronchoconstriction, upper airway edema, vasodilation, increased capillary permeability, and urticaria. Life-threatening.

Ig E (immunoglobulin E)

Anaphylactoid Reactions — involve Ig E. Foreign substances (i.e. drugs, hetastarch) directly stimulate the emptying of — & —.

do not ; mast cells and basophils

Anaphylactic and Anaphylactoid reaction = — S&S

same

Top 5 Causative of Anaphylactic Reactions

NMB 60% Latex 17% Abx 15% Colloids 4% Hypnotics 3-4%

Latex Allergy: food allergies: 4

bananas, avocados, chestnuts, stone fruit

Intrinsic Path =

XII, XI, IX, VIII (12,11,9,8)

Vitamin K Dep:

II, VII, IX, X (2,7,9,10)

Extrinsic =

III, VII (3,7)

CFs Not in Liver:

III, IV, VIII (3, 4, 8)

Final CP =

V, X, I, II, XIII (5,10,1,2,13)

Heparin = — pathway = — & — labs

Intrinsic ; aPTT & ACT

Coumadin = — pathway = — & — labs

Extrinsic ; PT & INR

Bleeding time : — min : — measure

3-10 min ; platelet function

PT : —sec : — measure

12-15 sec - extrinsic pathway

PTT : — sec : — measure

25-35 sec. – Intrinsic pathway

ACT : —sec

80-150 sec.

TT : —sec : — measure

9-11 sec. – final common pathway

One PRBC = ↑ Hct —% 1g/dl

3-4

1cc/kg PRBC= ↑ Hct —%

1 unit plts = ↑ — mm3

5,000-10,000

— = 1 complete blood volume in 24 hours

Massive transfusion

PRBC: universal donor and universal recipient

Donor: O & recipient: AB

Platelets: universal donor & universal recipient

Donor: AB & recipient: O

— drugs competitively inhibit vitamin K so synthesis of Vitamin K-dependent factors (II, VII, IX, and X) is diminished.

Coumadin

— is the fraction of plasma that precipitates when FFP is thawed at 40 C. (The drug of choice for — disease)

Cryoprecipitate ; Von Willebrand’s

Cryoprecipitate contains factors —

I, VIII, XIII

— inhibits plasmin and therefore inhibits the breakdown of fibrin.

Aprotinin

—: Contains all clotting factors but plts

FFP

FFP uses: 4

1. isolated coagulation factor deficiencies 2. reversal of Coumadin 3. liver dz- reverse coagulation issues 4. after massive transfusion and still bleeding

Max allowable EBL = equation

EBV x [(Hbi-Hbf)/Hbi]

Hct = — x Hbg

Hct of PRBC = —

PRBC replacement= equation

[(blood loss - MABL) x desired Hct]/Hct of PRBC

Estimated Blood Volume (EBV): Premie (

95ml/kg

Estimated Blood Volume (EBV): term

90ml/kg

Estimated Blood Volume (EBV): infant (< 6wks)

80 ml/kg

Estimated Blood Volume (EBV): toddler (6wk-2yr)

Estimated Blood Volume (EBV): child (2yr-12yr)

72 ml/kg

Estimated Blood Volume (EBV): men

75 ml/kg

Estimated Blood Volume (EBV): women

65 ml/kg

Total Body Water (TBW): adult

60% ; 42 L

Total Body Water (TBW): neonate

80%

Total Body Water (TBW): premie

90%

ICF: % and L

60-66% ; 25-28 L

ECF: % and L

33-40% and 14-17 L

Interstitial fluid %

80%

Plasma water %

20%

—: pH 6.5 - contains K 4, Na 130,lactate 28– hypo (osm 273)

Too much of this fluid = metabolic alkalosis

— : Na = 154 meq/L = Isotonic (osmol = 308)

Too much of this fluid = hyperchorlemic acidosis

—: Hypotonic (osmolality 252 mOsm)

—- colloid osmotic pressure of 20mmHg

5% Albumin

—- No Ca++ (osmol 294)

Normosol

—: 6% hydroxyethyl starch in NS =/> 20ml/kg/day = ↑ serum amalayse levels

Hespan

—- 6% hydroxyethy starch in solution w/ electrolytes, glucose and lactate

Hextend

Hypotonic ~ <— mOsm/L - — vascular volume

285 ; ↑

Hypertonic ~ > — mOsm/L - — cells shrink

305 ; ↓

—: Improves blood flow through the microcirculation presumably by decreased blood viscosity. Maximal dose = 20 ml/kg/day or about 58 ml/hr for 70 kg patient. -Side effects: interference with blood typing, prolonged bleeding time, renal failure, and anaphylactoid reactions.

Dextran 40

Five adverse effects of Mannitol administration:

1. Pulmonary edema and Cardiac decompensation 2. Rebound increase ICP 3. Hypovolemia 4. Hyperkalemia 5. Hyponatremia

Virchow Triangle:

1. endothelial injury 2. stasis or turbulent blood flow 3. hypercoagulability of blood

—: A hereditary hemolytic anemia resulting from the formation of an abnormal hemoglobin (Hb S). Red cell survival is reduced to 10-15 days, compared with up to 120 days in normal individuals. It occurs only under extreme hypoxemia or in low-flow states.

Sickle Cell Disease

Avoid in Sickle Cell Disease: 6

1. hypo- and hyperthermia 2. acidosis 3. mild degrees of hypoxemia 4. hypotension 5. hypovolemia 6. avoid the use of tourniquets.

Sickle Cell Anemia is a mutation of the — globin chains – glutamic acid instead of valine

beta

Four diseases associated with thrombocytopenia:

1. Chemotherapy or unrecognized cancer 2. Liver disease and splenomegaly 3. DIC 4. Pre-eclampsia

—: Metabolic d/o affecting biosynthesis of heme = thick blood

Porphyria

Porphyria Signs & Symptoms: 3

1. Acute abdominal pain, N & V 2. Neurotoxicity: confusion, SIADH, difficulty swallowing, HTN & tachycardia 3. Sensory & motor neuropathies

AVOID Triggering Agents for porphyria: “—”

KEPT MAN Barbs, Nifedipine, Phenytoin, Benzos, Ketorolac, Hydralazine, Ketamine, Enflurane, mepivicaine, Etomidate, Sulfamides, lidocaine GA- no regional

Hemophilia : x-lined recessive —- Factor VIII Deficiency —- Factor IX Deficiency

A ; B

Hemophilia : Prolonged — & normal —

Prolonged PTT & normal PT

Heat loss:

Radiation >Convection >Evaporation >Conduction

The center for Heat Loss is located in the — hypothalamus

anterior (preoptic)

Heat Gain center is located in the — hypothalamus.

posterior

Greatest decrease of core temp occurs in — of surgery

1st hour

— – from atrial muscle in response to local wall stretch

ANP- atrial

—- ventricle muscle when distended

BNP- brain

—- endothelial walls natriuretic peptides

CNP

Natriuretic Peptides: Induces — of arterial and veins = — RBF & GFR

vasodilatation ; ↑

Natriuretic Peptides: -Suppress actions of —, —, — -Inhibit – —, —, —

NE, angiotensin, endothelin ; renin, angiotensin II, aldosterone

↑ — & — = mortality predicator in CHF

ANP & BNP

4 Reasons for difficulty breathing after Thyroidectomy:

1. Laryngeal edema 2. Bilateral cord paralysis 3. Hematoma formation 4. Hypocalcemia secondary to hypoparathyroidism

Six hormones of the Anterior Pituitary: (Adenohypophysis) (Blood flow through Hypothalamic-Hypophyseal Portal System)

1. Adrenocorticotropic hormone (ACTH) 2. Thyroid stimulating hormone (TSH) 3. Growth hormone (GH) 4. Prolactin 5. Leutinizing hormone (LH) 6. Follicle stimulating hormone (FSH)

2 hormones of the Posterior Pituitary: (Neurohyphosis)

1.Anti-Diuretic hormone (ADH) 2. Oxytocin

Thyroid: Regulated by — release from anterior pituitary

TSH

Thyroid: —% Thyroxine (T4) —% Tri-iodothyronine (T3)

93 ; 7

About 80% of Tri-iodothyronine (T3) is produced outside the thyroid gland by — of thyroxine.

de-iodinazation

Tri-iodothyronine (T3) is —x — potent than thyroxine (T4).

four times more

T4 is converted to T3 in the —

tissues

Thyroglobulin = —

protein

Grave’s Disease: (—)

Hyperthyroidism

— is the drug of choice for treating hyperthyroid-related ventricular dysrhythmias.

Beta antagonist

S/S of —: 1. Intolerance to heat 2. Increase Sweating 3. Mild to extreme weight loss 4. Varying degrees of diarrhea 5. Muscular weakness 6. Nervousness 7. Extreme fatigue 8. Inability to sleep 9. Tremor of the hand 10. Exothlamous

Grave’s Disease: (Hyperthyroidism)

Four causes of Hypothyroidism:

1. Subtotal lobectomy of thyroid 2. Goiter 3. Autoimmune disease (myxedema) 4. Radiation therapy of thyroid (Can cause cretism in infant = large tongue)

S/S —: 1. Slow mental function 2. Slow movements (weight gain) 3. Dry skin 4. Cold intolerance 5. Depressed ventilatory responses 6. Abnormal cardiac conductivity (decrease cardiac function) 7. Renal disease

Hypothyroidism

—: ↓ Anesthesia requirements – however, no Δ in MAC

Hypothyroidism

—: Severe exacerbation of hyperthyroidism

Thyroid Storm

Thyroid Storm: S/S - — hrs. post-op

6-8

— s/s: 1. Hyperthermia 2. Tachycardia 3.CHF 4. Dehydration 5. Shock 6. Hyperglycemia

Thyroid Storm

Thyroid Storm Tx:4

Na Iodide, cortisol, propranolol, Propylthiouracil

—: Regulates Ca++ & Phosphate

Parathyroid

Parathyroid hormone increase [Ca++] by: 1. Increase Absorption of Ca++ from — 2. Increase Reabsorption of Ca++ from — 3. Increase Resorption of Ca++ from —

intestine ; renal tubule ; bone

Complications of —: 1. Hypocalcemia 2. Parasthesias 3. Muscle spasm 4. Tetany 5. Laryngospasm 6. Bronchospasm 7. Apnea 8. Hematoma 9. Airway compromise 10. Pneumothorax

Parathyroidectomy

Major postop concern after Parathyroidectomy: 4

1. Airway obstruction 2. Laryngospasm secondary hypocalcemia 3. Bilateral recurrent laryngeal nerve damage 4. Hematoma

Ca > — mEq/L Ionized Ca++ >— mEq/L

5.5 ; 2.5

— is a bone disease caused by hyperparathyroidism. Leaking of Ca out of bones= broken and brittle bones

Osteitis Fibrosa Cystica

— promotes the deposition of calcium in the bones and decreases [Ca++] in the ECF. (opposite of PTH)

Calcitonin

Clinically significant hypocalcemia: 2

1. ECG changes (prolonged Q-T interval) 2. decrease Myocardial contractility

S/S of — following parathyroidectomy: 1. Perioral parasthesias 2. Restlessness 3. Neuromuscular irritability

hypocalcemia

3 Neuromuscular irritability seen from hypocalcemia following parathyroidectomy:

Chvostek’s sign Trousseau’s sign Inspiratory stridor

Four effects of acidosis on CNS function:

1. Depressed neuronal activity (coma) 2. Cerebral vasodilation (increase CBF, increase ICP) 3. Decrease Cerebral perfusion pressure (cerebral ischemia) 4. Increase Seizure threshold

Anion Gap: = equation

[Na+] – [Cl-] + [HCO3-]

Anion Gap: Normal range = — mEq/liter

9-15

Anion gap: Used in the differential diagnosis of —

metabolic acidosis

Four causes of metabolic acidosis:

1. Ketoacidosis 2. Lactic acidosis 3. Renal failure 4. Toxic dose of salicylates

Three causes of Metabolic Alkalosis:

1. Vomiting 2. NG suctioning 3. Hypokalemia secondary diuretics

Plasma K+ increase approximately — mEq/L for each 0.1 decrease in pH

0.6

The kidneys excrete H+ as titratable acids — & —

H2PO4 & NH4+

Six physiologic functions that require Ca++:

1. Action potentials in smooth and cardiac muscle 2. Blood coagulation 3. Bone formation 4. Muscle contraction 5. Membrane excitability (Ca++ controls threshold) 6. Neurotransmitter release- Ca is REQUIRED

A rapid decrease in plasma — leads to skeletal muscle spasm (laryngospasm) and tetany.

[Ca++]

Nine S/S of —: 1. Numbness 2. Circumoral paresthesia 3. Confusion 4. Seizures 5. Hypotension 6. Increase LV filling pressures (due to decrease contractility) 7. Prolonged QT interval 8. Skeletal muscle weakness 9. Fatigue

Hypocalcemia

— (contracture of facial muscle with tapping) monitors hypocalcemia

Chvostek’s sign

Three ECG changes with Hypocalcemia:

1. Prolonged QT interval 2. Increase ST segment duration 3. Flat or inverted T-waves

7 Functions of Magnesium:

1. Functions as a cofactor in many enzyme pathways 2. Regulates the Na+/K+ pump 3. Regulates adenylate cyclase 4. Regulates slow Ca++ channels 5. It antagonizes Ca++ (an endogenous Ca++ channel blocker) = vasodilatation 6. Controls the threshold potential (membrane stabilizer) 7. Regulation of the release of acetylcholine from nerve terminals

—: (It both resembles and antagonizes Ca++)

Magnesium

↑ Mg = — excitability

↓

— Caused from: excess dietary intake of it, excess ingestion of oral antacids, hypothyroidism, hyperparathyroidism, Addison's disease, & lithium therapy

Hypermagnesemia

Tx for hypermagnesemia: 2

forced diuresis with saline and loop diuretics

—: Impairs coagulation by causing platelet dysfunction. Impairs ventricular contractility & leukocyte function.

Hyperphosphatemia

Causes of —: 1. Ingestion of large # antacids containing aluminum & Mg 2. Severe burns 3. DKA 4. ETOH WD 5. Prolonged respiratory alkalosis

hypophosphatemia

hypophosphatemia Tx: 4

aluminum based antacids, Carafate, Ca citrate, dialysis

Eight signs of Hyponatremia:

1. Arrhythmias 2. Hypotension 3. Pulmonary edema 4. Mental changes 5. Muscle cramps 6. Weakness 7. Myoclonia 8. Edema

Hypernatremia = — is what hydration status?

dehydration

Treatment of hyponatremia: 2

diuretics and hypertonic saline

S/S develop with [Na ] < — mEq/L

120

Three factors that promote Hypokalemia:

1. Alkalosis 2. Insulin 3. Beta-2 adrenergic stimulation

Seven ways to treat Hyperkalemia:

1. Give calcium gluconate 2. Give glucose/insulin 3. Give sodium bicarbonate 4. Give diuretics (to increase excretion) 5. Give kayexalate (potassium exchange resins) 6. Use hemodialysis 7. Hyperventilate the patient

Plasma [K+] is decrease — mEq/L for each 10 mmHg decrease in PaCO2

0.5

Cardioplegia – — mEq/L of K+

15-40

— should be given to the hyperkalemic pt. when ventricular dysrhythmias appear. (↑ threshold away from RMP)

Calcium

5 Medications that cause an ↑ K:

Triamterene, spironolactone, NSAIDs, ACE inhibitors, BB

ECG Δ with Hyperkalemia: 3

Prolongation of P-R interval Widening of QRS Peaked or tented T waves

ECG Δ with Hypokalemia 3

Prolongation of P-R & Q-T interval Flattening of T waves Appearance of prominent U wave

—: glucocorticoid & mineralocorticoid deficient

Addison’s disease

— - autoimmune destruct of the adrenal cortex

Hypoadrenocorticism

—: S/S 1. Hypotension 2. Hyponatremia 3. Hyperkalemia 4. Hypoglycemia (secondary decrease cortisol levels) 5. Hemoconcentration (d/t to ↑ H2O excretion 2nd to hyponatremia) 6. Skin pigmentation

Addison’s disease

2 electrolytes to indicate decrease in aldosterone:

Hyponatremia and hyperkalemia

Give — intraop for Addison’s disease

glucocorticoid

—- ↑ cortisol & ↑ ATCH in anterior pituitary

Hyperadrenocorticism

— disease: Hypoadrenocorticism

Addison’s disease

— disease: Hyperadrenocorticism

Cushing’s disease

— S/S: 1. HTN (secondary to Na retention) 2. Hypokalemia 3. Hyperglycemia (20 increase cortisol levels) 4. Moon face & buffalo hump 5. Skeletal muscle weakness 6. Skin pigmentation

Cushing’s disease

— Disease: Primary hyperadolteronism

Conn’s Disease

Conn’s Disease electrolytes :

↑ Na+ ↓ K+

—: Tumor of the adrenal medulla chromaffin tissues which results in an ↑ catecholamine release

Pheochromocytoma

— S/S: 1. Paroxysmal HTN 2. Diaphoresis 3. Tachycardia 4. Headache

Pheochromocytoma

Pheochromocytoma Tx: 2

α block- phenoxybenzamine 20-30mg/day &↑to 60-250mg/day β block- tx for tachy

3 drugs to Avoid in Pheochromocytoma:

Trimethaphan, droperidal, histamine

—: A group of syndromes characterized by tumor formation in several endocrine organs.

Multiple Endocrine Neoplasia: (MEN)

MEN — = tumors in pancreas, pituitary gland, & parathyroid gland

MEN — = medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism (type IIa) or multiple mucosal neuromas (type IIb or type III)

Kidney: —% CO

25-30

Kidney: 4 Functions:

1.ECF composition 2. Maintenance of EFV- NA & H2O excretion 3. Endocrine 4. Regulation of arterial BP

ECF composition: Osmolality: — mOsm/kg Urine osmolality — mOsm/kg H2O

285-305 ; 50-1200

Erythropoietin- CRF = —

anemia

— System- BP reg, Na/K excretion

RAA

Vitamin D: CRF = —

hypocalcemia

RBF = equation

(MAP- Venous Pressure) x Vascular resistance

Labs: — is single best indicator of renal status

Creatine Clearance

Creatine: — mg/dl BUN: —mg/dl

0.7-1.5 ; 10-20

GFR: nml —ml/min, mild dsyfx —, mod dsyfx —, failure — ml/min

95-150 ; 50-80 ; <25 ; <10

Glomerulus: freely filters 4

Na, Cl, K & H2O

Proximal tubule: —% of glomerular filtrate

Proximal tubule: reabsorbed —, ONLY place permeable to —

H2O > Cl > Na = K ; glucose

Descending LOH: filters 2

Urea & H2O (no Na, Cl or K)

Descending LOH: Osmotic gradient via —

countercurrent multiplier

Ascending LOH: Filters 3

Na, Cl, K – No H2O in thick branch

Loop Diuretics – — inhibit reabsorption

Na+, K+, 2CL-

Lasix ↑ —= — = ↓BP

prostaglandins ; venodilitation

Loop Diuretics –Side effects: 4

↓ K, fluid volume deficit, orthostatic HoTN, reversible deafness (CNVIII)

Distal Tubule: Filters 2

Na & Cl (No K or H2O)

Distal Tubule: Early: drug —: — K

Thiazides: ↓ K

Distal Tubule: Late & CC: drug —: — K

Potassium Sparing Diuretic: ↑ K

5 drugs that affect late distal tubule:

Triamterene, amiloride Spiratalctone ADH & Aldosterone

CollectingDuct: filter 4

Na & Cl-out, K-In, Low perm H2O, (no urea)

CollectingDuct: Site of Action — & —

ADH & Aldosterone (principle cells)

6 Nephron Sections:

1. Glomerulus 2. Proximal tubule 3. Descending LOH 4. Ascending LOH 5. Distal tubule 6. Collecting duct

3 nephrons sections in Cortex:

Glomeruli, Proximal Tubules, Distal Tubules

2 parts of the nephron in Medulla:

loops of Henle, Collecting Ducts

—= most vulnerable to ischemia of nephron

Inner stripe of the outer medulla

Carbonic Anhydrase Inhibitor: —

Acetazolamide(Diamox)

Carbonic Anhydrase Inhibitor: Acetazolamide(Diamox)-↓ — 2 to ↓ — formation

IOP ; aqueous humor

Acetazolamide(Diamox)- Inhibit — in — tubule = — Na reabsorption = diuresis – — Metabolic Acidosis

carbonic anhydrase ; proximal ; ↓ ; Hyperchorlemic

Mannitol:— Osmotic pressure in renal tubule= — reabsorption of H2O

↑ ; ↓

Mannitol: S/E: —

↓ K +

Renal Failure: S/S & lab findings normal until —% ↓ in Fx

Anuric: UO — Oliguric: UO — NonOliguric: —

<100ml/day or < 0.5ml/kg/hr ; 100-400 ml/day ; UO >400ml/day

Renal Failure: Electrolytes: —

↑ K, Mg, Phos, ↓Ca , Na , metabolic acidosis

Renal Failure: — is # 1 issue and cause of death

Infection

— DA1 agonist

Fenoldapam

Fenoldapam DA1 agonist: — RBF (6x more potent than —)

↑ ; dop

Renal Failure: Avoid — & —

Meperidine & Morphine (metabolite-6)

—: (vasopressin)

ADH

ADH: (vasopressin) : — Concentration

NA+

ADH: (vasopressin) : Synthesized Periventricular and Supraoptic nuclei of the — , stored in and released from the — (neurohyposis).

hypothalamus ; posterior pituitary

ADH: (vasopressin) : where does it work and effect 3

1. Primary on collecting ducts in the nephron = passive water reabsorption 2. Vascular smooth muscle and cardiac myocytes. 3.Dramatic vasoconstriction and has an inotropic effect

— Released in response to increase ECF osmolarity, decrease plasma volume, & drugs, stress, HoTN, Pain, CPAP, PEEP, VA, Trauma

ADH (vasopressin)

ADH (vasopressin): Works in the — & — to increase H2O reabsorption

distal tubule & collecting duct

In the absence of ADH the collecting duct and distal tubule are impermeable to — ie: excretion happens.

H2O

ADH = — = — (concentration)

Osmolality ; increase [Na+]

Extra Cellular Fluid Volume: — = ECFV

Na+

Aldosterone: controls —

VOLUME

Aldosterone: It controls — volume and works in the — & — tubule.

intravascular ; collecting duct and the late distal convoluted

Aldosterone: — Na+ reabsorption, and K+ —.

Increases/conserved ; secretion/excretion

—: Release is triggered by Angiotensin II and increase [K+]; also increase ACTH and low serum Na+. It also regulates the total amount of Na+.

Aldosterone

— is secreted by the zona glomerulosa of the adrenal cortex.

Aldosterone

— (a mineralocorticoid)

Aldosterone

— (a glucocorticoid)

Cortisol

— is secreted by the zona fasciculata, the middle zone of the adrenal cortex.

Cortisol

—, —, & — are catecholamines released from the adrenal medulla.

Epinephrine (80%), norepinephrine (20%), and dopamine

Epinephrine (80%), norepinephrine (20%), and dopamine are catecholamines released from the adrenal medulla. This is controlled by — preganglionic neurons that release — to — receptors.

sympathetic ; acetylcholine ; nicotinic

3 Stimuli for the release of Renin:

1. Decrease Renal perfusion pressure 2. Hyponatremia 3. Sympathetic NS stimulation of beta-receptors in JG apparatus

Normal GFR = — ml/min

125

Clinical features of Diabetes Insipidus: — - HALLMARK

Polyuria, > 2-15 L/day

3 Clinical features of Diabetes Insipidus:

1. Polyuria, > 2-15 L/day- HALLMARK 2. Hypernatremia (plasma hyperosmolality) 3. Dilute urine (osmolality < 200 mOsm/kg)

S/S of —: 1. Polydipsia (increase thirst) 2. Polyuria – (2-15L/Day) HALLMARK 3. Hypernatremia 4. Hypovolemia 5. Hypotension 6. ↓ Urine osmol (<200 mosm/kg) 7. ↓ specific gravity (1.005 or less)

Diabetes Insipidus

3 Diagnosis of SIADH: ↑ ADH

1. Decreased plasma osmolality (< 270 mOsm/kg) 2. Increase urine [Na+] (> 100-150 mOsm/kg) 3. Hyponatremia d/t retention of H2O

SIADH: Tx: —4

remove underlying cause, Limit H2O , 3% Saline, demecolcine

Liver: —% CO

Liver: Blood Flow: —% Portal vein - splenic & mesenteric —% Hepatic artery

70 ; 30

“—” An increase in hepatic arterial flow in response to a decrease in portal blood flow (1) to maintain hepatic O2 supply, and (2) to maintain total hepatic blood flow, which is essential for clearance of many compounds.

Arterial Buffer Response

Hepatic Blood Flow Arteries: —, —, —, & —

α-1, β-2, D1 &cholinergic

Hepatic Blood Flow Arteries: Blood flow receptors: —

Ohms

Hepatic Blood Flow Veins: — & —

α-1 & D1

Hepatic Blood Flow Veins: blood flow depend on — & —

GI & Spleen

Hepatic Blood Flow Arteries: — % of Blood flow, —% of oxygen supply

30 ; 50

Hepatic Blood Flow Veins: —% of blood flow, —% of oxygen supply

70 ; 50

Seven functions of the Liver:

1. Storage and filtration of blood (500ml) 2. Metabolic functions such as carbo, fat, and protein metabolism 3. Secretion of bile 4. Storage of vitamins 5. Blood coagulation 6. Storage of iron 7. Detoxification & excretion of drugs

P450’s Inducers: 7

chronic ETOH, barbs, ketamine, benzo’s, phenytoin, cigarette smoke, St. Johns wort

P450’s Inhibition: 4

cimetidine, chloramphemocel, fluoxetine, grape fruit Bile vomitus is usually alkaline

Puke your acids = —

alkalosis

Poop your bases = —

acidosis

Alcoholic Hepatic Issues/Liver Disease: 4

Thrombocytopenia, leukopenia, anemia, megoblastic anemia d/t folate deficiency

Maintain BP- ETOH depends on — FLOW

ARTERIAL

Alcoholic Hepatic Issues/Liver Disease: —- agent of choice

Isoflurane

Alcoholic Hepatic Issues/Liver Disease: — Vd= — loading dose, — main = prolonged Vec, Roc, Pan

↑ ; ↑ ; smaller

Alcoholic Hepatic Issues/Liver Disease: prolonged —

Vec, Roc, Pan

Alcoholic Hepatic Issues/Liver Disease: Labs: — total bilirubin,—AST/ALT (ALT more sensitive), — albumin & PT

↑ ; ↑ ; ↓

Alcoholic Hepatic Issues/Liver Disease: Hemodynamics: —SVR, —CO, —circ blood volume, —portal blood flow, — plasma osmotic pressure

↓ ; ↑ ; ↑ ; ↓ ; ↓

— Syndrome: (aspiration pneumonitis)

Mendelsons

Mendelsons Syndrome: (aspiration pneumonitis) Gastric pH < — Gastric volume < —

2.5 ; 25 ml

Seven conditions that delay gastric emptying:

1. Obesity 2. Pregnancy 3. Opiods 4. Diabetes mellitus 5. Trauma 6. Pain 7. Anxiety

Drugs that ↓ LES Tone: (↑ risk of aspiration)

1. Anticholinergics 2. Dopamine 3. Thiopental 4. Opioids 5. Propofol 6. Tricyclic antidepressants 7. Sodium nitroprusside

5 Patients who benefit from antiemetics:

1. Eye surgery patients 2. Gynecological patients 3. Obese patients 4. History of vomiting 5. ECSW Lithotripsy

Antiemetics: Competitive Dopamine Antagonists; 3

Droperidal, Compazine, Metoclopramide

Competitive Dopamine Antagonists; Droperidal, Compazine, Metoclopramide: Do not give to — Patients

Parkinson’s

Droperidol: 1. An antiemetic (secondary — blockade) 2. Produces extrapyramidal signs (secondary — blockade) 3. May decrease BP (secondary weak — blockade)

dopamine ; dopamine ; alpha

Treatment for droperidol-induced extrapyramidal symptoms is an 4

anticholinergic (Benadryl or benztropine, Cogentin).

Droperidol: Do not give to: — or —

Pheo or Parkinsons

Metoclopramide: (NO Δ in — )

Metoclopramide: 1. — pyloric sphincter 2. — gastric motility = ↑ gastric emptying 3. — LES tone = ↓ reflux 4. — the small intestine 5. Has — actions

Relaxes ; Promotes ; Increase ; Relaxes ; antiemetic

Metoclopramide: also inhibits —

plasma cholinesterase

Metoclopramide: Used to treat: 4

Diabetic gastroparesis Reflux esophagitis Pts. at risk for aspiration pneumonitis (Mendelsons syndrome) Parturients

Drugs that — gastric pH and — gastric volume: (H2 blockers)

Increase ; decrease

3 H2 blockers:

1. Cimetidine (Tagamet) 2. Ranitidine (Zantac) 3. Famotidine (Pepcid)

Which H2 blocker inhibits p-450 the most?

Cimetidine (Tagamet)

Which H2 blocker is the most potent?

Ranitidine (Zantac)

Proton pump inhibitors: - inhibits the — pump -—secretion of HCl into the lumen of stomach

hydrogen ; ↓

— : proton pump inhibitor

Omeprazole

most powerful agent for ↓ acid secretion

Proton pump inhibitor (omeprazole)

—: Raise gastric pH by neutralizing HCl also ↑ gastric volume

Antacids

How fast is antacids effect?

Immediate

How long does antacids loose effectiveness?

30-60min

Chemoreceptor Zone: —

4th ventricle (area posterema)

4 Neurotransmitters & Receptors in N/V:

Dopamine & DA-2 Serotonin & 5-HT Acetylcholine & muscarinic Substance P & NK-1

—: S/S caused by vasoactive substances released from enterochromaffin tumors or carcinoid tumors

Carcinoid Syndrome

Carcinoid Syndrome: Most carcinoid tumors are in —

GI tract- especially appendix

Carcinoid Syndrome: Cause overproduction: 5

serotonin-hallmark, bradykinin, histamine, kallikrein, prostaglandins

Carcinoid syndrome hallmark overproduction?

Serotonin

Carcinoid syndrome: Avoid activating tumor causing: 3

HoTN, catecholamine release, histamine releasing medications

Five clinical manifestations of nonintestional tumors:

1. Cutaneous flushing 2. Bronchospasm 3. Diarrhea 4. Large BP swings 5. Supraventricular dysrhythmias

— used to blunt vasoactive and bronchoconstritive effects of carcinoid syndrome

Octreotide (somatostatin)

Pancreas: Beta cells: — Alpha cells: — Delta cells: —

insulin ; glucagon ; somatostatin

Evaluation of pancreatitis: 3

1. Malnutrition 2. Abnormal liver FX 3. ETOH WD (alcoholism frequent cause of pancreatitis)

Symptoms of pancreatitis: 4

1. Dehydration 2. Hypocalcemia 3. Hyperglycemia 4. ARDS Alcoholism is a frequent cause of pancreatitis.

5 “F’s” of Cholelathiasis:

1. Fat 2. Female 3. Fertile 4. Forty 5. Fair

— is not needed by brain or RBC to utilize glucose

Insulin

—: Insulin secreting tumor causing massive insulin release.

Insulinoma

Insulinoma: —- during resection —- after resection Check Blood sugar every — mins

Hypoglycemia ; Hyperglycemia ; 15

Diabetic Neuropathy: Anesthetic considerations: 3

orthostatic Hotn, Silent MI, Gastroparesis

Diabetic Neuropathy: HR response blunted w/ use of —

antimuscurinics - Atropine

Normal A1C = — %

DM with autonomic neuropathy: 6 Cardiac Concerns

Orthostatic Hotn, Resting tachycardia, absence of beat to beat variability in HR, dysrhythmias, silent MI, painless myocardial ischemia

DM with autonomic neuropathy: HR response blunted in these medications: 2

Antimuscarinics & Beta-Blockers

MOA of DM neuropathy: High concentrations of glucose are converted to — within nerve via the polyol pathway. The high levels of it (and fructose) that develop — ATP→ — NO levels. Because this acts as a vasodilator, the loss of it leads to unopposed vasoconstriction and ischemia of the nerve

sorbitol ; ↓ ; ↓

—: Where T-Lymphocytes mature

Thymus

— is most commonly removed d/t Thyoma & MG

Thymus

Thymus removal has Pneumo most likely on — side

RIGHT

Scoliosis: — curvature of the spine

Lateral

Scoliosis: — lung dz

Restrictive

Scoliosis: most likely to have this heart issue

Mitral valve prolapse

—: Painless degenerative & atrophy of skeletal muscles

Muscular Dystrophy

Muscular Dystrophy: — (most common & severe)- x-linked, recessive

Duchene’s

Muscular Dystrophy (Duchenne’s): EKG- — PR, QRS, ST abnormalities, BBB, Q waves, R waves (tall), CHF

prolonged

Muscular dystrophy (Duchene’s): Resp: —TLC & RV, recurrent pulm infections

↓

Muscular Dystrophy (Duchene’s): NO — (↑MH)

succs

—: Random & multiple sites of demyelination of corticospinal tracts in brain & SC (NO PERIPHERY)

Multiple Sclerosis- MS

Multiple Sclerosis- MS: No — (may exacerbate)

spinals

Multiple Sclerosis- MS: Avoid – rises in —

temps

Multiple Sclerosis- MS: — in response to Succs

Hyperkalemia

—: Loss of dopanergic fibers basal ganglia (dop is a inhibitory NT)

Parkinson Disease

—: s/s: skeletal muscle rigidity, resting tremor, diaphragmatic spasm

Parkinson Disease

Parkinson Disease tx:

Levodopa

Parkinson Disease: Avoid: 3

droperidal, reglan, Compazine

—: Chronic inflammation disease w/cervical vertebral involvement

Rheumatoid Arthritis

Rheumatoid Arthritis: -—lung disease, pulmonary fibrosis, FOB, pulm fx test -Hoarseness or stridor – — involvement

Restrictive ; Cricoarytenoid

—: Cyanide binds to cytochrome oxidase resulting in inhibition of oxidative phosphorylation causing inhibition of cell respiration.

Cyanide Toxicity:

Cyanide Toxicity: caused by administration of —

Nitroprusside

—: Chronic autoimmune @ NMJ, weakness

Myasthenia Gravis- MG

Myasthenia Gravis- MG: Tx: 3

steroids, anticholinesterase meds, plasma phoresis

Myasthenia Gravis- MG: Avoid —

muscle relaxants

—: A disorder of neuromuscular transmission associated with carcinomas. An autoimmune disease in which immunoglobulin G (IgG) antibodies against voltage-gated sodium channels cross-react with calcium channels at the neuromuscular junction. The result is a decreased release of acetylcholine in response to nerve stimulation.

Lambert-Eaton Syndrome ~ Myasthenic Syndrome

Lambert-Eaton Syndrome (Myasthenic Syndrome): — sensitivity to NDMRs and succinylcholine is seen.

Increased

Lambert-Eaton Syndrome (Myasthenic Syndrome): ↓ Weakness with — activity

↑

—: A familial d/o associated w/ histocompatibilityantigen HLA-B27. Low back pain associated w/ early morning stiffness young men progressively restricted movement of the spine. Some patients develop arthritis of the hips and shoulders.

Ankylosing Spondylitis

Ankylosing Spondylitis: — dose if needed

Stress steroid

—: characteristic manifestations: antinuclear antibodies, nephritis, serositis, thrombocytopenia, or a characteristic rash

Lupus

Drug most likely to cause lupus like symptoms:

Hydralazine

4 Complications of TURB:

1.Blood Loss 3. bactermia 2. Hypothermia 4. Bladder perforation

TURP: Preference for —: ↓ blood loss, ↓ thrombus risk, atonic bladder, prevents postop bladder spasms, awake pt. can assist detecting issues

SAB

Bladder Perforation during TURP –Signs & Symptoms: 2

1.Abdominal pain & spasm 2. HTN & tachy—followed by sudden & severe HoTN

TURP Syndrome: Triad of S/S:

↑ PP, bradycardia, mental status Δ Other symptoms: HTN, CV collapse, ↑ CVP, Dyspnea, N, anxiety

TURP Syndrome: Tx:

Give O2, notifiy surgeon, invasive monitors, blood to lab, 12-lead ECG,

— - complication from TURP syndrome- d/t the rapid tx of hyponatremia

Central Pontine Myelinolysis

TURP Syndrome: Management: stop resection, Labs, fluid restriction, Lasic, NS3% Amount of NS 3% = Dose (mEq) = — Stop NS 3% when NA > —

kg x (140-(Na)mEq/L) ; 120

Na+ levels: — mEq/L = restlessness & confusion, (psbl. wide QRS), N/V

120

Na+ Levels: — mEq/L = nausea, somnolence, ECG (wide QRS, ST elevation)

115

Na+ levels: — mEq/L = seizures & coma with VT, VF

110

Irrigating fluid = — ml/min of surgery time

Blood loss is ~ — ml/min of resection time

3-5

Gas Embolism – laparoscopic surgery S/S: HoTN, Tachy, bilateral wheezing & ↓ ETCO2 Halt insufflation, eliminate N2O, release pneumoperitoneum, place in — lateral decub, aspirate gas via central venous cath

LEFT

Fat Emboli Syndrome – — hrs

12-72

Fat Emboli Syndrome 5 major signs:

axillary, subconjuctival petechial, hypoxemia,↓CNS, pulm edema

S/S of Intraop PE: 7

1. Hypotension 2. Tachycardia 3. Hypoxemia, decrease SpO2 4. Bronchospasm 5. Hypocapnia, decrease ETCO2 (1st sign d/t dead space ventilation) 6. PVR > 300 7. +D-dimer

—: Skeletal muscle necrosis d/t tissue injury Myoglobin: oxygen transport protein Common causes: major crush injury, thermal or electrical injury, arterial occlusion, acute muscle injury, prolonged immobility, compartment syndrome, MH, extreme lithotomy, hyperlordotic position

Rhabomylosis

—: To improve blood flow to ischemic areas: causalgia, Raynaud’s, frostbite, gangrene, ischemic ulceration of lower extremities L2-L3

Surgical Lumbar Sympthathectomy

Cyanide Toxicity: Tx:

Na Thiosulfate 150ml/kg over 15 mins

— = muscle cell

Myocyte

—: ECG = peaked P waves in leads II, III, and aVF which are consistent with right atrial hypertrophy & right axis deviation and right bundle branch block which are consistent with right ventricular hypertrophy.

Cor Pulmonale

Surgical Stimulation: 6

Intubation > upper ab surgery > breast surgery = lower ab = skin incision > skin closure

ASA classes: Healthy

ASA class: mild systemic disease- HTN, DM, Anemia, age, obesity, chronic bronchitis

ASA class: severe systemic disease- Cardiac dz with limiting activity, Uncontrolled HTN, DM w/vascular issues, MI or Angina

ASA class: incapacitating systemic dz – CHF, persistent angina, advanced kidney or liver dz

ASA class: moribund pt. – Not expected to live 24 hours after surgery- PE, AAA, cerebral trauma

ASA class: brain dead- organ procurement

ASA class: not elective- i.e appy

Mallampati: Pillars, soft palate, fauces, uvula

Class I

Mallampati: Uvula, soft palate, fauces

Class II

Mallampati: Soft palate, uvula

Class III

Mallampati: Hard Palate

Class IV

Mallampati score mnemonic:

PUSH (from I to IV)

ECT: 1st response

parasympathetic- HoTN, ↓HR

ECT: 2nd response

sympathetic- HTN, ↑HR ↑CBF = ↑ICP

ECT: Medication of choice:

Brevital (0.5mg/kg)

ECT: Desired Duration

30-60 seconds, sz sec needed= 400-700

ECT: 6 Absolute contraindications:

1. Pheo 2. Recent MI (4-6 wks) 3. CVA <3mos 4. recent intracranial surgery- <3mos 5. Intracranial mass lesion 6. Unstable C-spine

ECT: 9 Relative contraindications

angina, CHF, Pacer/ICD, pulm dz, major bone fx, glaucoma, retinal detachment, thrombophlebitis, pregnancy

Fetal heart Circulation:

RA to foramen ovale and RV (foramen ovale to LA), RV to PA, PA to patent ductus and lungs (PDA to aorta)

Fetal circulation: — arteries-deoxygenation blood & — vein- oxygenated

2 ; 1

Hemoglobin levels are lowest at — of age —mg/dl

3 months ; 10-11

Basal metabolic rate is highest at — of age

2 years

Oxyhemoglobin curve: Newborn= — shift & — @ —

Left ; Right ; 3-4 mos.

Peds Inspiratory pressure more negative than — to open alveoli

25-40

—: hyaline membrane disease, 50-75% mortality rate d/t result of inadequate surfactant in the alveoli

Respiratory distress syndrome (RSD)

Premie: less than —

37 weeks

Neonate: less than — of age

30 days

Infant: — of age

1-12 mos.

Children: — of age

1-12 years

Post conceptual Age = equation

gestational age + post maternal age

Apgar scores: taken at — min & — min

1 ; 5

Apgar scores: 1 min = — & 5 min = —

survival ; neurologic outcome

Differences in body systems in Pediatrics: Cardiac: -CO is dependent on — -fixed SV & noncompliant & poorly developed — (depends on —)

HR ; L vent ; Ca++

Differences in body systems in Pediatrics: Cardiac: Innervation: — = SPARSE, —-complete

Sympathetic ; parasympathetic

Differences in body systems in Pediatrics: Respiratory:— RR, — Lung compliance + — chest wall compliance = — FRC (↑ IA induction), Deficient in Type — fibers, high closing volumes

↑ ; ↓ ; ↑ ; ↓ ; I

Differences in body systems in Pediatrics: Respiratory: larynx are — & — (@ —), Adult —

Anterior and cephalad ; C3-C4 ; C4-C5

Differences in body systems in Pediatrics: Respiratory: Obligate — breathers

nasal

— airway narrowest point in children less than 5 yrs.

Cricoid cartilage

MAC highest — of age

6 mos.

Differences in body systems in Pediatrics: Kidney: — glomerular development, ↓ size of glomerulus ↓ perfusion pressure, ↓ ability to concentrate urine, obligate — losers

Incomplete ; Na

Differences in body systems in Pediatrics: Hepatic: — hepatic biotransformation, ↓ protein binding, fetal liver = hematopoiesis, — risk of hypoglycemia, — LBF

Immature ; ↑ ; ↓

Peds spinal cord and dural sac end at:

Spinal cord: L2-L3 and dural sac: S3

Adult spinal cord and dural sac end at:

Spinal cord: L1-L2 and dural sac: S2

— cortex- unmylenated and poorly developed until 2 years

Motor

— cortex- mylenated @ birth, nerves poor develop until 3 mos.

Sensory

Peds CBF —ml/100g/min (adults 100/100/g/min)

Peds Neuro surgery: PaCO2 → — mmHg

20-25

Peds Non-shivering thermogenesis (inhibited by: 4 )

IA, BB, fent, prop)

Best way to maintain infants body heat = heat up OR to —

26C (78.8)

Peds O2 consumption — an adults

Peds Large volume of distribution 2nd to higher — content

total body water

Peds Higher ratio of body — to body —

surface area ; weight

Hypotension: SBP NB <—

Hypotension: SBP 1year <—

Hypotension: SBP >1yr —

70+(agex2)

Peds ETT Diameter:

4 + Age /4 (uncuffed) = -.5(cuffed)

Peds ETT Length:

10 + age/2

Wt in kg NN-5: size LMA and ETT

LMA: 1 and ETT: 3.5

Wt in kg 5-10: size LMA and ETT

LMA: 1.5 and ETT: 4.0

Wt in kg 10-20: size LMA and ETT

LMA: 2 and ETT: 4.5

Wt in kg 20-30: size LMA and ETT

LMA: 2.5 and ETT: 5.0

Wt in kg >30: size LMA and ETT

LMA: 3 and ETT: 6

French Suction Catheter: neonate

8 Fr

French Suction Catheter: 2mths - 2yrs

10 fr

French Suction Catheter: 2-12 yrs

14 Fr

Precordial Stethoscope: — intercostal — of sternal border

3rd-4th ; left

Propofol < 2 y.o = IV induction — mg/kg.

3-4

Propofol >2 y.o. = — mg/kg

2.5-3

Peds Propofol — mg/kg/min GA

200-300

Peds Midazolam IV dose = —mg/kg PO dose= — mg/kg

0.05 ; 0.5 to 0.75

Peds Flumazenil IV — mg/kg → — mg total

0.05 ; 1

Peds thiopental —mg/kg

4-6

Peds Succinylcholine = ↑ intubate dose IV —mg/kg IM — mg/kg

2-3 ; 4

Peds NDMR dose —

Same dose as adults

Less than — weeks post conceptual = > risk of post anesthesia comp

Elective surgery: at least — weeks post conception

—: vasoconstriction of retinal vessels- leading to permanent scarring, blindness and retinal detach

ROP- retinopathy of prematurity

ROP- retinopathy of prematurity: most likely < — (post conception)

44 weeks

ROP- retinopathy of prematurity: Causes: 4

Hyperoxia, hypercarbia, Hotn, Sepsis Maintain PaO2 60-80mmHg O2 sats 89-94%,

—: Recurrent pauses in ventilation no longer 5-10 seconds. During REM sleep not associated with any physiologic disorder.

Periodic breathing

—: Unexplained cessation of breathing > 15 sec or shorter resp pauses w/ HR < 100, cyanosis, pallor or loss of muscle tone.

Central Apnea

Central Apnea has highest risk in premies. Most important risk of —.

Postop apnea

MOA of foramen ovale: 2

1. Decrease PVR and increase pulmonary flow 2. Increase SVR = increase L vent = increase LAP

MOA of ductus arteriosus: 2

1. Increase PaO2 and decrease prostaglandins 2. Increase SVR and decrease PVR

Function foramen ovale closure:

Rapidly after birth

Anatomical closure of foramen ovale:

3-12 mths

Functional closure of PDA:

2-4 days

Anatomical closure of PDA:

1-4 mths

Foramen ovale problem:

Cyanosis

Ductus arteriosus problem:

Increase work of L side of heart - L ventricular hypertrophy

Foramen ovale: IV induction time

Faster

Foramen ovale: inhalational induction time

Slower

Ductus arteriosus: IV induction time

Slower

Ductus arteriosus: inhalational induction time

Faster

RAP — LAP (causes of return or continuation of fetal circulation)

RAP > LAP: 5 problems

1. Hypoxia 2. Hypercarbia 3. Acidosis 4. Hypothermic 5. Coughing, bucking & Valsalva

RAP>LAP: — underestimates AaCO2

ETCO2

RAP > LAP: Preductal Monitoring :

Right Hand or Finger

RAP > LAP: Postductal monitoring:

Left foot or toe

RAP > LAP: ABG’s best obtained from —

Right Artery

—: Narrowing of the descending aorta.

Neonatal Coarctation of the Aorta

Neonatal Coarctation of the Aorta: If severe – perfusion is dependent on open — shunt. — use to maintain patency

PDA; PGE1

Neonatal Coarctation of the Aorta: BP monitoring in —

Right Radial artery

—: Foramen of Bochdaleck or anterior foreman of Morgagni Larger on left & 90% of diaphragmatic hernias on left.

Congenital Diaphragmatic Hernia (CDH)

Congenital Diaphragmatic Hernia (CDH): Larger on — & 90% of diaphragmatic hernias on —.

left ; left

Congenital Diaphragmatic Hernia (CDH): Maintain preductal saturation > — w/ PIP < — cm H2O

85 ; 25

Congenital Diaphragmatic Hernia (CDH): Keep them —, — stomach and avoid barotrauma

breathing ; Decompress

Congenital Diaphragmatic Hernia (CDH): — shunt – monitor pre and post ductal perfusion

R to L

Congenital Diaphragmatic Hernia (CDH): problems: 3

Cyanosis, Dyspnea & Dextrocardia

4 issues with Tetralogy of Fallot:

1. Large single ventricular septal defect 2. Aorta that overrides the right & left ventricles 3. Obstruction to right ventricular outflow 4. Right ventricular hypertrophy

Tetralogy of Fallot: — shunt

RIGHT to left

Tetralogy of Fallot Goals: 2

maintain volume status and SVR (need to ↑ = NEO)

—: Most common form ends in blind pouch & lower esophagus that connects to trachea – C (then B & E) Associated with VACERTL syndrome Principle cause of death = pulmonary complications

TEF: Tracheoesophageal Fistula

TEF: Tracheoesophageal Fistula: — secretions and No — prior to intubation

↑ ; PPV

—: Infants: projectile vomiting & visible peristalsis Adults: Peptic ulcer scarring

Pyloric Stenosis

Pyloric Stenosis: problems 3

1. Hyperchorlemic metabolic alkalosis- ↓Cl, K, Na, Ca 2. ↑ Aldosterone secretion 3. Cleft palates & esophageal reflux

Pyloric Stenosis: Anesthetic Considerations: 3

correct electrolytes, rehydration, OG

Is pyloric stenosis a surgical or medical emergency?

Medical

Pyloric stenosis: post op complication

Respiratory depression

Down’s syndrome (trisomy 21) Concerns: 3

1. Difficult intubation: use small than usual ETT (Large tongue Short neck Small mouth) 2. Neck flexion- Cervical spine dislocation- antlanto-occipt (Instability & Weak ligaments) 3. Congenital heart disease (40% incidence)

Which is more common: omphalocele or gastroschisis

Omphalocele

Location of omphalocele:

Base of umbilicus

Location of gastroschisis:

Lateral to umbilicus

Anomalies with omphalocele:

Yes, cardiac

Anomalies seen with gastroschisis:

Omphalocele presence of sac:

Yes

Gastroschisis presence of sac:

3 concerns with gastroschisis:

Infection, hypothermia, and hydration

Omphalocele and gastroschisis: steps 4

1. Decompress stomach with tube 2. No nitrous 3. Hydrate 8-16ml/kg/hr 4. If PIP >25-30 cmH2O

Which is emergency: epiglottis or croup?

Epiglottis

Onset of epiglottis:

Rapid, 24 hrs

Onset of croup:

Gradual 24-72 hrs

Radiograph sign of epiglottis:

Thumb (swollen)

Radiograph sign of croup:

Steeple (narrow)

Age with epiglottis:

1-7 year old

Age with croup:

Most < 2yrs

Cause of epiglottis:

Haemophilius B-flu

Cause of croup:

Cold (viral)

Fever with epiglottis:

Yes - high

Fever with croup:

Low grade

Respiratory with epiglottis:

Inspiratory stridor

Respiratory with croup:

Croupy cough “bark” with inspiratory stridor

Tube size with epiglottis:

1/2 size small with leak

Tube size with croup:

1/2 size smaller

Tx with epiglottis:

Ampicillin &/or vaccine before 2 yrs

Tx with croup:

Epi neb, O2, cool humid, steroids

Anesthesia with epiglottis: 2

-do not attempt to visualize glottis -sedate while sitting

Anesthesia with croup: 3

-intubate if high PaCO2 -epi neb-2.25% in 3ml -NS @ 0.05ml/kg up to 0.5ml/kg Q 1-4hr

—: Hereditary disease of exocrine glands of resp and GI

Cystic Fibrosis

Cystic fibrosis: Cl- transport — w/ — Na & H2O transport — Thickness of secretions= avoid antisialogogues — RV & airway resistance, — VC & exp flow rate

↓ ; ↓ ; ↑ ; ↑ ; ↓

Cystic fibrosis: No — secondary to increase secretions

ketamine

—: Most common surgical emergency in the neonate. Decreased mesenteric blood flow = ischemia → intestinal mucosal injury

Necrotizing enterocolitis

Necrotizing enterocolitis: — @ > risk for developing

Premature infants

— is most common pediatric surgical emergency

Foreign body aspiration

—- abn fusion of embryologic neural groove

Neural Tube Defect

—: herniation of brain & meninges through defect in skull producing a fluid filled sac

Encephalocele

—: hernia protrusion of a saclike cyst of meninges filled w/ CSF & no neurological deficits

Meningocele

—: (spina bifida) hernial protrusion of saclike cyst containing meninges, CSF & portion of spinal cord

Myelomeningeocele

Encephalocele, Meningocele, Myelomeningocele: — precautions & — is key

LATEX ; Positioning

—: Nerves blocked: ilioinguinal and iliohypogastric

Inguinal hernia

— is neuroprotective for global ischemia in neonates

Hyperglycemia

Tonsillectomy:↑ Blood loss- — ml/kg

Tonsillectomy: 3 complications:

bleeding, laryngospasm & emesis

NPO Guidelines: Solid Food

NPO Guidelines: Commercial Formula/Milk

NPO Guidelines: Breast Milk

NPO Guidelines: Clear Liquids

Mendelsons Syndrome: Volume > — ml/kg or pH <—

0.4 ; 2.5

Peds Regional Anesthesia: CSF volume — of adults = dilution of LA = — dosing & — DOA

x2 ; ↑ ; ↓

High spinal – decreasing — #1 sign

oxygen saturation

Caudal: tip of — to fix the midline & sacral — on either side of sacral —

coccyx ; cornua ; hiatus

— LA is not metabolize in the NN

Mepivicaine

Peds Regional Anesthesia: — determines height of block

Volume

Regional Anesthesia: Caudal: —ml/kg analgesia T4-T6- concentration no > 2.5 mg/kg

1.2-1.5

Regional Anesthesia: Epidural Blood Patch: —ml/kg

0.3

Laryngospasm: 3 steps in peds

1. CPAP- 10-15cm H2O 2. atropine 0.02mg/kg 3. Succs 1mg/kg IV or 4mg/kg IM

Maternal Physiological & Physical Changes: Cardiac: — CO, SV, HR, LVEDV, EF, Femoral venous pressure — PVR, MAP, SBP, DBP, SVR, PADP, PCWP

↑; ↓

Maternal Physiological & Physical Changes: Cardiac: — ↑ the most immediately post-partum

Maternal Physiological & Physical Changes: Cardiac: ↑ — & — x12

Renin & angiotensin II

Maternal Physiological & Physical Changes: Respiratory: ↑ Alveolar vent & ↓ FRC = — inhalation agent uptake & — MAC

↑ ; ↓

Maternal Physiological & Physical Changes: Respiratory: Respiratory — CO2 = —

Alkalosis ; 30

Maternal Physiological & Physical Changes: GI: Metabolic — – HCO3 = —

Acidosis ; 20

Maternal Physiological & Physical Changes: GI: ↑ Gastric emptying time &↓ LES secondary to ↑ —

progesterone

Maternal Physiological & Physical Changes: Renal: — RBF & GFR (50%) → — BUN & serum creatinine ↑ Kidney size & weight & ureters and renal pelvis dilates — & — common

↑ ; ↓ ; Glucosuria & proteinuria

Relative — maternal anemia

hemodilutional

Maternal Physiological & Physical Changes: Hemostasis: Hgb > — w/PIH or HTN = low volume

Maternal Physiological & Physical Changes: Hemostasis: — Blood volume, plasma volume, RBC, Hbg — Hct —, ↑ Factors —, —, —, —, —, —

↑ ; Hbg 11.5 Hct 35.5 , 1, 7, 8, 9, 10,12

Maternal Physiological & Physical Changes: Hemostasis: No change in —, —, —, and —

2 & 5, platelets, bleeding time

Maternal Physiological & Physical Changes: Hemostasis: Shortened or ↓: 4

PT, PTT, AT, Factors 11

Maternal Physiological & Physical Changes: Hemostasis: —, —, and — that are greater than twice the normal value represents a high-risk state that should be corrected prior to initiating a neuraxial anesthetic.

PT, PTT, and bleeding times

Platelet < — too low to perform a neuraxial anesthetic

100,000

Maternal Physiological & Physical Changes: Anesthetic considerations w/ Δ: Do not — = ↓ maternal alkalosis = ↓ — blood flow

hyperventilated ; uterine

Maternal Physiological & Physical Changes: Anesthetic considerations w/ Δ: GA = RSI — gestation to — of postpartum

8 wk. ; 6 week

Most common cause of maternal death during GA =

Hemorrhage

Most common cause of maternal death with anesthesia =

Airway issues

Maternal Physiological & Physical Changes: Anesthetic considerations w/ Δ: — MAC & — sensitivity to LA

↓ ; ↑

DO NOT give — to PIH/HELLP parturient

esmolol

Maternal — & fetal — = ↑ fetal ion trapping

alkalosis ; acidosis

— receptors: relaxes smooth muscles & stops contractions via activation of adenylyl cyclase = ↑ cAMP = myometrial relaxation

β2

Tocolytics 2

Methergine Hemabate

Uterine Blood Flow:

800ml/min (10% maternal CO)

Uterine Blood Flow:↓ Perfusion pressure: 6

supine, hemorrhage/hypovolemia, HoTN, contractions, sz, Valsalva

Uterine Blood Flow:↑ Uterine Vascular resistance: 2

catecholamines, vasopress

Maternal — is only factor influence blood flow through placenta

uterine blood flow is — autoregulated

NOT

— receptors predominate uterine vasculature

α adrenergic

Greatest risk to fetus from Maternal issues: 3

Severe hypoxia, HoTN, acidosis

Three layers in placental membrane:

1. Fetal trophoblasts 2. Cytotrophoblasts 3. Syncytiotrophoblasts

Placental Transfer of Drugs: 4

1. Concentration gradient 2. Molecular weight of drugs – MW < 500 = easier transfer 3. Lipid solubility- lipids soluble drugs = easier crossing 4. Ionization – ions inhibited

—: Compression inferior vena cava = ↓ venous return = ↓ SV & Hotn

Maternal supine hypotensive syndrome

Maternal supine hypotensive syndrome: tx:

LUD (i.e Right hip up) 15degrees

—: Regular uterine contractions until cervix fully dilated.

First stage

—- Cervical effacement 2-3 cm

Latent

— – frequent contractions 3-5 mins & dilatation is 4 cm in a primiparous patient & 3 cm in a multiparous patient.

Active

—: From the end of the first stage until the delivery of the baby is completed.

Second stage

—: From the delivery of the baby until the placenta and the membranes are expelled.

Third stage

—: excessive amniotic fluid around unborn infant

Polyhydramnios

First stage: uterine contractions & cervical dilatation. Pain travels via — fibers accompanying sympathetic nerves.

visceral afferent

Pain Pathways for Stages of Labor: First stage: Enter cord at —&— → —,—,—,— spinal segments. —-Fibers

T11 & T12 ; T10, T11, T12, & L1 ; C

Second stage: Caused by distention of lower vagina, vulva, and perineum. Pain travels via the — nerves

Pudendal

Pain Pathways for Stages of Labor: Second stage: enters the cord at —,—,— sacral segments. (— dermatomes)

S2, S3, & S4 ; T10-S4

NO —: they inhibit uterine contractions & promote closure of the fetal DA.

NSAID

Early Decelerations (Type —)

Late Decelerations (Type —)

—: Etiology: head compression or stretching of neck during uterine contractions. Start & end w/ contraction & UNIFORM

Early Decelerations (Type 1)

Early Decelerations (Type 1): Mild decrease in FHR < — BPM

—: Etiology: uteroplacental insufficiency & fetal compromise w/ ↓ HR Onset: begin or near end of contraction Uniform in appearance + or - variability

Late Decelerations (Type II)

Late Decelerations (Type II): SEVERE: if FHR > — BPM

—: Etiology: cord compression Nonuniform with variable waveform Typically associated with fetal asphyxia when: > 60 bpm FRH, duration > 60 seconds or pattern persists > 30 mins

Variable Decelerations

Variable Decelerations: Severe: FHR ↓ — by BPM, FHR < — BPM or decels — secs +

60 ; 60 ; 60

Fetal bradycardia & late decelerations = —

fetal hypoxia (asphyxia)

Obstetrics & Regional Anesthesia: SAB ↓ dose by —% d/t ↓ epidural space secondary to venous congestion &/or progesterone-induced sensitivity

Obstetrics & Regional Anesthesia: Most common S/E = —

Hotn

—: used during 1st stage of labor when traditional neuraxial analgesia is contraindicated

Paravertebral lumbar sympathetic block

—: quickly metabolized no opportunity to accumulate in any significant amount.

Chloroprocaine

—: 1/3 less motor block than bupivacaine & causes less CNS & cardiac toxicity, 0.08-0.15% can be administered via an epidural catheter at a rate of 8-12 mL/hour to provide continuous analgesia during labor

Ropivacaine

— level sufficient for caesarean section

Injuries: Dorsiflex to foot= — nerve

common peroneal

Injuries: Loss of sensation to lateral thigh = — nerve

lateral femoral cutaneous

Injuries: Most common nerve injury during ab hyster= — nerve

femoral

Injuries: Nerve injury most common w/ vaginal delivery= —

lumbosacral

Spotty spinal: 5 helpful things

1. 2.5mg diazepam up to 10mg IV 2. Fentanyl 1μg/kg IV 3. 40% N2O 4. 0.25mg/kg ketamine IV 5. 10-20ml 0.5% lidocaine intraperitoneally

Morphine intrathecal and epidural dose:

Intrathecal: 0.5-1mg and epidural: 7.5-10mg

Meperidine intrathecal and epidural dose:

Intrathecal: 10-20mg and epidural: 100mg

Fentanyl intrathecal and epidural dose:

Intrathecal: 10-25 mcg and epidural: 50-100 mcg

Sufentanil intrathecal and epidural dose:

Intrathecal: 3-10mcg and epidural: 10-30mcg

—: Placed through sacrospinous ligament- via Transvaginal approach

Pudendal block

— block: 2nd stage of labor

Pudendal block

Pudendal block risk:

hitting the scalp

—: Anesthetizing nerve fibers innervate uterus, cervix, upper vagina. Submucosally in the vagina @ 3 & 9’oclock

Paracervical block

— block: 1st stage of labor

Paracervical block

Paracervical block risk:

Fetal Brady (33%)

Signs of Fetal distress: 7

1. Repetitive late decelerations 2. Loss of beat to beat variability associate w/ late or deep decels 3. Sustained FHR < 80 BPM 4. Meconium-stained amniotic fluid 5. Oligohydramnois 6. Fetal Scalp pH < 7.2 7. IUGR

—: Inadequate uterine contractions following delivery

Uterine Atony

Uterine Atony risk factors: 7

multiple gestations, fetal marosomia, prolonged/rapid labor, tocyotlitcs, VA, retained placenta, chorioamniotis

—: One of the most common infections during pregnancy

Chorioaminoitis

Chorioaminoitis: Based on S/S: Temp > — = CARDINAL symptom

—: May lead to fetal hypoxia

Uterine Cord Prolapse

—: Dx: sudden fetal bradycardia or profound decels w/ physical exam

Uterine Cord Prolapse

Uterine Cord Prolapse: tx:

immediate steep trendelenburg or knee to chest position

Placenta Previa:- is there pain?

No pain

Placental Abruption: is there pain?

Yes, pain

—: The partial or total covering of the cervical os by the placenta

Placenta Previa

Placenta Previa:↑ incidence of asymmetric —

IUGR (intrauterine growth restriction)

—: Separation of the placenta from deciduas basalias before delivery

Placental Abruption

Placental Abruption tx:

Delivery of fetus

—: placenta adheres to the surface of the myometrium w/o invasion or passage through uterine muscle

Placenta accrete

Placenta accrete is the most common indication for — surgery.

Hysterectomy

—: refers to placental implantation within the myometrium (confined to myometrium)

Placenta increta

—: refers to the condition where the placenta completely penetrates the myometrium or other pelvic structures

Placenta percreta

3rd cause of death in pregnant pts?

Amniotic fluid embolism (AFE)

—: Amniotic fluids into maternal circulation

Amniotic fluid embolism (AFE)

— S/S: tachypnea, cyanosis, shock, generalized bleeding, ↓ CO, acute PE, uterine atony, ARDS, arrhythmias, bleeding, SZ

Amniotic fluid embolism (AFE)

Amniotic fluid embolism (AFE) Tx: 3

aggressive cardioplulamony resuscitation, stabilization, fast delivery

—: Uterine wall defect resulting in fetal distress or maternal hemorrhage

Uterine Rupture

Uterine Rupture Risk Factors: 5

prior C-section, uterine scar, trauma, forces, hard labor

Most diagnostic sign for Uterine Rupture =

fetal distress- loss of fetal heart tones

Uterine Rupture s/s:

Continuous abdominal pain & Hotn (↑ in VBAC)

Uterine Rupture tx:

volume resuscitation & immediate laparotomy & hyster poss

Pregnancy Induced Hypertension: (↑ —)

thromboxane A2

Pregnancy Induced Hypertension: — = ↓ CI & ↓ blood volume

HTN

Pregnancy Induced Hypertension: —= HTN w/o edema or proteinuria

Gestational hypertension

Pregnancy Induced Hypertension: —= HTN w/proteinuria and edema during pregnancy

Preeclampsia

Pregnancy Induced Hypertension: —= preeclamptic patient w/ sz

Eclampsia

Pregnancy Induced Hypertension: —= form of preeclampsia characterized by hemolysis, elevated liver enzymes, and a low platelet count.

HELLP

S/S Severe pregnancy induced HTN:

1. BP 160/110 2. Proteinuria increase 5 g/day 3. Oliguria, < 500 ml/day 4. Pulmonary edema 5. Hepatic tenderness or HELLP syndrome 6. CNS: HA, visual disturbances, or seizures

Complications that necessitate pregnancy induced HTN delivery: SBP >/= — or DBP >/= — – 24-48 hrs

160 ; 110

Complications of pregnancy induced HTN: 1. —- #1 death 2. Renal failure 3. DIC 4. —- #2 death 5. Cerebral edema 6. Airway obstruction

Cerebral hemorrhage ; Pulmonary edema

—: MOA: ↓ presynaptic release of AcH & ↓ post synaptic sensitivity preeclamptic patients & works @ NMDA → ↓ SVR & ↑ CI

Magnesium

—: Beneficial: Anticonvulsant, vasodilatation, ↑ UBF, ↑ RBF, ↑ prostacyclin, ↓ ACE, ↓ renin activity, tocolytic & bronchodilitation

Magnesium

Magnesium IV load = — over 15-20 mins → —g/hr IV gtt

4g ; 1-4

—: drug of choice sz prophylaxis in PIH

Magnesium

Tx for Mg overdose : —

Calcium Gluconate

—: useful in pregnancy—mainstay, decrease BP increase Uteroplacental BF

Hydralazine

Heart Disease in the Parturient: —: -mitral valve dz, aortic insufficiency, L to R shunt -Regional Anesthesia: especially continuous epidural -NEO

Group One

Heart Disease in the Parturient: —: AS, R to L shunt, primary pulm HTN, Regional anesthesia CONTRAINDICATED

Group Two

Four findings that suggest DIC:

1. Thrombocytopenia 2. Prolonged PT 3. Prolonged PTT products 4. Decrease Serum fibrinogen, increase Fibrin split

DIC is associate with 3 OB problems:

1. retention of dead fetus 2. Placental abruption 3. AFE

Lab Tests for —: Plasma fibrinogen <150 mg/dL Plasma fibrinogen <50,000/mm3 Thrombin time >100 sec Prothrombin time >100 sec Partial thromboplastin >100 sec Fibrin split products >200 mcg/ml Red blood cell fragment Yes

DIC

Geriatrics: Progressive loss of functional reserve in ALL organ systems 1 % decline each year after — years old

Geriatrics: A-A gradient: >/= —

20 (normal 8)

Geriatric System Changes Cardiac: fx declines —% (20-80 y.o)

Geriatric System Changes Cardiac: increase, decrease, or no change : left ventricular wall thickness, LVH d/t chronic ↑ afterload, left ventricular wall tension (law of Laplace), afterload, cardiac workload 2nd to ↓ aortic compliance - AC, SBP, PVR, Circulation time, conduction fibrosis, dysrhythmias, SA node cell loss, Vagal tone – d/t ↓ sensitivity of adrenergic receptors, systolic

Increase

Geriatric System Changes Cardiac: increase, decrease, or no change: cardiac reserve, CO –d/t ↑ in AL, CI, HR, left ventricular compliance, chronotropic & inotropic responses, baroreceptor fx, adrenergic sensitivity

Decrease

Geriatric System Changes Cardiac: increase, decrease, or no change: DBP, resting systolic fx, excitation-contraction coupling, ionized Ca levels, contractile proteins, SV

No change

Geriatric System Changes: Respiratory: Obstructive or Restrictive

Restrictive

Geriatric System Changes: Respiratory: increase, decrease, or no change : vocal cord stimulation for closure, airway obstruction, risk of aspiration, pulmonary complications, physiologic dead space, WOB, potential for hypoxia, FRB, Closing volume and Closing capacity, alveolar compliance, resp depression w/opioids, collagen PaCO2-PACO2 gradient d/t V/Q mismatch, VD/VT

Increase

Geriatric System Changes: Respiratory: increase, decrease, or no change: elastin fibers, tissue elasticity, lung recoil, ability to cough, chest wall compliance – kyphosis, VC, ERV, IRV, response to hypoxia & hypercarbia, protective reflexed, cervical spine & TMJ mobility, ease of mask ventilation, PaO2 (0.4mmHg/yr. after 20)

Decrease

Geriatric System Changes: Respiratory: increase, decrease, or no change : PaCO2, PAO2

No change

Geriatric System Changes: Respiratory: CC—FRC @ 44 y.o CC — FRC @ 66yo

= ; >

Geriatric System Changes: Respiratory: Closing volume is —% of VC in the young & —% in the elderly

10 ; 40

Geriatric System Changes: Respiratory: PAO2-PaO2 gradient = equation

0.21 (age +2.5)

Geriatric System Changes: Respiratory: PaO2 = equation

102-Age/3

Geriatric System Changes: Endocrine: increase or decrease : Insulin resistance, heat loss

Increase

Geriatric System Changes: Endocrine: increase or decrease : heat production, hypothalamic temp regulation

Decrease

Geriatric System Changes: GI/Hepatobiliary: increase, decrease, or no change : gastric pH, AAG-1 (↑ binding of basic-LA, opioids)

Increase

Geriatric System Changes: GI/Hepatobiliary: increase, decrease, or no change : liver mass, HBF, liver fx, biotransformation, albumin production, PCHE – MEN, gastric emptying, plasma clearance

Decrease

Geriatric System Changes: GI/Hepatobiliary: increase, decrease, or no change : Hepatocellular fx

No change

Geriatric System Changes: Nervous System: increase, decrease, or no change : skeletal muscle atrophy, degeneration of peripheral nerve cells, Threshold –proprioceptor, hearing, temp thresh, touch thresh, vision thresh, CSF, cerebral cortex neuron loss, SNS

Increase

Geriatric System Changes: Nervous System: increase, decrease, or no change : CBF, intracranial volume, gray matter, brain mass, skeletal muscle steadiness-strength-control, conduction velocity, response to β

Decrease

Geriatric System Changes: Nervous System: increase, decrease, or no change : Auto regulation

No change

Geriatric System Changes: Renal: increase, decrease, or no change: BUN, ADH response to hypertonic saline load (caution w/fluids), ability to develop hyper/hypo kalemia

Increase

Geriatric System Changes: Renal: increase, decrease, or no change: kidney mass, RBF d/t ↓CO (50%), renal plasma flow, GFR, renal fx, muscle mass, creatinine production, fluid handling (prone to fluid overload), Na handling, concentrating ability, response to ADH, response to aldosterone

Decrease

Geriatric System Changes: Renal: increase, decrease, or no change: serum creatinine

No change

Geriatric System Changes: Pharmacology: increase, decrease, or no change: circulation time, body fat, Vd for lipids, recovery of VA

Increase

Geriatric System Changes: Pharmacology: increase, decrease, or no change: muscle mass, body head production, core body temp, basal metabolic requirements, MAC, Total body water, Vd for water soluble drugs, dosing for barbs-- opioid antagonists-- benzos

Decrease

— is most sensitive indicator of renal fx in elderly

Creatine Clearance

Creatine Clearance fx in elderly —ml/min @ y.o

Geriatric System Changes: Thermoregulation: > 80 shivering @ — vs. younger pt. at —

35 degrees ; 36.1 degrees

Geriatric System Changes: Pharmacology: increase, decrease, or no change Atropine, Isoproterenol & other Beta agonists

Increase

Geriatric System Changes: Pharmacology: increase, decrease, or no change Thiopental, Propofol, Etomidate, Midazolam, Opioids, remifentanil, pan, vec, roc, succ

Decrease

Decrease opioids and midazolam by —% in elderly pts.

Geriatric System Changes: Pharmacology: increase, decrease, or no change: atracurium, neostigmine, Edrophonium

No change

Geriatric System Changes: Pharmacology: — responsiveness secondary to↓receptor affinity & alterations in signal conduction -↓cAMP

Beta receptor

Geriatric System Changes: Preoperative concern: 5

Heart> renal> hepatic > pulm > multi- DM

Geriatric System Changes: postop concern: 2

Heart and lungs

Geriatric System Changes: IV induction = —

SLOWER

Geriatric System Changes: Inhalation Induction= —

FASTER

Geriatric System Changes: Postop Delierum: @ risk: > — yrs, hx of delirium, etoh abuse, narcotic

Geriatric System Changes: Postop Delierum: greatest with — procedures.

Orthopedic

Geriatric System Changes: Geriatric & Regional: — Cmin for LA

↓

Geriatric System Changes: Geriatric & Regional: SAB —DOA —Sensory block — Dose

↑ ; ↑ ; ↓

Geriatric System Changes: Geriatric & Regional: Epidural — DOA, — Motor Block, — segment dose, — volume cephalad spread

↓ ; ↓ ; ↓; ↑

Geriatric System Changes: Geriatric & Regional: — for TURPS

Geriatric System Changes: Geriatric & Regional: cysto SAB @ —

T10

Similarities of Neonates to Geriatrics:

1.↓ ability to ↑ HR 2nd to hypovolemia 2.↓ arterial O2 tension 3. impaired ability to cough 4.↓ renal tubular function 5.↑ susceptibility to hypothermia

— (Aka: —): premature aging

Progeria ; Hutchinson-Gilford Syndrome

Progeria (Hutchinson-Gilford Syndrome): average death is — y.o.

Progeria (Hutchinson-Gilford Syndrome): Airway effects: 3

mandibular hypoplasia, micrognathia, glottis opening is narrow

Progeria (Hutchinson-Gilford Syndrome): Anesthesia concerns: 2

organ systems fx, positioning

—: Deposition of amyloid beta peptides produces neuritic plaques & neurofibrillary tangles= ↓ NT fx & death of neurons.

Alzheimer’s

Alzheimer’s: The — system and — are most affected.

limbic ; cortex

Alzheimer’s: Tx:

Cholinesterase inhibitors: rivastigmine, donepazil, & Galantamine

Alzheimer’s: Anesthesia/Pharm: -Acetylcholinesterase inhibitors may have a ↑ DOA w/ — -Anticholinergic – Use — is blood brain -May be resistance to — d/t use of acetylcholinesterase inhibiting drugs

succs; glycopyrrolate ; NDMR

Obesity Values: BMI < 18.5 = —

Underweight

Obesity Values: BMI 18.5 -24.9 = —

Normal

Obesity Values: BMI 25-29.9 = —

Overweight

Obesity Values: BMI 40-49.9 = —

Extreme obesity

Obesity Values: BMI 30-39.9 = —

Obesity

Obesity Values: BMI 50-59.9 = —

Superobesity

Obesity Values: BMI 60+ = —

Super super obesity

IBW = equation

ht in cm – 100 (m) or 105 (f)

1 in = — cm

2.54

BMI = equation

kg/m2

BMI > — is cut off for ambulatory surgery center

35- 40

Obesity: cardiac: increase, decrease, or no change: CO, Blood Volume (50ml/kg), incidence of HTN

Increase

Obesity: cardiac: — ♥ effects: polycythemia, pulmonary & systemic vasoconstriction, ↑ risk for ischemic heart dz & cerebrovascular dz, & RHF, cardiomegaly, CHF

OSA

Obesity: cardiac: EKG changes: — ventricular hypertrophy and — atrial enlargement

Left ; left

Obesity: Extra — L/min of CO for each additional kilogram of fat.

0.1

Obesity: Respiratory: increase, decrease, or no change: Diaphragm, O2 consumption, CO2 production, WOB, RR, Hypoxemia

Increase

Obesity: Respiratory: increase, decrease, or no change: ERV, IC, FRC, VC, PaO2, chest wall compliance

Decrease

Obesity: Respiratory: increase, decrease, or no change: PFT’s, lung compliance

No change

Obesity: obstructive or restrictive respiratory?

Restrictive

Obesity: renal: increase, decrease, or no change: GFR renal tubular resorption, impaired Na+ excretion = worse HTN

Increase

Obesity: renal: increase, decrease, or no change: RBF

No change

Obesity: Endocrine: —- activates SNS = Na retention = ↑ HTN

Hyperinsulinemia

Obesity: — single best predictor of difficult airway

Neck circumference

Obesity: ↑ — nerve injury

Brachial plexus

Obesity: Appetite suppressant – — = catecholamine depletion

SSRI’s

Obesity: Regional:— LA dose by 20% secondary to vascular engorgement of the epidural space, the level and onset of an epidural block can be —

↓; unpredictable

Obesity: Pharmacology: — Vd for meds

↑

Obesity: Drugs distributed mainly to lean tissue dosed on — & include: Thiopental, propofol, rocuronium, vecuronium, atracurium, midazolam cisatracurium, fentanyl, sufentanil, & remifentanil

LBW

Obesity: Drugs distributed to lean & adipose dosed on — & include: Succinylcholine and Dexmedetomidine

TBW

Obesity: Hetastarch- 20ml/kg – based on —

IBW

—= males & females, awake PaCO2 > 45 mmHg, doesn't exhibit nocturnal airway obstruction unless concomitant OSA, pulmonary HTN, somnolence, sleep apnea, hypercapnia, & hypoxemia,↓ alveolar ventilation, cyanosis Polycythemia, enlarged heart, hypoxemia – PaO2 < 65mmHg Rales

OSH (pickwickian): Obesity hypoventilation syndrome

—: males > females, normal awake PaCO2 ,sleep induced obstruction, normal paCO2, pH, pulm compliance

OSA: obstructive sleep apnea

—: 1ml of wetting solution per 1ml of fat. >5000 ml – fluid overload concern may promote- hypoxemia, HTN, & pulm edema

Liposuction

—: used to emulsify fat, provide anesthesia, create hemostasis – solution is dilute epi 1:100,000 & lidocaine 0.05- 0.1%

Wetting solution

— is # 1 concern = 25% of liposuction deaths

Positioning: Lateral Position: ↑ risk of —

rhabdo

Ax roll/chest roll – to protect — = relief of pressure from axillary neurovascular bundle & prevent ↓ blood flow to hand

brachial plexus

lithotomy: 5 nerves that may be injured:

Common peroneal (most common), saphenous, sciatic, femoral, obturator

lithotomy: decrease —

FRC

Upright to prone = ↓3

SV, CO, FRC

Supine to prone = ↑ —

FRC

Trendelenberg position — MAP, PCWP, SVR, venous return, CVP, ICP — CI, oxygen delivery, O2 consumption, CO — TLC, VC, FRC

↑ ; ↓ ; ↓

Sitting 90 degrees = — 45 degrees = —

sitting ; beach chair

Lawn chair ↓ — nerve injuries

sciatic

Prone: Large breast = positioning —and —

medial and cephalad

vision loss during prone procedures in — optic neuropathy and central retinal artery occlusion account for 89% of cases of postoperative vision loss in prone

Ischemic

—: Caused because air enters the cranium while the pt. is in a head up position at a time when the volume of intracranial contents has been reduced as a result of some combo of ↓ CO2, good venous drainage, osmotic diuresis, CSF loss from field.

Pneumocephalus

Pneumocephalus: Manifests: delayed — from GA, severe —

emergence ; HA

Bladder perforation Awake- — pain

shoulder

Bladder perforation Anesthetized – —, — or —

tachy, htn or hotn

Total parotidectomy: spares the — nerve

facial

Radical parotidectomy removes the — nerve

facial

— of neck = compression of ipsilateral and/or contralateral vertebral arteries

Hyperextension

Bone Cement: Methylmethacrylate toxicity = sudden —

hotn

— = MOA – transient fat/air embolism from bone marrow or causes vasodilatation & ↓ SVR

Methylmethacrylate toxicity

Radial prostectomy - complications: #1 is — and — nerve injury can happen

Hemorrhage ; obturator

8 causes of rhabdomyolysis

1. Major crush injury 2. thermal/electrical injury 3. Acute muscle ischemia d/t arterial occlusion 4. Acute muscle injury 2nd prolonged immobilization 5. Compartment syndromes 6. MH 7. Extreme lithotomy 8. Hyperlordotic position

6 Congenital syndromes associated with difficult intubation:

1.Downs 4. Pierre Robin 2. Goldenhar 5. Treacher Collins 3. klippel-fiel 6. Turner

—: Overwhelming generalization septic cellulites of submandibular region. Usually after dental procedures. S/S: chills, fever, drooling, ability to open mouth, difficulty speaking.

Ludwig’s Angina

Ludwig’s Angina : Caused by hemolytic —.

streptococci

Ludwig’s Angina: Airway management: preliminary — using LA in awake patient = Safest

tracheotomy

Contraindications for Cricothyrotomy: 2

Children < 6 years old Laryngeal fractures

—: Severe jaw limitation

Scleroderma

Scleroderma: Decreased — = difficult ventilation

compliance

Scleroderma: — hypoxia secondary to decreased diffusion of O2 across alveoli

Arterial

Scleroderma: No RSI – — intubation with head up position= safer

awake

Mouth opening – —mm -- — fingerbreadths

40 ; 2

Thyroidmental distance - > — cm normal < —= difficult airway

6.5 ; 6

ETOH – what kinda of 3 electrolytes

Hypomagnesium, hypokalemia, metabolic alkalosis

Medications to Hold before surgery: 2

Oral Glycemic & Diuretics

Postoperative — complications: with thoracic and upper Abdominal surgery = highest risk.

pulmonary

Post op complications: — in the PACU: hypoventilation & ↑ R to L intrapulmonary shunting secondary to ↓ — (#1)

Hypoxia ; FRC

Post op complication: — secondary to #1- Hypovolemia

HoTn

Post op complication: — 2nd #1 Pain

HTN

#1 Postoperative Complication – —

PONV

High risk PONV = 10

children, women, previous hx, hx of motion sickness, anxiety, abd, gyn , laparoscopic, opioids, surgical duration

Carotid Endarterectomy: PaCO2 — mmHg – Avoid ↓ CO2 → —

35-45 ; vasoconstriction

Carotid Endarterectomy: Stump pressure transmitted pressure through the —, < — = shunting

circle of willis ; 50

Carotid Endarterectomy: Avoid —

hyperglycemia

Carotid Endarterectomy: Post-operative HTN = bc —

carotid sinus baroreceptors

Carotid Endarterectomy: Causes of morbidity & mortality #1- — & #2-—

MI ; Stroke

Carotid Endarterectomy: Nerves: Smile: — nerve, say "EEE": — & — nerves, shrug shoulders: — nerve, swallow: — nerve, stick his tongue out: — nerve

facial ; superior and recurrent laryngeal ; spinal accessory ; glossopharyngeal ; hypoglossal

6 brainstem reflexes absent in brain death:

1. Pupillary response to light 2. Corneal reflex 3. Oculocephalic reflex (dolls eyes) 4. Oculovestibular reflex (caloric response) 5. Gag & cough reflex 6. Facial motor response

Goals of anesthetic management of organ donors: *Maintain — 1. SBP > — 2. PO2 > — 3. Urine Output > —ml/hr 4. Hbg concentration —g/L 5. CVP — 6. FiO2 < —% (if tolerated) 7. Glucose < —mg/dl 8. Peak airway pressures < —

euvolemia ; 100mmHg ; 100mmHg ; 100ml/hr ; 100g/L ; 5-10mmHg ; 40% ; 200 ; 30mmHg

Absolute contraindications for transplants: —

active infection

Transplant: Intraoperative renal considerations: 1. SBP > — 2. MAP > — 3. CVP > —

90mmHg ; 60mmHg ; 10mmHg

Liver Transplant Severe — – THAM – trishydroxymethl

acidosis

Pneumoperitoneum: Hemodynamic Δ’s: 3

↑SVR&MAP,↓CI

Eye Surgeries Normal IOP: —mmHg based on rate of aqueous humor formation & rate of aqueous humor outflow

10-22

IOP ↑ with — IOP ↓ with —

hypercarbia ; hypocarbia

—: cardio effects of ocular meds, oculocardiac reflex, MH, PONV

Strabismus

—- the single most effective means to increase PaO2 w/OLV

CPAP

OLV: —- non-dependent lung 5-10cm H2O

CPAP

OLV: —- dependent lung 5-10cm H2O

PEEP

OLV: Other actions: 2

periodically inflate collapsed lung, ligate PA

OLV: Greatest risk = —

hypoxemia

Inhibition of HPV: 6

1. Hypocapnia 2. Vasodilators 3.VA 4. High or low pulmonary artery pressure 5. High or low mixed venous partial pressures 6. Pulmonary infections

TRAM: Avoid —&— during abd closure

vasopressors and N2O

—: Surgical procedure where a mediastinoscope is inserted into the mediastinal space in order to view and biopsy lymph nodes.

Mediastinoscopy

Mediastinoscopy: Monitors: Art-line & pulse ox - — BP cuff – —

Right ; Left

Mediastinoscopy: The most common reason for doing this —

bronchogenic carcinoma

Mediastinoscopy: Compression: innominate or Right —

brachiocephalic

Mediastinoscopy: Complications: #1- — & #2 — tearing of great vessels, chylothorax,bronchospasm from airway manipulation, air embolism, arrhythmias, & esophageal laceration.

hemorrhage ; pneumothorax

—: Hypotension, tachycardia, cutaneous hyperemia, and hypoxia are signs caused by the release of vasoactive amines (principally prostacyclin) from the vascular bed of the mesentery. As a result, serum prostaglandin levels increase substantially

Mesenteric Traction Syndrome

Mesenteric Traction Syndrome: Tx: 4

H1 & H2, Ketorolac, Neo

Tourniquet Inflated: Arm —mmHg > SBP (—) Leg —mmHg > SBP (—)

50 (250mmHg) ; 100 (300mmHg)

Tourniquet: Tourniquet times should not exceed —

1.5 to 2 hours

Tourniquet: —CVP & SBP — HR, ETCO2, PaCO2, serum K, & serum lactate

↓ ; ↑

Restrictive Lung Disease Extrinsic: 7

pectus carinatum, pectus excavatum, kyphosis, scoliosis, and flail chest as well as obesity, neuromuscular disorders

Restrictive Lung Disease Intrinsic: —

Sarcoidosis

Bowel Obstruction: — should never be administered to a patient suffering from a bowel obstruction due to the possibility of perforation from its prokinetic effects

metoclopramide

—: projects to the medial thalamic nuclei - associated with autonomic & emotional responses to pain.

Paleospinothalamic tract (medial spinothalamic tract)

— possesses fibers that ascend to the lateral cervical nucleus and then cross to the contralateral thalamus.

spinocervical tract

— projects to the midbrain reticular formation and may generate nondiscriminatory pain sensations

spinomesencephalic tract

—: and sends fibers to the posterior nuclei of the thalamus- location and intensity of pain.

Neospinothalamic tract (lateral spinothalamic tract)

— burn: consists of erythema w/ only microscopic damage to the superficial epidermis.

First-degree

— burn: (partial thickness), extend through the epidermis into the dermis. Spontaneous regeneration of the skin is possible

Second degree

— burn: total destruction of the skin, dermal appendages, & epithelial elements occurs with no spontaneous regeneration of the skin possible.

Third-degree

— burn: involve muscle, fascia, and bone

Fourth-degree

Burns: Fluids: first 24 hours is = equation

% body surface area X Kg X 2 to 4. (hct)

Rule of Nines: adults:

each arm 9%, each leg 18%, the entire trunk is 36%, head 9%, perineum 1%.

Burns; Hct & viscosity: — significantly

↑

Burns: UO: Adults —ml/kg/hr < 30kg peds —ml/kg/hr

0.5 ; 1

Burns: Anesthesia: OR —C

28-30

Burns: most heat loss from burns = —

evaporation

Burns: Resistant to — d/t ↑ # of cholinergic nicotinic receptors

NDMB

Most common cause of trauma coagulopathy = —

Dilutional thrombocytopenia

Cardiogenic shock: —PAOP >15mmHg, —CI, —SVR

↑ ; ↓ ; ↑

Hypovolemic shock: —PAOP, — CI, — or—SVR

↓ ; nml ; nml/↑

Autonomic Hyperreflexia: 65-80% ↑— (unlikely below —)

T7 ; T10

—: Triggering stimuli: bladder, or bowel distention, heat/cold, uterine contractions, pyelonephritis

Autonomic Hyperreflexia

Autonomic Hyperreflexia: S/S: Hallmark – —&—

HTN & reflex bradycarda

Autonomic Hyperreflexia: — level of injury – SNS activation = vasoconstriction & HTN

Below

Autonomic Hyperreflexia: — level of injury- SNS blockade = vasodilatation

Above

— block for pancreatic cancer = most effective ; Blocked with alcohol or phenol

Celiac plexus block

— nerve block = relief from cluster headaches

Greater occipital

— fibers from the head are carried within the trigeminal, facial, glossopharyngeal, and vagus nerves.

Pain

— are the most common multipurpose coanalgesic used for cancer pain

Corticosteroids

Post-operative shivering medications: 4

1. Clonidine 2. Physostigmine 3. Serotonin antagonists 4. Propofol

— = large voltage applied to skin/tissue

Macroshock

— = small voltage/current directly to the ♥

Microshock

V-fib caused by — microamp-micro or — milliamp- macro

50 ; 100-2500

Grounded in OR: 3

Power supply, Patient, The floor

Units & Measurements PO2 = —

760mmHg

Units & Measurements 1mmHg= —cm H2O

1.36cmH2O

Units & Measurements 1atm = —mmHg=— psi = — kPa = — bar

760 ; 14.7 ; 101 ; 1

CO2 Absorber -Baralyme = 80% Ca(OH)2 + 20% Ba(OH)2 (no silica) -—L of CO2/100g

10.2L

CO2 Absorber -Soda Lime = 94% Ca(OH)2 + 5% NaOH + 1% KOH -—L of CO2/100g

-26L

E cylinder: O2 = — Liters, — psi

660L ; 2200 psi

E cylinder: Air = — Liters, — psi

625L ; 1800 psi

E cylinder: N2O = — Liters, — psi

1590L ; 750 psi

Law of Laplace T=equation

P x r

When N2O < 745 psi= no more — & ~ —L of N2O remains

liquid ; 400L

—- Quick connectors indexed for specific gas- SAFETY & is a check Valve- Wall Hose to machine – pressor of 40-50psig

DISS

— value on back of gas machine at pressure of 1380 kPa (200 psi) or less. Closes if cylinder pressure is on & pipeline pressure is off.

free floating value

O2 pin index — & N2O is —

2,5 ; 3,5

1st stage regulator- —psig (intermediate)

40-50

2nd stage regulator- 40-50 to — psig

O2 Flush Valve- —L/min, —psig (intermediate)

35-75 ; 40-50

Pressure Sensor Shut-Off Valve: (only senses PRESSURE) Senses O2@ 50 psig, shuts of N2O if O2 pressure falls O2 pressure @ —psig to keep open

Components of the High Pressure system of AM : > 55psig (4)

1.hanger yoke 2. yoke block w/ check valves (free floating) 3. cylinder pressure gauge 4. cylinder pressure regulators

Components of intermediate pressure system of AM: 40-50 psig (6)

1. Ventilator power inlet 2. pipeline inlets, check valves, pressure gauges 3. flow meter valves 4. oxygen pressure- failure devices 5. oxygen second stage regulators 6. flush valve

Components of the low-pressure system of AM: 16 psig (4)

1. flow meter tube 2. vaporizers 3. check valves 4. CGO

—: dual circuit, gas vapor blender, 39C & pressurized to 2 atmospheres (1300mmHg) @ high elevation – need to ↑ concentration to raise PP

Tec 6 vaporizer

Oxygen supply failure alarm: Sets off an alarm if the oxygen pressure falls below a standard set by the manufacturer typically —psig. Must engage within —seconds of the disconnect and cannot be disabled by the anesthetist.

30 ; 5

—: Prevent hypoxia from lack of oxygen flow, but does not prevent the flow of anesthesia gases (still possibly allow a hypoxic mixture of gases to be delivered).

Oxygen supply failure alarm

—: An intermittent back pressure caused by positive pressure ventilation or use of the oxygen flush valve results in ↑ vaporizer output. (not happening on newer machines)

Pumping Effect

Pumping Effect: —: flows, vapor dial settings, levels of anesthetic in vaporizer

Low

Pumping Effect: —: RR & PIP

High

Tipping of the vaporizer = — agent to the patient

most

— System- no mask on the face ie. NC

Open

— system: mask on face- no rebreathing = ↑ FGF

Semi-Open

— system: mask on face- some rebreathing w/ regular flows

Semi-Closed

— system: Mask on Face: - complete rebreathing APL closed & low flows (150-500ml/min physiological requirements)

Closed

Mapleson Systems: Prevention of rebreathing – spont ventilation: —> DFE > —

A ; CB

Mapleson Systems: Prevention of rebreathing Controlled vent: — > BC > —

DFE ; A

All Mapleson can ventilate the — patient

Apneic

Mapleson — modified = Bain → best for controlled vent

Mapleson — only one w/o reservoir bag

Mapleson — = Jackson Reese - peds d/t ↓ WOB but heat loss

Forced Air Warmer: Maximum temp —C Average contact —C

48 C ; 46 C

Blood Salvage Contraindications: 5

1. Infection 2. malignant cells 3. Urine 4. bowel contents 5. Amniotic fluid

Blood Salvage Contraindications: 5

1. Infection 2. malignant cells 3. Urine 4. bowel contents 5. Amniotic fluid

Pacemaker Chamber — A,V,D Chamber — A,V,D — – Inhibit, Trigger, Double, O-none

paced ; sensed ; Response

Pulse Oximetry: — law

Beer Lambert

Pulse Oximetry: Fx w/ 2 wavelengths: Red light —nm – — Hbg Infrared light —nm- — Hbg

660 nm ; Deoxygenated ; 940nm ; Oxygenate

— are one of the last places to showing desat (central first)

Fingers

Changes in Pulse Oximetry False —: Caboxyhemoglobin & methemoglobin, severe anemia, SpO2 < 85%

High

Changes in Pulse Oximetry False —: Methylene blue, prominent venous pulsations, injection (if dyes- indigo carmine, lymphazurin, nitrobenzene, indocyamine green, patent blue)

Low

5 monitors that can detect disconnection:

1.pulse oximetry 2. mass spectrometer 3. capnography 4. stethoscope 5. spirometer

Mass Spectrophy: Gases analyzed: —,—,—&— (Not —)

CO2, O2, N2 & inhaled agents ; PaO2

Mass Spectrophy: — is ionized by an electron beam and passed through a magnetic field.

Gas sampled

Mass Spectrophy: —: measures gas concentrations by analyzing the intensity of light emitted when a gas sample returns to an unexcited state after being energized by a laser beam

Raman

Mass Spectrophy: —: they detect gases based on the amount of this light that is absorbed by the sample- can not detect oxygen content Most popular in the OR & based on beer lambert

Infrared

Mass Spectrophy: — drug= high false measurements

Isoproterenol

TOF – —Hz – — twitches per — second or — every — seconds

2Hz ; 2/1sec ; 1/.5

Tetany- — seconds @ —Hz

5 ; 50Hz

DBS- — trains of — impulses @ —Hz – separated by 750 ms

2 ; 3 ; 50Hz

—- best to determine fade

DBS

Post Tetanic- —Hz x — seconds – — second pause – stim @ —Hz

50Hz ; 5sec ; 3sec ; 1Hz

# of visible post tetanic twitches correlates — to time required for return of single twin or train-of-four responses

inversely

— nerve = adductor pollicis- —

Ulnar ; abdomen

— nerve = orbicularis oculi – —

Facial ; laryngx

Twitches: 1. one visible twitch = —% blockade G 2. two visible twitch= —% blockade 3. three visible twitches= —% 4. four visible twitches = <—%

95 ; 80-85 ; 75-80 ; 75

— – based on HYPNOSIS

BIS

BIS: —- Awake

100

BIS: —- Light/Moderate Sedation

90-70

BIS: —- Deep sedation (low probablility of recall)

70-60

BIS: —- general anesthesia

60-40

BIS: —- deep hypnotic state

40-10

BIS: —- flat line EEG

10-0

BIS: < — reflect burst suppression.

BIS: — can be produced by: Output from cardiac pacemakers, muscle activity such as twitching, shivering, or blinking, incorrect electrode placement, & high frequency electrical devices such as IV pumps and warming devices can all produce artifact.

Artifact

BIS: — waves may occasionally be seen during anesthetic maintenance and emergence.

Paradoxical delta waves

Blood Pressure Cuffs: —% of arms circumference

Blood Pressure Cuffs: — if cuff: too loose, too small, or positioned below the level of the heart

Overestimation

Pacemakers Most common indications = —&—

SSS & complete ♥ block

Pacemakers: ID codes 1st = chamber — 2nd= chamber — -- eletrocautery affects 3rd= — to sensing 4th= programmability — modulation 5th= fx

paced ; sensed ; response ; rate ; antitachyarrythmic

Pacemakers: ID codes: —= eletrocautery affects

2nd

Pacemakers: ID codes: AICD affects which letters?

4th and 5th

Pacemakers: — can inhibit the pulse generator d/t fasiculations

Succs

Pacemakers: Avoid — if implanted within 1-2 days ago

nitrous

Magnet —- converts to a fixed rate (asynchronous) mode

Pacer

Magnet —- disables it – loud continuous high pitch sound

AICD

—: destroys most microorganisms- except SPORES

Disinfection

—: all viable forms of microbial life – yes to spores

Sterilization

7 —: quaternary ammonium, alcohols, glutaraldehydes (Cidex), hydrogen-peroxide, formaldehyde, phenolic compounds, chlorine ( bleach)

chemical disinfectants

—- for objects that can’t be heated in steam autoclave

Ethylene oxide

Glutaraldehyde (Cidex) & hydrogen peroxide = — destruct

SPORES

Quaternary ammoniums – WILL NOT kill —

tuberculosis

Lasers can be both long (—) and short (—) wavelengths.

CO2laser ; YAG laser

— laser risks: Thermal injury, eye injuries, electrical hazards, fire, transmission of viruses, and contaminants in the smoke plume

Major

Nd-YAG laser – OD(optical density) 5 or > for 1,064 nm/—

Green

—: Laser vaporization of condylomatous lesions d/t release toxic chemicals: benzene & formaldehyde as well as viable viruses capable of transmitting the disease

N-95 respirator mask

Gas Laws mnemonic:

“Can These Girls Possibly Be Virgins”

Boyle = equation

P1V1 = P2V2

Charles = equation

V1/T1 = V2/T2

Gay-Lussac = equation

P1/T1 = P2/T2

— = 1 mole of gas @ STP = 22.4 Liters

Avogadro’s Hypothesis

Avogadro’s Number: — = 1 mole

6.023 X 10^23

1 mole = 00 = 1 atm = 760 mmHg = —L

22.4L

Gases liquefy if: 2

(1) sufficient pressure is applied and (2) temperature is below critical temperature

critical temperature: N2O = —C O2 = —C

39.5C ; -119C

—: (P1 –P2) (Area) (Solubility)/ (Membrane thickness) (square root Molecular Weight)

Fick Diffusion

Fick Diffusion: the — is the most important factor in determining the rate of diffusion of a drug across a membrane

concentration gradient

% Concentration = equation

(Partial Pressure/Atm) X 100

Partial Pressure = equation

(% Concentration X Atm)/100

Partial Pressure H2O @ 370 C = —mm Hg

Laminar Flow: —Law

Poiseuilles

Poiseuilles Law = equation

F=πr4ΔP/8nl Flow F= flow, r = radius, n= viscosity, l= length

Poiseuilles : Doubling the radius = — the flow

16x

Tripling the radius = — the flow

81x

Angle < — degrees = laminar flow

— #- turbulent flow

Reynolds

— Reynolds # = turbulent flow

>1,500-2000

— determines flow when turbulent flow present

Density (p)

—: Flow through constricted region of the tube = ↑ Flow & corresponding ↓ in pressure in area of narrowing

Venturi/Bernoulli

—: Law of mass action

LeChatelier’s

LeChatelier’s: ↑ concentration of reactant→ reaction to — products

↑

LeChatelier’s: Law of mass action ↑ concentration of reactant→ reaction to — reactant (— products)

↑ ; ↓

—: Calculation of dissolved O2 & CO2 in blood

Henry’s Law

—: Total pressure in a mixture is = to the sum of pressures of each gas

Dalton’s Law of Partial Pressure

Dalton’s Law of Partial Pressure: of O2, N2, and total

O2: 160mmHg (21%) N2: 600mmHg (79%) Total: 760mmHg

—: A cylinder cools and condenses after opening a valve – Joule is cool

Joule-Thompson

—: The intensity of light is altered as transmitted through liquid. The intensity of the light falls exponentially as light passes through the liquid.

Beer Law

Law of Laplace; T= equation

P x r – cylindrically shaped structures thus ↑T = ↑ r

Law of Laplace: Applies to: 2

blood vessels, left ventricle (Frank-Starling)

Law of Laplace: Applies to alveoli – ARDS equation T=

(P x r) /2 -- spherically- shaped structures thus ↑r = ↑ T, ↓r = ↑ P

Humidification Relative Humidity (%) =

(actual vapor pressure/Saturated vapor pressure) x 100

Humidification: ↓ T = — capacity to hold H2O → H2O condenses

↓

— Law: SVR

Ohms

—: Solubility of a gas in a fluid

Ostwald Solubility Coefficient

Ostwald Solubility Coefficient: -Amount of gas in solution is — proportion to temp -—= ↑ solubility of VA in blood & tissue

inversely ; Hypothermia

—: Non-ideal gas behavior

Van Der Wals

—: Distance from source = amount of exposure

Inverse Square Law

Fires in OR: Components needed for Fire: —,—&—

fuel, oxygen & ignition source

Fires in OR: Steps if fire occurs: 6

1. Stop ventilation 2. Stop O2 Flow 3. Extubate patient 4. Extinguish the fire 5. Mask ventilate 6. Reintubate

—→ formed the AANA in 1931

Agatha Hodgins

— → 'Mother of Anesthesia

Alice Magaw

— → first LA

Cocaine

—= an order by a court to force a party to commence some required action.

A writ of mandamus

—= refers to the doctrine of common law in which courts adhere to the prior decisions of other courts.

Stare decisis

—= (the thing speaks for itself) refers to an event that would not have occurred 'but for actions of the defendant'.

Res ipsa loquitor

— = Civil Wrongdoing

Tort

— = Failure to use reasonable care, which is that level of care recognized as acceptable and appropriate given the circumstances.

Negligence

—= is a lawsuit to recover goods improperly taken by another.

Replevin

—= intentionally causing harmful or offensive contact with a person or to something close to them

Battery

—= intentionally causing the apprehension of an immediate and harmful contact

Assault

Four Elements of Malpractice:

1.Duty- prove defendant had a duty to the plaintiff 2.Breach of Duty- prove defendant failed to fulfill duty to defedant 3. Causation - reasonably close relationship proven to exist between breach of duty by defendant and the injury that resulted 4.Damages - prove some injury occurred due to the breach in duty

Informed Consent Includes: 4

1. Risks 2. Benefits 3. Complications 4. Alternatives

—: defines compressed gas standard

Department of Transportation

—: sets specification for compressed gas cylinder construction

Interstate Commerce Commission

—: defines compressed gas standard

Federal Food, Drug & Cosmetic Act

—: develops purity standards for gases

United States Pharmacopeia

—: recommendations for the construction and location of BULK oxygen containers

National Fire Prevention Association

—: sets standards of practice

Compressed Gas Association

—: performance & safety requirements for components of the AM, ETT, connectors,vacuum & gas pressure regulators

American National Standards Institute (ANSI)

—: promulgates standards for medical devices and gases

Food and Drug Administration

—: voluntary accrediting agency

Joint Commission

—: assess technology & revises standards

American Society for Testing Materials (ASTM)

—: standards to protect the health & safety of workers

National Institute of Occupational Safety & Health

—: When researchers, on the basis of a statistical test, erroneously concludethat there is evidence of an association between two variables when, in fact, there is not

Type I error

—: When researchers, on the basis of a statistical test, erroneously conclude that there is evidence of no association between two variables when, in fact there is

Type II error

Acute hypoparathyroidism & hypocalcemia usually presents w/in —hrs following surgery

24-96

Hypoalbuminemia, hypomagnesemia, hyperphosphatemia, vitamin D deficiency, PTH deficiency, pancreatitis, RF, massive blood transfusions, burns, & sepsis are all causes of —.

hypocalcemia

Factor — is the only clotting factor that decreases w/ pregnancy.

— is active myocardial relaxation

Lusitropy

— or contractility

Inotropy

— is a genetic condition affecting a protein in the body called the fibroblast growth factor receptor. This protein begins to function abnormally, slowing down the growth of bone in the cartilage of the growth plate.

Achondroplasia

— syndrome is a disorder of your immune system identified by its two most common symptoms, dry eyes & a dry mouth. The condition often accompanies other immune system disorders, such as rheumatoid arthritis & lupus.

Sjogren's

— are the MOST SENSITIVE to anesthetic technique & are rarely ever used.

Visual evoked potentials (VEP)

The evoked potentials in order from least to most sensitive to anesthetic technique are:

BAEP < SSEP < MEP < VEP. Another way to remember: BAEP=Barely affected, SSEP=Somewhat affected, MEP=Mostly affected, & VEP=Very affected.

ASA —-A normal healthy pt. (Healthy, non-smoker

ASA —-A pt w/ mild systemic disease w/o functional limitation. (Smoker, Pregnancy, Controlled Diabetes)

ASA —-A pt w/ severe systemic disease. (Morbid obesity, ESRD with regular dialysis)

ASA —-A pt w/ severe systemic disease, constant threat to life. (Recent (< 3mths) TIA or MI, ESRD not on regular dialysis)

ASA —-A moribund pt who is not expected to survive w/o the operation (Massive trauma, ICH with mass effect)

ASA —-A declared brain-dead pt whose organs are being removed for donor purposes.

— are associated w/ leukocytosis, increased Hb, hyperglycemia, hypokalemia, mild hypernatremia, alkalosis, increased urinary uric acid, & increased urinary Ca+.

Corticosteroids

— act on the kidney to stimulate reabsorption of Na+ & excretion of K+ & H+ ions resulting in normal/slightly high plasma Na+, hypokalemia, & alkalosis (not causing uric acid & urinary Ca+).

Mineralocorticoids

— can result in decreased O2 delivery to the tissues through an impairment in the production of 2,3-diphosphoglycerate. Decreased ATP production will also tend to cause diaphragmatic weakness &, in severe cases, cardiac failure. Other sequelae include hemolytic anemia, neurologic deficits, seizure, & eventual death.

Hypophosphatemia

— is characterized by adrenal gland dysfunction manifesting as fatigue, weakness, anorexia, N&V, cutaneous mucosal hyperpigmentation, hypovolemia, hyponatremia, hyperkalemia, HoTN, & metabolic acidosis.

Primary adrenal insufficiency (Addison disease)

During prolonged fasting the brain uses — bodies as an alternate source of energy. The other organs use —.

ketone ; fatty acids

— syndrome is due to an excess secretion of serotonin into the systemic circulation. Diagnosis made by measuring 24hr urinary levels of 5-HIAA.

Carcinoid syndrome

The primary pathophysiology of MH is an uncontrolled release of — by the — that causes a profound hypermetabolic state.

Ca+ ; sarcoplasmic reticulum

— may be used as a 1st-line vasopressor for neurogenic diabetes insipidus following TBI.

Vasopressin

W/ morphine 10mg IV as the standard potency of “1”: — 1/8th as potent, — 8-10x as potent, — & — 100x as potent, — 1000x as potent, & — 10x as potent.

meperidine ; hydromorphone ; fentanyl & remi ; sufent ; alfent

Verapamil & diltiazem are the — & watch for —

Ca+ channel blockers ; hyperkalemia

— is a mast cell stabilizer that works to prevent the release of histamine, leukotriens, & other allergic mediators by preventing degranulation of mast cells.

Cromolyn Na+

— is an inhaled steroid useful in the prevention of attacks, & prednisone may be taken orally for the same purpose.

Fluticasone

— is a leukotriene modifier.

Montelukast

— is a long acting beta agonist that should be administered only w/ a rapid acting beta agonist inhaler available, as it has been linked w/ severe asthma attacks.

Salmeterol

Beta blockers that begin w/ letters after “—” are non-selective (— is an exception).

N ; labetalol

— is a degenerative disease caused by a loss of dopaminergic neurons in the substantia nigra along w/ the presence of Lewy bodies.

Parkinson’s disease

— is a drug administered for Parkinson’s instead of dopamine, as dopamine cannot cross the —.

Levodopa ; BBB

— must be avoided as they worsen symptoms of Parkinson’s

Antidopaminergic drugs (metoclopramide & prochlorperazine)

demyelination & axon degeneration is —.

multiple sclerosis

The inherited autosomal dominant neurodegenerative disorder is — disease.

Huntington’s

immune response directed towards myelin or peripheral axons is —.

Guillain Barre

All — can cause spasm of the sphincter of Oddi & can lead to biliary colic when the gallbladder contracts against a closed sphincter

opioids

spasm of the sphincter of Oddi can be treated w/: 4

naloxone/other opioid antagonist, glucagon 1-2mg IV, nitroglycerin or atropine.

Pancuronium & hydralazine both cause an — in HR

increase

— syndrome may be heralded by sudden onset of refractory bradycardia, HLD, metabolic acidosis, hyperkalemia, RF, & rhabdomyolysis. >4 mg/kg/hr or 67 mcg/kg/min, long term propofol therapy, defined as >48hrs

Propofol infusion

— are contraindicated in decompensated HF pts & in the presence of AV conduction blocks greater than 1st degree.

Beta adrenergic antagonists

— is a potent antiHTN that also increases renal perfusion.

Fenoldopam

— is a non-selective beta blocker that is useful to treat HTN, anxiety disorders, & Grave’s disease/hyperthyroidism.

Propranolol

— is a thyroid hormone replacement for pts w/ hypothyroidism.

Levothyroxin

— is used in the treatment of Grave’s disease & hyperthyroidism.

Propylthiouracil (PTU)

Using — can cause suppression of the hypothalamic-pituitary-adrenal axis (HPA).

exogenous glucocorticoids (prednisone)

— is the most likely neuromuscular blockade agent to cause an allergic reaction of muscle relaxants.

Succ

— treatment of SVT & rapid rate a-fib due to its ability to block the Ca+ channels of the AV node.

Diltiazem (benzothiazepine Ca+ channel blocker)

ACE-I typically cause —kalemia

Hyper

— is broken down by Erythrocyte Esterase hence its short DoA. Anemic pts can experience a prolonged effect.

Esmolol

— for the treatment of carcinoid syndrome

octreotide

— is an opioid that blocks the neuronal re-uptake of serotonin in combo w/ MAOIs. This has lead to serotonin syndrome & caused seizures & deaths in pts when these are combined.

Meperidine

Treatment for beta blocker OD: 4

atropine, glucose & insulin, glucagon, Ca+ chloride

Liver failure decreases amount of acetylcholine that is being produced by the liver, thus — NDMB.

prolonging

— should be avoided in pts w/ sepsis. Adverse outcomes have been reported w/ its use in pts likely due to suppression of adrenal cortisol production.

Etomidate

— agonists (Spinal) provide for analgesia & also provide some of the negative side effects of opioids, including ventilatory depression, physical dependence, & constipation.

Mu2

— receptors activated by intrinsic endorphins & exogenous opioids.

Reversal of GP IIb/IIIa inhibitors (abciximab) can be accomplished w/ — transfusion, but is less effective w/ the smaller molecules of tirofiban.

plt

— is a selective phosphodiesterase inhibitor that decreases hydrolysis of cyclic AMP & cyclic GMP, leading to increased intracellular cAMP & cGMP. This increases inward movement of Ca+ ions, causing positive inotropic effects & relaxation of vascular & airway smooth muscles. It is thus a positive inotrope & preload & afterload reducer.

Amrinone (inamrinone)

— works upon the activation of beta 2 receptors after inhalation of the aerosolized drug. Beta 2 receptor activation causes relaxation of the bronchial smooth muscles through activating adenylate cyclase & thus increasing cAMP.

Albuterol

Drugs that can be administered through the ETT:

NAVEL or ALIEN V: A – atropine, L – lidocaine, I – Isoproteronol, E – epinephirine, N – naloxone, V – Valium (diazepam).

— work to strongly inhibit factor Xa (traditional heparin effects antithrombin III & inhibits Xa).

Enoxaprin & other LMW heparin

— is an alpha 1 agonist only at all doses.

Phenylephrine

Dobutamine has only — effects

beta 1

isoproterenol has — only

beta 1 & beta 2 agonisim

Dopamine: Doses —mcg/kg/min activate dopamine 1 receptors which produces renal dilation (once believed helpful to pts needing renal protection but evidence does not support the usefulness of dopamine for this). Doses —mcg/kg/min beta 1 receptors are activated. Doses —mcg/kg/min to greater concentrations alpha receptors are activated causing vasoconstriction.

1-3 ; 3-10 ; 10

75% of initial dosage of fentanyl is removed from circulation on the first pass through the —, & repeated doses of fentanyl may cause saturation of the pulmonary sites leading to a prolonged DoA.

lungs

Ventilatory depression is not seen with activation of — opioid receptor activation.

Mu1

Remifent has the advantage of providing a rapid & dense analgesic response (w/in —min), w/ an equally quick termination of action in —min.

1-3 ; 3-10

— disease should not receive droperidol as it antagonizes dopamine receptors. Droperidol can cause extrapyramidal symptoms.

Parkinson’s

one of the greatest challenges in treating the pt on tricyclic antidepressants is the unpredictability of the patient’s —.

— blocks ADP receptors on the surface of platelets, inhibiting platelet activation and aggregation.

Clopidogrel

— is a phenylalkylamine Ca+ channel blocker that blocks slow Ca+ channels of vascular smooth muscle & myocardium, greatly slowing conduction through the AV node. It also has negative chronotropic effects on the SA node (decreasing HR) & is a negative inotrope on cardiac muscle. It also relaxes the coronary vasculature & causes coronary vasodilation. used to treat supraventricular dysrhythmias such as SVT but should be avoided in pts with WPW syndrome.

Verapamil

— should be avoided in pts with WPW syndrome.

Verapamil

— should be avoided to decrease the chances of iatrogenic seizures. Morphine-3-glucuronide also has proconvulsant properties as a metabolite of morphine, but is not listed as a choice here. Morphine-6-glucuronide is the active pain relieving molecule derivitive of morphine.

Meperidine (Demerol)

— acts by decreasing hepatic production of glucose by decreasing gluconeogenesis through increasing hepatic sensitivity to insulin–thus it only works in the presence of insulin. It does NOT cause hypoglycemia.

Metformin

— NDMR is known to increase HR, MAP, & CO. SVR is not changed to a great degree. It produces a slight blockade at cardiac muscarinic receptors, inhibiting parasympathetic activity allowing for an increase in HR.

Pancuronium

A — in SVR may be seen w/ giving midazolam

decrease

Alfentanil is — metabolized extensively

heptically

Most anesthesia providers will use — mA as the goal of optimal position for nerve blocks

0.5

—, a derivative of PABA (para-aminobenzoic acid) & a popular preservative used in multi-dose LA, & is most commonly implicated in anaphylactic reactions from LA adminstration.

Methylparaben

LA w/ the highest amount of — binding have the longest anesthetic duration.

protein

—,—,—,— have high levels of protein binding & are long-acting LA.

Bupivicaine, Etidocaine, Ropivcaine & Tetracaine (BERT likes protein)

— fibers are preganglionic sympathetic neurons located at the outer most area of the nerve root. These fibers are small & myelinated.

Sympathetic — fibers are attenuated 1st so the sympathectomy is the 1st sign of the LA starting to work.

The — fibers are small & unmyelinated while the — fibers are also small but myelinated.

C ; A-delta

— and — fibers are involved in transmitting pain, temp, & touch w/ a subset of the — fibers, the — fibers, transmitting for various autonomic functions since they are postganglionic sympathetic neurons.

C & A-delta ; C ; sC

The large myelinated fibers —,—&—. These fibers are motor efferents involved in muscle movement, propioception, touch & pressure.

A-gamma, A-alpha & A-beta

— are the abnormal sensation of the skin (tingling, prickling, numbness, or burning) that has no objective cause.

Paresthesias

—&— are 2 LA that can cause methemoglobinemia.

Prilocaine & benzocaine

—: These pts are most often middle age females, but people of a broad spectrum of ages & genders have been diagnosed. Pts may complain of “fibro-fog,” a feeling of impaired concentration & memory problems, & to pain sensitivity. Times of emotional stress seem to bring on exacerbations, & exercise & antidepressants have been proven helpful to many pts w/ this condition.

fibromyalgia

— was the 1st FDA approved med for fibromyalgia. Other meds: —,—&—

Pregabalin (Lyrica) ; SSRI (citalopram) & SNRI (duloxetine) are useful, tricyclic antidepressants (amitriptyline).

Absolute contraindications to neuraxial anesthesia: 7

infxn at site of injection, severe mitral or aortic stenosis, severe hypovolemia, increased ICP, bleeding diathesis, coagulopathy, or pt refusal

Relative contraindications: 4

sepsis, severe scoliosis or kyphosis, demyelinating lesions, & valvular heart lesions

— means painful response to a typically non-painful stimulus. Seen in: migraines, cluster headaches, postherpetic neuralgia, complex regional pain syndrome, neuropathies & fibromyalgia.

Allodynia

Morphine is more likely to spread to — than fentanyl.

CNS

Due to its antagonism, — exhibits a “ceiling effect” & doses >30mg don’t produce further respiratory depression if no other depressants are present.

nalbuphine

Unlike atracurium, — doesn’t cause elevations in plasma histamine levels which may lead to urticaria.

cis-atracurium

— is still one of the most common meds to be implicated in OD & death, w/ its main area of destruction being the liver hence the high AST & ALT levels.

Acetaminophen

For elective surgery, warfarin should be discontinued at least —days prior to procedure if normal INR is desired.

5dys

— acts to inhibit the release of acetylcholine, & — decreases the release even more. It also competitively inhibits Ca+ influx into the presynaptic nerve channels at the Ca+ channel. Other drugs such as Ca+ antagonists also can interfere w/ neurotransmitter release.

Mg+ ; hypermagnesemia

4mg of — is equivalent to 20mg of cortisol or 0.75mg of dexamethasone.

methylprednisolone

—&— steroids both have characteristically low Na+ retaining abilities while providing adequate anti-inflammatory potency.

Methylprednisolone & prednisone

— steroid has no Na+ retaining ability & potent anti-inflammatory properties.

Dexamethasone

—&— steroids can be useful for a variety of inflammatory & immune conditions.

Both dexamethasone & methylprednisolone

All — cause an increased incidence of potential dangerous CV incidents which may include HF, MI, & stroke.

steroids

—: the risk of dyskinesia is elevated due to the presence of Parkinson’s disease & is best avoided

Promethazine (Phenergan)

— is a delayed dyskinesia due to prolonged use of drug.

tardive dyskinesia

— (drooping eyes) & — (double vision) are often the earliest & most commonly seen signs in MG

Ptosis ; diplopia

treatment of — is largely supportive, w/ particular attention to respiratory support. Autonomic dysfunction occurs in up to 70%, w/ tachycardia being the most common reported finding. These pts also need to have proper bowel & bladder care taken, & DVT prophylaxis should be undertaken w/ low molecular weight or unfractionated heparin.

Guillain-Barre

CMRO2 averages — mL/100g/min in adults.

3.5

Cerebral blood flow avg — mL/100g/min in peds (avg — mL/min in the adult pt).

50 ; 750

Cerebral blood flow is regulated b/n — mL/100g/min.

10-300

MG commonly affects — gender more.

females

Volatiles should be limited when evoked potentials are being conducted since they affect the amplitude (—) & latency (—) (below 0.5 MAC recommended).

decrease ; increase

Opioids have — on CMR or ICP.

no net effect

Volatiles — CMR & — ICP.

decrease ; increase

Nitrous — CMR & — ICP, but not as much as volatiles do.

decreases ; increases

Barbiturates profoundly — CMR & ICP w/ etomidate closely following suit.

decrease

CSF is produced at around — ml/hr, or approximately 0.3 cc/min.

The CSF is produced by the — in the lateral, third, & fourth ventricles. It circulates in the brain in the subarachnoid space.

choroid plexus

The normal CSF volume is — ml.

125 ml

Profound hypoxemia below tensions of 50mmHg will produce a significant — in CBF.

increase

Pts w/ Lambert-Eaton syndrome will have — sensitivity to succ & — sensitivity to NDMB.

increased ; increased

— is a condition resulting in impaired renal Na+ reabsorption in the proximal tubules leading to excessive urinary Na+ excretion. This leads to hyponatremia & a solute mediated diuresis of free water. The result is hyponatremia combined w/ hypovolemia. Can be caused by many CNS conditions & pathology including (Brain tumor, Tertiary syphilis, Meningiococcal Meningitis, Central nervous system surgery).

Cerebral Salt Wasting

— has had positive effects on pts w/ vasospasm after subarachnoid hemorrhage

Nimodipine

—% of CO in adults is taken as cerebral blood flow.

Intracranial HTN is defined as a sustained increase in ICP >— mmHg

— is an autoimmune disease in which IgG antibodies act against the voltage-gated Ca+ channels to interfere w/ Ca+ influx required to release acetylcholine at the motor end plate.

Myasthenic syndrome (Lambert-Eaton syndrome)

Vasospasm after subarachnoid hemorrhage usually doesn’t occur for — after the initial bleed

72hrs to upwards of 2wks

Cerebral blood flow — by approximately 3% or 1-2 cc/100g/min for every 1 mmHg decrease in PaCO2.

decreases

CPP is normally between — mmHg.

80-100

At — mL/100g/min an isoelectric wave is produced, & below — mL/100g/min is irreversible brain damage. <—ml/100g/min, there is slowing of the EEG demonstrating cerebral impairment.

15-20 ; 10 ; 25

Anticonvulsants (anti-epileptics) cross placenta & responsible for a — risk of birth defects when taken during pregnancy.

high

CO will eventually increase to —% greater than that of a nonpregnant female.

Terbutaline is a — agonist. Terbutaline’s — effects cause increases in cAMP levels leading to decreases in intracellular Ca+, causing the desired uterine smooth muscle relaxation. Side effects: HoTN, tachycardia, anxiety, chest tightening/pain, ECG changes, hyperglycemia, hypokalemia, & pulmonary edema. It is relatively contraindicated in pts w/ CAD & RF.

beta 1 & beta 2 ; beta 2

Infants delivered to mothers on — may develop hypoglycemia secondary to hyperinsulinemia, & infants may also develop tachycardia & MI.

terbutaline

HELLP stands for: —.

Hemolysis, Elevated Liver enzymes, & Low Platelets (less than 100,000/mm3)

—is a prostaglandin E1 analogue that can be useful to decrease uterine hemorrhage by increasing uterine tone.

Misoprostol (Cytotec)

Mg+ — acetylcholine at neuromuscular junction

decreases

indomethacin (NSAIDs) — prostaglandin synthesis.

inhibit

Beta adrenergic blocking drugs have — role in tocolysis

Pain in the 1st stage of labor should be relieved by — epidural blockade & is — pain.

T10-L1 ; visceral

The 2nd stage of labor adds — fibers of the birth canal entering at —.

somatic ; S2-S4

in the infants of hyperglycemic/poorly controlled diabetics mothers, -Congenital — lesions are increased (Transient subaortic stenosis due to ventricular septal hypertrophy) -vertebral, skeletal, renal, & CNS anomalies. -—is common & may be related to placental insufficiency & fetal hypoxia common to reduced O2 delivery. -—, a birth weight >4000 gm, increases risk of Erb’s palsy or phrenic nerve palsy due to shoulder dystocia. -—may be seen -—is caused by delay in the normal rise of PTH.

cardiac ; Polycythemia ; Macrosomia ; Jaundice ; Hypocalcemia

—&— are peptides activated in response to increased ventricular volumes & pressures.

BNP & ANP

Increased oxytocin levels causes release of —. -released in increased amounts w/ fluid loading, as done prior to administration of neuraxial anesthesia. -decrease vasospasm seen in uteroplacental circulation & provide benefit in uteroplacental perfusion. -promotes dilation of the vessels & excretion of Na+ by the kidneys.

ANP

— produces selective afferent arteriolar vasodilation & inhibits Na+ reabsorption in proximal convoluted tubule, but is not released by oxytocin–elevated. -seen in pts w/ CHF among other causes. Risk factors associated w/ nausea in spinal anesthesia includes a block height of T5 or greater, omission of neuraxial opioids, & a hx of motion sickness.

BNP

— is seen in infants of poorly controlled diabetic mothers, — is most often seen in macrosomic infants; & respiratory — secondary to immature fetal lungs-fetal lungs are immature as high levels of insulin block lung maturation.

Macrosomia ; hypoglycemia ; distress ;

—,—,&— is considered safe to use during pregnancy to treat BP.

Labetalol, Hydralazine & methyldopa

The period of greatest susceptibility to teratogenic agents is from —wks after conception

2-8wks

— (highest risk of malformations if taken while pregnant) (carbamazepine, phenobarbital, phenytoin, & valproic acid): neural tube defects & dysmorphic facial features, Cleft lip & palate, congenital heart disease.

Anticonvulsants

The grouping of orofacial, CV, & digital malformations is called fetal — syndrome.

anticonvulsant

— causes kid higher chance to have spina bifida at a rate of around 1-2%.

Valproic acid

— may increase the risk of cleft palate in 1st trimester exposure

Benzodiazepines

—&— depressants meds are thought to be safe.

Tricyclic antidepressants & SSRIs

— b/n 6-9wks gestation, can result in fetal — syndrome. It consists of nasal hypoplasia, mental retardation, growth restriction, & a depressed nasal bridge. It is not safe in any trimester, adverse effects in the 2nd & 3rd trimesters can result in microcephaly, deafness, blindness, & growth restrictions.

Warfarin

— doesn’t cross placenta & is the drug of choice for pregnant females requiring anticoagulation.

Heparin

— doesn’t cross placenta, but is cleared more rapidly in pregnancy than in non-gravid patients & dosing may need adjusting. Twice daily dosing should be considered.

Low molecular weight heparin

— antiHTN were shown to cause fetal renal dysplasia & oligohydramnios.

ACE inhibitors

If steroids are to be used, — is the drug of choice as only a small amount cross the placenta. — readily crosses the placenta & may be used as an aid to accelerate fetal lung maturity.

prednisone ; Dexamethasone

For nausea —,—&— are all considered safe during pregnancy.

promethazine, metoclopramide, & ondansetron

—&— Abx are safe for use during pregnancy.

Penicillins & cephalosporins

The — are probably safe the 2nd trimester, but must be avoided the 3rd trimester due to risk of neonatal pulmonary HTN & other negative outcomes, many recommend avoiding all pregnancy.

NSAIDs

During the 2nd stage of labor variable decelerations are the result of —.

compression of the fetal head

In the 1st stage of labor, variable decelerations are caused by —.

umbilical cord occlusion

— can cause fetus HR variability that is minimal (<5 BPM) to marked (>25 BPM). Variable decelerations are considered severe when they last >60sec or drop 60 BPM below the baseline rate. A healthy fetus can tolerate HR drops into the 80s in some cases

Hypoxia

The 1st trimester is considered the most risky due to the — that takes place during this period (3-8wks).

organogenesis

Due to lack of studies, risk can’t be ruled out in category — drugs.

Category — drugs are ones that controlled studies have shown no risk.

Category — drugs show no evidence of human fetal risks. These are typically animal reproduction studies w/o performing controlled studies in pregnant women.

Fetal abnormalities have been clearly demonstrated w/ administration of category — drugs, & these drugs shouldn’t be given in any pregnancy situation.

In Category — Evidence of human fetal risk exists, but the benefits may outweigh the risk in the pregnant woman (gentamycin, phenobarbital, ACE inhibitors (ACEIs are category C in 1st trimester only), & thiazide diuretics).

Amniotic fluid embolism resembles — shock.

anaphylactic

Amniotic fluid embolism: The — phase is caused an intense but temporary pulmonary vasospasm secondary to vasoactive mediators being released. This causes severe pulmonary HTN & right HF w/ sudden cardiopulmonary collapse. This collapse leads to the hypoxemia, cyanosis, & HoTN seen in these pts. Severe anxiety or a sense of impending doom may be seen early on as well. In some cases, the right HF will resolve & this phase generally lasts <1hr.

1st

Amniotic fluid embolism: The — phase shows a left HF & pulmonary edema. It is a hemorrhagic phase with massive hemorrhage, uterine atony, & coagulopathies or DIC.

2nd

Amniotic fluid embolism is diagnosed based on 4 criteria:

1) acute HoTN or cardiac arrest 2) acute hypoxia 3) coagulopathy or severe hemorrhage in the absence of other explanation 4) occuring during labor, c-section, or w/in 30min postpartum.

Amniotic fluid embolism coagulopathy should be treated w/ 3:

1. FFP for prolonged PTT 2. cryoprecipitate for fibrinogen levels <100 mg/dL 3. plt transfusions certainly for plt counts <20,000/uL

The detrusor muscle is responsible for micturation & urine storage, & is innervated by the sacral roots —.

2-4

Chest compressions are indicated if HR falls <— after 30sec of assisted ventilation, & should be ceased if the HR >—BPM

60 ; 60BPM

—: # of pregnancies a woman has had.

Graviditiy

—: # of pregnancies beyond 20wks gestation.

Parity

Abortions is the # of pregnancies that ended prior to —wks gestation.

20wks

Preterm pregnancies are deliveries between —wks.

20-36

The format used for reporting pregnancies is GPPAL:

G = Gravida P = Para , followed by Preterm pregnancies, Abortions, & # of Living children.

Rh immune globulin (RhoGAM) should be given to Rh negative mothers w/ Rh positive fetuses w/in —hr of delivery or abortion. This only protects for the D antigen of the Rh system & not any other of the possible blood system antigens.

72hr

Chronic untreated hyperglycemia from mom can cause fetal — is frequently due to reduced CO or hypovolemia.

bradycardia

— symptoms are characterized by slight to severe pain in buttocks & legs, & can develop w/in a few hrs up to 24hrs after the spinal anesthetic is administered. It lasts at most 2dys. Lidocaine is more likely to cause this than bupivacaine, prilocaine, & procaine.

TNS

suggested therapy is — ml/kg of 20% intralipid as an initial bolus for any pt suffering from significant LA toxicity, followed by — ml/kg for 30-60min.

1.5 ; 0.25

— cause the relaxation of uterine muscle, & are used to prevent or delay preterm delivery. As the administration of steroids to the mother can decrease the incidence & severity of fetal lung immaturity & respiratory distress, these are frequently used to delay delivery until steroids have had at least some time to work

Tocolytics

— should be avoided in these pts that labor pts who are abusing heroin bc they are relatively contraindicated as they can precipitate a withdrawal syndrome.

Mixed opioid agonist/antagonists (nalbuphine)

4 functional stages of labor.

1st stage occurs b/n the onset of labor & full cervical dilation (10cm). This includes 2 phases, the latent phase (cervical effacement & early dilation) & the active phase (begins around 4cm, more rapid cervical dilation). 2nd stage of labor encompasses complete cervical dilation through delivery of the infant. 3rd stage begins immediately after delivery of the infant & ends with delivery of the placenta. 4th stage is the immediate postpartum period of 2hrs after deliver of the placenta, when the patient undergoes significant physiologic adjustment.

The root cause of increased airway edema is due to an increased level of — & increased circulating —.

estrogen ; blood volume.

A lack of fetal alcohol dehydrogenase prevents alcohol from being properly metabolised in the unborn infant, contributing to the development of —.

fetal alcohol syndrome.

The pregnant female at term requires smaller doses of LA than a nonpregnant female due to —.

venous engorgement.

Normally the fetus has a — pH than the mother.

lower

—: The lower fetal pH allows basic drugs (lidocaine) to cross the placenta in their non-ionized state, mostly by diffusion. Once in the fetal circulation, the non-ionized weakly basic drug (lidocaine or other LA) will become — in the lower pH fetus.

Ion Trapping ; ionized

A normal vaginal delivery & the period immediately afterwards typically sees blood loss of around —ml while a C-section typically results in —ml blood loss.

600mL ; 1000ml

— prevent Ca+ entry into muscle cells by blocking voltage-dependent cell membrane channels that are selective for Ca+, decreasing uterine muscle tone & providing for —.

Ca+ channel blockers (nifedipine) ; tocolysis

—: the most common side effects in pregnancy are HoTN, headache, & flushing. Adverse effects: possible decreases in uteroplacental blood flow, fetal hypoxia, pulmonary edema & MI. Short term use doesn’t seem to cause the decrease in uteroplacental blood flow or negatively effect fetal oxygenation.

Nifedipine

Ca+ channel blockers may also — side effects of Mg+ sulfate.

potentiate

Uterine blood flow increases greatly during pregnancy, from the baseline of 50-100 ml/min before pregnancy to ~700-900 ml/min at term. The increase in uterine blood flow is achieved by a — in uterine vascular resistance.

decrease

Increased circulating — causes up to a 40% decreased MAC requirement during pregnancy as well as a decreased requirement for LA used in neuraxial blockade.

progesterone

Propofol requirements are — during pregnancy.

unchanged

Greater levels of circulating — act as a respiratory stimulant & increases CO2 receptor sensitivity. alveolar dead space is decreased. These factors combined w/ an increase in total body CO2 production cause an increase in resting minute ventilation. This leads to faster uptake of inhaled anesthetics lowering MAC requirements.

progesterone

Increased circulating blood volume will — the duration of other meds (thiopental) as the increased volume lowers clearance of the drug.

increase

Sensitivity to LA is — lowering doses required by about 25% in the term pregnant pt compared to non-pregnant pt.

increased

Mg+ sulfate competes with Ca+ entry into the cells, — intracellular Ca+. It also — release of acetylcholine at the neuromuscular junction, reduces sensitivity of end plate to acetylcholine, & decreases excitability of muscle membrane. Side effects: flushing & headaches, & pts on Mg+ may appear sedate.

decreasing ; decreases

Therapeutic Mg+ levels b/n 6-8 mg/dL, but these levels do not correlate well to adequate — for every pt. Mg+ levels should be titrated to desired results & side effects. At high blood levels Mg+ may cause respiratory depression (12-15 mg/dL) or cardiac depression (> 15 mg/dL).

tocolysis

Mg+ is contraindicated in pts with — or —, & is renally excreted (pts w/ RF should receive very cautiously).

hypocalcemia or MG ;

— presynaptically decrease sympathetic output from the CNS.

Alpha 2 agonists (clonidine)

There is a 40% increase of CO by the end of the — trimester, & CO continues to rise through the 2nd trimester. It will eventually increase to —% greater than that of a nonpregnant female.

1st ; 50

The greatest increase in — is seen just after delivery of the fetus when there is up to an 80% increase in CO.

Terbutaline is a — agonist w/ — effects, being more selective for — effects. This drug works by increasing cAMP, & is not commonly used in modern medicine due to significant side effects. Plus, the use of this adrenergic agents has not been associated w/ a decrease in overall perinatal morbidity & mortality resulting from preterm labor & birth.

beta ; beta 1 & beta 2 ; beta 2

—: main undesired side effects seen are maternal HoTN, tachycardia, pulmonary edema, hyperglycemia, hypokalemia, & other side effects. Glucose levels rise rapidly after start of beta-adrenergic therapy secondary to glycogenolysis, & fall w/in 24hrs of cessation. Hypokalemia is seen as increased levels of insulin causes greater transport of K+ & glucose into the cell, but there is no “loss of K+” & treatment is not necessary. Fetal side effects include increased fetal HR & neonatal hypoglycemia (secondary to maternal hyperinsulinemia secondary to maternal hyperglycemia), but no long-term fetal effects have been noted.

Terbutaline

Apgar scores are taken at —&— & continue every 5min until either 2 scores of 8 are obtained OR 20min time has elapsed.

1min & 5min

Apgar scores of — indicate an infant that requires no active resuscitation, & — show a mildly to mod depressed infant. Scores of — shows a severely depressed infant & requires immediate resuscitation.

7-10 ; 4-7 ; <4

—: a woman who is currently in labor

parturient

—: a woman who has just recently given birth

puerpera

—: a woman who is in or who has just experienced her 1st pregnancy

primagravida

—: a woman who has delivered 1 pregnancy that progressed beyond the gestational age of an abortion.

primapara

An infant who weighs <—g at birth is considered a low birth weight infant regardless of gestational age. An infant who weighs <—g at birth is considered a very low birth weight infant. <—g at birth is an extremely low birth weight infant.

2500g ; 1500g ; 1000g

During pregnancy, — levels & clotting factors (—,—,—,—,—) are all increased leading to a hypercoagulable state.

fibrinogen ; VII, VIII, IX, X, & XII

The axillary roll, placed just —, is designed to take the weight off the upper thorax & place it on the chest rather than the axilla itself. This decreases the likelihood of injury to the —.

caudad to the axilla ; brachial plexus

Pressure alopecia may occur where a pts hair falls out secondary to pressure on the head when a pt is —

supine

Overextension of the neck has not been associated w/ — injuries.

brachial plexus

Most inhalation agents decrease cerebral metabolic O2 requirements, — increases them. Like the other inhaled agents, nitrous oxide also — ICP through increases in cerebral blood flow & cerebral blood volume.

nitrous oxide ; increases

Sevoflurane, isoflurane, & desflurane will — blood flow through the hepatic artery to varying degrees.

increase

Increasing CO would — be of benefit sevo increasing level

not

During pregnancy, —,—,— decrease, while —&— increase.

Plt levels, albumin levels, & Hb levels ; white cell counts & blood volume

Hypothermic pts, on alpha 2 agonists, elderly, acutely alcohol intoxicated, pregnant pts, IV or neuraxial opioids, lidocaine, & pts w/ hyponatremia have — MAC requirements.

decreased

From least to most metabolized of the volatile anesthetic agents is —,—,—,—,—.

nitrous oxide, des, iso, sevo, & halothane

—&— are considered least irritating of inhaled anesthetics making them the recommended choices for inhaled inductions.

Halothane & sevo

Irritating Volatile Anesthetics =

DIE = Desflurane, Iso & Enflurane

— is by far the most potent trigger of MH of the volatile agents.

Halothane

— is a respiratory depressant, decreasing pts hypoxic drive, but its effects are < other volatile anesthetics.

Nitrous oxide

Nitrous oxide causes the — amount of overall CV change in an otherwise healthy, euvolemic pt. As nitrous oxide releases catecholamines to cause sympathetic stimulation, the net result of CO, BP, & HR is a largely — overall cardiac function. This is despite nitrous oxide causing a — in cardiac contraction.

least ; unchanged ; decrease

MAC requirements by age from highest to lowest MAC concentration needs: 5

infant, neonate, children, adults, geriatrics.

All volatile anesthetics produce a dose dependent — in the ventilatory response to hypercarbia & hypoxemia.

depression

Isoflurane will cause an increase in serum fluoride levels but does not lead to — even after prolonged exposure. Halothane does decrease GFR & overall renal blood flow, but not — does not occur due to its use the decrease is likely due to the myocardial depressant activity of halothane with a fall in CO.

nephrotoxicity ; nephrotoxicity

Nonsmoking pts administered — will not have a great change in airway pressures or resistance. Smoking pts may see a transient increase in airway resistance that is typically mild.

desflurane

—,—,— w/ poor or no vascularization makes up the vessel poor group.

Bones, cartilage, & other connective tissue

The vessel rich group receives —% of the total CO & is the 1st group to take up the most volatile anesthetic agent. This is followed by the muscle group & then the fat group.

— is best avoided in pts w/ hepatic pathology. It is the greatest metabolized inhalational agent w/ ~20% being metabolized by the liver. It decreases CO to the greatest degree & causes decreased coronary blood flow as the output falls.

Halothane

Although — is a pungent, irritating agent that is ill-suited for inhalational induction, it is an effective bronchodilator.

isoflurane

— is best avoided due to the possibility of causing or worsening anemia.

Nitrous oxide

The mechanism of anemia & neurological changes is that — converts vitamin B12 (cobalamin) from the active form to the inactive form, leading to a megaloblastic (in this case B12 deficient) anemia. As vitamin B12 is a coenzyme of methionine synthase (& methionine synthase is required to develop DNA and RNA), symptoms such as paresthesias & other neurological findings may occur w/ it. Anemia & neurological symptoms are known to be caused by it when used for long durations or when it is used by pts w/ low amounts of B12 stores (elderly or chronically malnourished). While there are many causes of megaloblastic anemia & neuropathies, it induced causes are of particular concern to anesthesia bc they are causes that we directly affect.

nitrous oxide

— abuse or overuse can also lead to other problems related to low serum B12, including myeloneuropathies causing paresthesias & motor dysfunction. Bone marrow depression & aplastic anemia have also been reported, usually related to long term use at high concentrations. Other related problems :neurological deficits, including dizziness, inability to concentrate, & possible negative reproductive effects.

nitrous oxide

— should be avoided in pts w/ CAD or renal disease, but not necessarily in pts w/ a primary anemia (ie. not caused by RF).

Ketorolac

— should be avoided in diabetics but not in anemics.

Dexamethasone

—&— cause the least decrease in RBF.

Sevoflurane & desflurane

—,—&— cause the greatest degree of RBF reduction.

Halothane, isoflurane, & nitrous oxide

All inhaled agents cause a — in hepatic blood flow as well.

decrease

Young pts, chronic alcohol abusers, & those acutely intoxicated w/ cocaine or methamphetamine have — MAC requirements.

increased

Chronic methamphetamine abusers, people on barbs or benzos, those acutely intoxicated w/ alcohol, & hypothermics all will have — MAC requirements.

decreased

Thyroid disorders — effect MAC requirements.

do not

Nitrous oxide — provide skeletal muscle relaxation.

does not

Nitrous oxide & all volatile anesthetics do — skeletal muscle blockade caused by depolarizing & non-depolarizing drugs.

potentiate

All of the currently used inhaled anesthetic agents — tidal volume & — RR. Cerebral blood flow is also — in all of the inhaled agents & renal blood flow is — in all agents as well.

decrease ; increase ; increase ; decreased

Induction of anesthesia produces 15-20% reduction in —.

FRC

The hyoid bone is felt at level of — & used as attachment muscles of floor of mouth, tongue, larynx, epiglottis, & pharynx.

— inhalational agent should be avoided in pts w/ long QT syndrome. Likely a dose-dependent prolongation of QT interval.

Sevo

—has the least impact on HR of all volatile anesthetics.

Sevo

— is not a very stable chemical compound, & as such it is stored in amber colored bottles & contains a thymol preservative (to prevent degradation by light).

Halothane

—causes least vasodilation. — causes most vasodilation, then —&— vasodilate about same extent.

Halothane ; Iso ; des & sevo

The muscle group receives —% of CO. The vessel rich group receives —% of CO. The fat group receives —% of CO.

20 ; 75 ; 5

— has some sympathomimetic properties & causes a slight increase or no change in CO.

Nitrous oxide

— may cause a decrease in HT along w/ CO as it blunts the normal increased HR response seen with a decrease in SVR.

Halothane

— may increase HR, & — does as well as volatile agent.

Des ; iso

External intercostal muscles can help augment —, & during labored breathing sterncoleidomastoid, pectoralis & scalene muscles also contribute to — effort.

inspiration ; inspiration

— dyspnea is a condition where a pt develops sudden severe shortness of breath & panic, often awakening the pt from sleep. may occur when a failing LV is being supplied by an adequately pumping RV, leading to sudden right sided HF & pulmonary congestion.

Paroxysmal nocturnal

—: where the pt has shortness of breath sitting up which is relieved by lying down.

Platypnea

—: is the term used to describe shortness of breath when laying flat.

Orthopnea

The trachea begins at the — cervical vertebrae in the adult. The level of the cricoid cartilage begins just below — & continues to — level.

6th ; C6 ; C7

During inspiration, unless it is max, the vocal cords will be found in positions in b/n —&—.

paramedian & lateral

Gas exchange begins at generation — (terminal bronchioles).

The avg adult minute ventilation in an adult pt is —L/min. Minute ventilation is measured as: Minute ventilation = RR x TV.

5-8

The — muscle is the only laryngeal muscle that is innervated by the external branch of the superior laryngeal nerve. The function of this system is to tense the muscle to control phonation & pitch.

cricothyroid

One of the biggest issues w/ single lung ventilation is the iatrogenic — that occur, meaning that oxygenated blood from the ventilated, dependent lung, mixes w/ blood from the non-dependent, non-ventilated blood causing lowered FiO2 values. Even with 100% Fi02 PaO2 values may be lower than 80% in about 25% of the population, & <60mmHg in about 10% of pts under the best anesthetic management. Although increased FiO2 requirements are problematic, they are expected in nearly all cases due to the complex changes that occur in pulmonary blood flow & ventilation during these procedures. Right ventricular preload is not generally a major issue due directly to the one lung ventilation, & increased peak airway pressures are also expected in these cases by definition.

right to left shunt

A single abnormal pulmonary function test — contraindicate surgery.

does not

The — nerve is responsible for bronchoconstriction & increased bronchial secretions via muscarinic cholinergic receptors. As this nerve is responsible for bronchoconstriction, anticholinergic drugs (inhaled ipratropium bromide) can be used to block cholinergic mediated bronchoconstriction. Other anticholinergics (atropine & glycopyrrolate) are used to block the mediated bronchial secretions.

vagus

The avg adult airway contains ~— alveoli in the adult. This compares to — alveoli in the newborn. The alveoli are the primary units of gas exchange, & mark the very end of the respiratory tree.

300 million ; 20-50 million

Vital capacity is —mL/kg in a healthy adult pt.

60-70

The — nerves supply the cricothyroid muscles, causing tension of the vocal cords.

superior laryngeal

The hypopharynx is innervated by the superior laryngeal nerve, a branch of the — nerve. The hypopharynx includes the area of the pharynx from the hyoid bone down to the cricoid cartilage.

vagus

Pulmonary embolism leads to a — pulmonary edema. This pulmonary edema is seen as fluid in the alveolar sacs that is not caused by a cardiogenic process.

non-cardiogenic

ARDS is a major cause of — pulmonary edema, & has causes including transfusion-related acute lung injury (TRALI), pulmonary embolism, opioid overdose, eclampsia, & sepsis. SARS also causes a — pulmonary edema, as can high altitudes & neurologic injury that causes significant catecholamine release.

noncardiogenic ; noncardiogenic

Alcohol intoxication, cocaine overdose, myocarditis, & mitral & aortic regurgitation can lead to — pulmonary edema.

cardiogenic

—: located in the interstitial alveolar tissue & supplied by the vagus nerve are responsible for responding to edema & swelling of the tissues. Besides responding to pulmonary edema, these receptors also respond to pulmonary microemboli, overinflation of the lungs, & pneumonia & anything else that causes stretching of the alveoli. When these receptors are stimulated, inspiration is prematurely terminated which results in more rapid & shallow breathing & an increase in minute ventilation.

Juxtacapillary receptors (or stretch receptors)

— position of vocal cords is found when a pt has received paralytic or during rest. This position is also found during end expiration.

Paramedian or cadaveric

Type — pneumocytes produce surfactant which is required to reduce surface tension in the alveoli & preventing the alveoli from collapsing during expiration. Pulmonary cells are differentiated during development, & by 25wks These are beginning to produce enough surfactant for the fetus to survive outside of the body. This is not enough surfactant however to prevent infant respiratory distress syndrome, & it is not until the mid 30wks that adequate surfactant is produced to provide more ideal pulmonary function after delivery.

Type — pneumocytes are tight junction cells that prevent passage of materials into the alveolar sacs.

— are glial cells in the brain that help provide support to various brain cells & help control the cerebral physiological environment.

Astrocytes

— cells are found in the dermis & are antigen presenting cells with functions similar to macrophages.

Langerhans

— cells are made up of a variety of subtypes in the pancreas.

Islet

The more commonly referred to cells are — cells which secrete insulin, — cells which secrete glucagon, & — cells which secrete somatostatin.

beta ; alpha ; delta

The avg adult trachea is —cm in length.

10-15

Thoracic roots — provide sympathetic activation which leads to bronchodilation & decreased secretions via beta 2 receptors agonism.

T1-T4

The respiratory bronchioles are where gas exchange starts & corresponds to generation — in the airway.

Nitrous oxide is — at room temperature.

liquid

Cirrhotic pts produce increased levels of nitric oxide which cause chronic —, — vascular resistance, & — CO. Bc of this they may be chronically HoTN.

vasodilation ; decreased ; increase

— is the most common sign of pulmonary embolism occurring in up to 70% of affected pts. —&— are the next most commonly found objective signs. Acute onset of — is the most commonly elicited historical component occurring in up to 75% of pts. Keep in mind that the s/s of PE are non-specific & rarely can be diagnosed by history & physical exam alone.

Tachypnea ; Rales & tachycardia ; dyspnea

Remember that —&— are not helpful in excluding or diagnosing PE as they are frequently normal.

ABG readings & pulse ox

— is used in the treatment of hyperkalemia however but it does not directly reduce serum K+ concentrations. It has been shown to stabilize the cardiac membrane to the arrhythmogenic effects of the elevated K+ concentrations allowing more time for treatment prior to arrhythmia development.

Ca+ gluconate

All that reduce K+ serum levels: 4

bicarbonate, Stimulation of sympathetic beta receptors, insulin, kayexalate

Plasma osmolality is a measurement of ions in the blood & is normally — mOsm.

280

Oculocardiac reflex, also known as trigeminocardiac reflex, is a decrease in pulse rate or new onset heart block caused by traction applied to extra-ocular muscles or compression of the eye, secondary to stimulation of the — nerve.

trigeminal

The trigeminal afferent nerves synapse with the vagus nerve of the — nervous system’s motor nucleus. Vagal stimulation then travels to the heart causing bradyarrhythmias & heart blocks.

parasympathetic

— coma is a severe hypothyroidism that presents w/ decreased mental status & hypothermia. A history of hypothyroidism or Iodine 131 therapy to treat hyperthyroidism may be indicators. HoTN, bradycardia, hyponatremia, hypoglycemia, & hypoventilation are often too.

Myxedema

— pts have severe & life-threatening symptoms of hyperthyroidism. HR can exceed 140BPM & CHF may be present. Temp of 104-106 degrees F are common, along w/ agitation, delierium psychosis & coma. Hepatic failure & jaundice can occur.

Thyrotoxicosis

— syndrome is a cause of sudden cardiac arrest & death in pts w/ apparently normal hearts. This syndrome is detected by obtaining an ECG on the effected pt. ECG will show ST segment elevation in leads V1 to V3.

Brugada

— syndrome is a cardiac condition in which a chronic left to right intra-cardiac shunt causes right ventricular (or atrial) hypertrophy eventually reversing the flow of blood through the defect. Due to the higher right side cardiac pressures systemic HoTN would cause an increase in deoxy blood flow through the defect causing hypoxemia. In these pts, conditions causing elevated PAP will increase the abnormal flow as well. Aggressive pulmonary physiotherapy post op to prevent atelectasis or pneumonia is indicated. Due to the dilation & hypertrophy caused by the syndrome these pts are at higher risk than avg for intraop arrhythmia & care should be taken to be prepared should such an event occur. In addition the risk of systemic air embolism is increased in these pts due to the abnormal right to left side blood flow. Air should be removed from all IV lines & air filter should be used.

Eisenmenger

Maintaining strict — is of key importance for MS pts.

temp

Droperidol is contraindicated in — disease, among other disease, due to its antagonism of dopamine receptors.

Parkinson’s

— meds (donepezil) (used commonly in Alzheimer disease) seem to help improve the cognitive function in pts w/ MS.

Anticholinesterase

— has no use in the treatment or management of a typical MS pt, & dehydration can cause stress leading to an exacerbation.

Fluid restriction

— deficiency is a congenital inherited disorder manifesting w/ early onset hepatic disease &/or early onset emphysema depending on the genotypic allele pattern present in the pt.

Alpha-1 Antitrypsin (AAT)

Propofol infusion syndrome are as follows: metabolic —, lipemia, rhabdomyolisis, HF, RF, hepatic dysfunction, elevated LFT, elevated troponins, elevated lactate. Recognize that these lab values represent hepatic, cardiac, renal, & muscular damage w/ lipemia & lactic acidosis. Treatment is w/ —,—,—

acidosis ; charcoal hemoperfusion, cessation of propofol, & supportive measures.

— is a disorder which occurs when a large amount of hypo-osmolar fluids are used in irrigation of the surgical field. Because this syndrome is caused by absorption of hypo-osmolar, non-electrolyte containing solutions, only 1.5% — solution holds a substantial risk of causing it. The reason is that the electrocautery devices used in these procedures are mono-polar. This leads to hyponatremia & serum hypo-osmolarity causing cerebral edema. The symptoms are thus confusion, nausea, & irritability, & in the case of associated glycine toxicity, temporary blindness.

TURP syndrome ; glycine

— occurs during an acidotic state bc the body attempts to normalize pH by exchanging extracellular H+ ions for intracellular K+. Peripheral — occurs because acidemia seems to augment peripheral responses to nitric oxide & other vasodilators & decrease responses to circulating catecholamines.

Hyperkalemia ; vasodilation

Glucose — affect the serum osmolal gap. Osmolal gap is a calculation to estimate excess osmotically active solutes in the blood.

does not

An elevated osmolal gap can be found in: 5

alcohol ingestions, excess glycine (during TURP), severe hyperlipidemia, DKA, severe RF.

Goiter is associated with —.

hypothyroidism

—&— slow the progression of CKD by lowering the glomerular filtration pressure in kidney.

ACE-I & angiotensin receptor blockers

The — # is used to test a pt for pseudocholinesterase deficiency.

Dibucaine

Classic pheochromocytoma triad: 3

1) sustained or paroxysmal HTN 2) headache 3) generalized sweating.

The mild release of K+ (—mEq) from muscle cells that normally accompanies the administration of succ is magnified & can result in life threatening hyperkalemia in pts w/ pre-existing neurologic & muscular disorders (—mEq increase). It has been well documented to happen in Guillain-Barre syndrome as well as chronic immobilization, spinal chord lesions, & other disorder resulting in muscle paralysis, disuse &/or chronic denervation. The phenomenon is likely due to over sensitization of the damaged myocytes to the depolarizing effects of succ.

0.5mEq ; 5-10mEq

3 stages of heat loss & movement during anesthesia:

1st phase (redistribution), 2nd stage (linear stage), 3rd stage (steady state)

— causes a drop of temp in the central core of the body w/in the 1st hr of anesthesia due to redistribution of heat from the core to the peripheral tissues. This is greatest loss of heat.

1st phase (redistribution)

— is that of combo of reduced heat production & increased heat loss to the environment. This 2nd phase starts at the beginning of surgery & lasts from 2-3 hours where there is decreased heat production due to anesthetic agents, decreased heat production due to limited muscle activity, & further loss of heat to the environment due to convection, radiation, evaporation & conduction. Cold IV fluids also contribute to this heat loss stage.

2nd stage (linear stage)

— is that of a thermal steady state where the body’s production of heat equals the loss of heat to the environment & core temp becomes stable. This stage often not reached during most surgeries, & occurs when the temp drops sufficiently to activate peripheral vasoconstriction & reduce loss of peripherally shunted heat.

3rd stage

Administration of excessive concentrations of normal saline (0.9%) can cause a — metabolic acidosis from the excess chloride concentrations administered & dilution of serum bicarbonate levels. Additional causes include disorders which cause a net loss of bicarbonate ions (diarrhea, renal tubular acidosis & early acute RF).

hyperchloremic

Hyperchloremic acidoses are — acidoses as the body is able to compensatory raise serum Cl- concentrations to maintain electrical neutrality in these examples.

non-anion gap

A rough estimate of renal function deterioration can be surmised by the rule that for every doubling of the — about 1/2 of renal function is lost.

creatinine

Severe — causes lab reports to falsely show low Na+ levels.

HLD

— is the greatest cause of heat loss in a pt & is estimated to be —% of heat loss.

Radiation ; 40

— is heat transfer by electromagnetic waves, which carry energy away from the emitting object. Keeping the body covered helps decrease the body’s area exposed to the energy into its environment.

Radiation

— is responsible for around 30% of heat loss.

Convection

— is the form of heat transfer in liquids & gases, caused by fluid flow around the pt. The ambient temp of the room being set below the pt’s temp is a cause of this heat loss.

Convection

— is responsible for an estimated 20% of heat loss.

Evaporation

—: Water takes heat to turn into a vapor, & the heat in our case is provided by the human body. As the pt breathes & sweat evaporates, the energy (heat) from the pt’s body provides the water the ability to take the water from liquid to vapor form. The heat is transferred from the body to the vapor that drifts away. The heat the body uses to warm the gas traveling to the lungs is not a major cause of heat loss in our pts. Once intubated, the ventilator assists w/ helping maintain humidity & temp, decreasing the rate of respiratory heat loss.

Evaporation

— is believed to be responsible for around 10% of heat loss in pts.

Conduction

— heat loss is caused by direct contact to a surface that is colder than the pt; ex.: laying a pt on a cold bed surface.

Conductive

— is generally believed to be the last sense to be lost before the unconscious state is reached, & may be the 1st sense regained upon your pt’s emergence.

Hearing

— interval is a manifestation of a congenital disorder or of Ca+ and Mg+ abnormalities.

Prolonged QT

Midazolams quick onset is due to its high — solubility.

lipid

— is useful for irregular narrow complex tachycardias at a dose of 0.25mg/kg initially, or 20mg as appropriate in this pt. In common practice for the adult pt, 15-20mg is typically used although it is technically a weight-based med. This initial dose is given over 2min & may be repeated at 0.35mg/kg after 15min.

Diltiazem (Ca Channel blocker)

— is frequently used for a-fib, however other choices such as —or— are also good depending on the clinical situation.

Diltiazem ; beta blockers or verapamil

— antiarrhythmic medications work to alter or block Na+ channels and inhibit Phase 0 of cardiac depolarization. They also have modest K+ channel antagonism.

Class I

Class I drugs are further subdivided into class IA, IB, & IC. Class IA drugs have an — time of onset & termination, class IB drugs have the rapid onset of action & termination, & Class IC drugs have the — onset & termination of action.

intermediate ; rapid ; slowest

The earliest sign of an ST elevation MI is — waves.

peaked (or hyperacute) T

pericardial tamponade will lead to:

lowered BP, muffled heart tones, & jugular venous distension (Beck’s triad)

Measurement of ST depression or elevation should occur at 0.08seconds (2 small boxes) past the — point.

The — is the point where the end of the QRS occurs, beginning the ST segment. It is where depolarization ends & repolarization begins.

J point

Defibrillation: Dosing for peds should start at —Joules/kg. If this fails to convert the rhythm, the 2nd dose should be at —Joules/kg or higher but not to exceed — Joules/kg or —J (the suggested adult dose).

2 ; 4 ; 10 or 200

— is indicated in the treatment of v-fib or ventricular tachycardia w/o a pulse, working by depolarizing the entire myocardium to allow restoration of normal electrical conduction. When possible, use ped adhesive pads instead of adult pads.

Defibrillation

A pt in pulseless v-tach or v-fib should be administered — at a dose of —mg in a bolus. After defibrillation & continued CPR, its dosing may be repeated at —mg if the 1st dose is unsuccessful.

amiodarone ; 300 ; 150mg

— is by far the drug of choice for ventricular & atrial dysrhythmias for any pt w/ an EF of <40% or CHF is otherwise present drugs such as verapamil are contraindicated in these pts.

Amiodarone

The PR interval is measured from the beginning of the P wave to the 1st part of the QRS complex (Q wave or R wave). It is normally <— seconds. The PR segment includes the period of atrial depolarization & conduction through the His-Purkinje system. Any prolongation of the PR interval is typically caused by slowed AV node conduction.

0.20

A normal QRS complex lasts <— seconds (<— very small EKG strip boxes).

0.12 ; 3

For peds pt, the 1st cardioversion dose is — Joule/kg w/ the next doses at — J/kg if needed.

0.5-1 ; 2

— is indicated for pts w/ a reentrant electrical dysrhymia. It stops the reentrant electrical conduction, allowing normal depolarization from the SA node through to the Purkinje system to resume. Pts w/ unstable vital signs who are in cardiac rhythms such as SVT, ventricular tachycardia w/ a pulse, a-fib, & a-flutter

Cardioversion

Lidocaine for v-fib or v-tach & pulsatile stable v-tach should be dosed at — mg/kg. Dosing may be repeated every 5-10min as a bolus at a rate of 0.5-1 mg/kg if the rhythm doesn’t convert the max dose is —mg/kg. After successful resuscitation, a drip of lidocaine should be started at a rate of 1-4 mg/minute (or 20–50 mcg/kg/min).

1-1.5 ; 3

Lidocaine: If there is no IV present, the same dosing schedule may be used through an intraosseous needle. ETT administration should be at — the IV dose diluted in 10mL of — (normal saline is adequate, but this has greater absorption).

2x ; sterile water

— provides K+ channel blocking (primary mechanism), Na+ blocking (class IB), Ca+ blocking, & sympathetic blocking properties. Blocking of K+ channels prolong the time of repolarization & the refractory period.

Amiodarone

Left ventricular hypertrophy causes — axis deviation.

left

Causes of — axis deviation: PE, COPD, cor pulmonale, lateral wall MI, & right ventricular hypertrophy.

right

ECG findings of ST elevation MI most likely seen in order: Peaked — waves, ST segment —, Q wave development, T wave —.

T ; elevation ; inversion

— at 1-2g should be administered to any pt w/ polymorphic v-tach (Torsades de Pointes) even if serum is thought to be normal. After initial dosing, an infusion drip of 0.5-1g/hr should be continued. It is also useful for pts w/ long QT syndrome who are at significant risk for conversion to polymorphic v-tach an excellent candidate for this is a pt w/ a QTc of >450millisecs who has a bradycardic rhythm & frequent PVCs.

Mg+ sulfate

— complicates diagnosis of MI, bc it changes how ventricles depolarize & leads to its own ST segment & T wave changes.

LBBB

— is not associated w/ QT prolongation & is useful to treat Torsades de Pointes & v-fib.

Lidocaine

Meds such as procainamide, amiodarone, methadone, droperidol, & ondansetron are known to — QT intervals. Antipsychotics (haloperidol) & tricyclic antidepressants also do to.

prolong

— is administered at 2.5-5mg IV for the treatment of irregular narrow complex tachycardic rhythms, including a-fib, multifocal a-tach, & a-flutter. Given over 2min & may be repeated in 15-30min at a dose of 5-10mg. It decreases SVR.

Verapamil

—: is absolutely contrainidacted in pts w/ WPW syndrome due to its ability to send the pt into v-fib.

Verapamil

ST-T wave changes seen in left ventricular hypertrophy are typically seen in — leads (—,—,—). These signs can be seen as T wave inversion & ST depression.

anterolateral leads (I, aVL, V4-V6)

Left axis deviation, left atrial hypertrophy, & increased amplitude of the QRS complex R wave in —&—.

aVL & V5-V6

Procainamide is dosed at —mg/min until rate controlled.

— is useful to treat hemodynamically stable v-tach & a-fib w/ an uncontrolled ventricular response. The dose is started at 20mg/min & continued until either the QRS widens by >50%, HoTN develops, or a max dose of 17mg/kg is administered. If an emergent situation is present, procainamide can be administered at 50mg/minute. After successful treatment of the dysrhythmia, a continuous infusion of 1-4mg/minute drip is administered.

Procainamide

— is not to be used for unstable v-tach or v-fib.

Procainamide

—&—, both useful for SVTs, should not be used in any pt w/ a QTc interval of >450 milliseconds.

Procainamide & sotalol

V-tach w/ a pulse should have an initial dose of —J, not —J.

100J ; 200J

A-fib dosing for cardioversion may start at —J biphasic, a-flutter —J biphasic, & v-fib or polymorphic v-tach (Torsades de Pointes) at —J.

50-100J ; 50J ; 200J

Use of antiarrhythmic agents can help result in more succesful cardioversion at lower doses. This has been successfully done by combining — or — w/ cardioversion in therapy for a-fib for instance.

amiodarone or sotalol

— drugs are the Ca+ channel blockers such as verapamil & diltiazem. Ca+ channel blockers slow firing of the SA node & slow conduction through AV node through increasing AV refractory period & prolonging AV conduction. On the EKG an increased PR interval may be seen.

Class IV

— rhythm is most often found during myocardial reperfusion. It is seen as a wide complex ventricular rhythm at a rate of 40-100 (typically 40-60). >100BPM it is referred to as v-tach. Reperfusion may occur as a pt comes off of cardiopulmonary bypass or after interventional cardiology procedures such as arterial stenting. In these cases beta blockers may be beneficial, but the rhythm typically should not be treated with anti-arrhythmics as the pt may convert to asystole.

Accelerated idioventricular

A pt w/ WPW syndrome must not be given certain — blocking drugs to control ventricular rate in the event of a-fib w/ a rapid ventricular response. The contraindicated drugs include —,—&—.

AV node ; verapamil, digoxin, & adenosine

Pts w/ — have their AV conduction travel through a path that bypasses the AV node, causing pre-excitation which is seen as rapid ventricular firing. Blocking AV nodal conduction further will cause the accessory tract to be favored. These drugs if given will enhance the ventricular rate & can lead to v-fib & death.

WPW

Pts with WPW syndrome, IV — is the most dangerous of these drugs to give. Not only does it block the AV node & increase its refractory period, it also has a direct effect in reducing myocardial contraction & SVR.

verapamil

— has lead to v-fib when given to a pt in a-fib w/ WPW syndrome.

Verapamil

— is contraindicated in a-fib in any situation.

Adenosine

When WPW is mentioned, — is the drug of choice according to current ACLS guidelines. See WPW, think this unless a contraindication to the drug exists.

procainamide

The vertical deflection on the ECG is a display of detected voltage. A 10mm deflection vertically equals — mV on the standard EKG. 10mm equals 10 of the small boxes.

Hypokalemia may lead to prominent - waves.

Although U waves may be normal in healthy individuals, certain conditions such as —,—, & certain meds such as — can also cause U waves.

hypokalemia, intracranial hemorrhage ; amiodarone

A pt in complete heart block can not be treated w/ —, which only increases the SA rate & is blocked from increasing the ventricular rate. AV dissociation can not be treated by increasing the SA rate due to the antimuscarinic effects of it only increasing the atrial contraction rate, which is not translated to increasing the ventricular rate. Interventions that are beneficial in this rhythm include transcutaneous pacing, epi infusion, & dopamine infusion which all work to increase the ventricular rate. These interventions can be used either until the situation resolves or until a permanent pacemaker is installed.

atropine

Anesthesia services typically use a minimum of —mm of ST segment depression as a sign of ischemia.

1mm

The auscultation of — prolapse is a mid-systolic click followed by a murmur through the remainder of the systolic cycle. The sounds represent the prolapsed valve reaching max prolapse, then, as the valve becomes incompetent, blood flow regurgitates into the left atria causing the murmur. The murmur has characteristics which can be changed by increasing or decreasing ventricular volume. The characteristic “click” of its prolapse will move closer to S1 when left ventricular volume is decreased such as w/ sitting, standing or valsalva. It will move further from S1 when left ventricular end-diastolic volume is increased such as w/ hand grip maneuvers, laying supine, or squatting. This murmur will be loudest heard over the apex.

mitral valve

“—” refers to cardiac contractile rate.

Chronotropy

“—” refers to cardiac muscle fiber relaxation.

Lusitropy

Pure — HF is is a condition in which the S/S of HF are present while there remains a preserved ventricular EF. The problem with this HF is w/ — of the ventricle.

diastolic ; filling

the problem w/ — HF is — which is directly correlated to EF.

systolic ; contraction

A dilated left ventricle w/ minimal EF & elevated end diastolic pressures best describes left ventricular — failure.

systolic

Low CO caused by decreased preload from hypovolemia & low left ventricular diastolic pressures is — shock.

hypovolemic

HoTN from an infectious cause w/ preserved CO & low end diastolic volume describes — shock.

septic

Elevated PAP w/ eventual decreased right ventricular EF describes a condition known as —.

cor pulmonale

— med (“coronary steal syndrome”) is useful for most indications

Nitroprusside

— med for cardiac ischemia or HF

nitroglycerin

— med for aortic dissection

beta blockade (esmolol)

— med for renal insufficiency

fenoldopam

— is a phenomenon w/ parenteral nutrition

Hyperglycemia

The — is the best test to determine the degree of anticoagulation present from heparin therapy.

activated PTT test (aPTT)

The PTT is used to assess the — pathway & the — pathway of clot formation. PTT evaluates factors —,—,—,—,—,—,—&—.

intrinsic ; common ; I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI, & XII

— inactivates factor II (prothrombin) which prevents the formation of thromboplastin. These actions are present for about 4-6hrs after dosing of heparin.

Heparin

Activated PTT has additives to the testing reagents to shorten & narrow the time of results, where normal values should be between —sec. Traditional PTT’s normal range is —sec.

30-40sec ; 60-70sec

LR produces a metabolic — as the lactate is converted to bicarbonate in the liver.

alkalosis

— metabolic — may be seen after large amounts of Na+ Cl- being administered. It produces a non-anion gap metabolic acidosis.

Hyperchloremic ; acidosis

—,—,—&— are all found in cryoprecipitate.

Factor VIII, XIII, fibrinogen, & vWF factor

Administration of plts is not indicated typically unless the plt count is <— cells/mm^3.

50,000

— for plts, cryoprecipitate, & FFP are considered universal donors. This is the exact opposite of blood in which — is the universal donor. Likewise, — plts, cryoprecipitate & FFP are considered universal recipients for these products.

AB+ ; O- ; O-

Cirrhosis, Viral infection, B12 deficiency, Sepsis may cause a — plt count.

decreased

— is also seen in polycythemia vera, rheumatoid arthritis, & postsplenectomy syndrome.

Thrombocytosis

— TSH & — T4/T3 values will be seen w/ secondary hyperthyroidism.

Low TSH & high free T4/T3

Hyperthyroidism is almost always a — endocrine problem meaning that there is an overproduction of thyroid hormone (T4 & T3) from the thyroid gland itself. This will lead to a suppression of TSH from the anterior pituitary gland in a negative feedback loop, to suppress continued CNS signaling for thyroid hormone production.

peripheral

Hyperthyroidism (Graves Disease): —or— should be started 6 weeks prior to the procedure in order to achieve this state. — is very useful for ameliorating the symptoms of hyperthyroidism & the doses are titrated according to HR. — has a slight advantage for induction in hyperthyroid pts as it decreases the peripheral conversion of T4 to T3 (a more active form of the thyroid hormone).

Propylthiouracil or methimazole ; Beta blockade ; Thiopental

Uncontrolled thyroid pts requiring prompt surgery can be quickly controlled by administering methimazole followed by high dose —. It reduces all stages of thyroid hormone production, IF given with a thyroid synthesis blocking agent (methimazole). It w/o premed will INCREASE thyroid hormone stores.

oral iodide

Preop, — 2mg IV Q 6hrs will decrease peripheral conversion of thyroid hormone to T3 (a more active from) allowing for better control.

dexamethasone

The most important step in the correction of DKA is adequate — followed by insulin administration. The insulin must be continued until the metabolic acidosis resolves to prevent further ketogenesis.

volume resuscitation

— anesthesia is preferred whenever possible in pts w/ Duchennes Muscular Dystrophy.

Regional

Pts w/ acromegaly suffer from narrowed upper airways and require — ETT.

smaller

Hyperosmolar Hyperglycemic State (HHS) is one of the 2 acute diabetic emergencies. Pts in HHS are usually older than 65 & suffer from —. They present with blood sugars >— & a serum osmolality of >—. Symptoms consist of lethargy, polyuria, & polydipsia, progressing to obtundation or coma over a matter of days (pts w/ DKA by comparison complain of severe abdominal pain & vomiting in the majority of cases that develops over 24-48hrs).

DM2 ; 600 ; 320

HHS pts generally suffer from a greater degree of — depletion than pts in DKA (9L on avg compared to 6L) as well as a greater deficiency in electrolytes such as —&—. Pts w/ HHS should not suffer from a — which can be useful in differentiating from DKA.

volume ; Na+ & K+ ; ketosis

Cricoid pressure must provide —lbs of force upon loss of consciousness (—Newtons) to be effective.

8-10lbs ; 30-40

Acute —, w/ its characteristic millwheel murmur.

venous air embolism

Correction of severe hyponatremia should be done to cause an increase in serum Na+ of no more than — mEq/hr. Repletion rates too fast can cause shifts in cerebral cellular water concentrations causing cellular swelling leading to seizures & death. More aggressive treatment is required in pts w/ severe symptoms such as seizure, coma, or obtundation regardless of Na+ level due to the risk of brain herniation.

0.5

In pts w/ — as the primary cause of their hyponatremia, hypertonic saline (1ml/kg body wt/hr) must be used to correct the imbalance when these symptoms are present. If these symptoms are absent then more gradual measures may be taken (fluid restriction).

SIADH

Always monitor the serum Na+ every 2-3hrs during correction to avoid — from overly rapid correction.

central pontine myelinolysis

—coagulability is seen with hypothermia

Hypo

Hypothermia — the rate of emergence (both inhalational & TIVA). It can also — the rate of drug metabolism causing prolonged action or decrease blood blow preventing redistribution. Hypothermia also causes post-op shivering, — the risk of infection, & prolongs the total time for recovery.

slows ; slow ; increases ;

helium cylinders are colored —.

brown

Equation = Hourly Insulin infusion rate

Plasma Glucose/150

Administering 75% nitrous oxide will expand closed air spaces to — the original volume. The amount of nitrous oxide that will diffuse into a closed air space will be that which results in an equal concentration of nitrous oxide to the inspired level. To get the concentration in the pneumothorax to be 75% nitrous oxide, the original air would only be 25% of the total air. Thus, 600mL of nitrous oxide added to the 200mL of air would result in the desired concentration. The total amount of gas in the pneumothorax would be —ml.

4x ; 800 mL

The fail-safe device decreases/stops flow of all gases when pressure falls <—psi.

30psi

Soda lime can absorb —L for every 100g of absorbent, & barium hydroxide lime (BaraLyme) can absorb —L of CO2 per 100g of absorbent.

14-23 ; 9-18

— absorbents are designed to remove CO2 to prevent re-breathing of carbon dioxide which may lead to hypercapnia. Initially the pt’s exhaled CO2 combines with water (there is additional water contained w/in the soda lime) to create carbonic acid. This carbonic acid enters the carbon dioxide absorbent canister & interacts w/ the soda lime (or other absorbent) producing —,—,— carbonate.

Carbon dioxide ; water, heat, & Ca+

The actual VO2 is based on the pt’s —&—.

O2 content (CaO2 or CvO2) & CO.

The NMDA antagonism is non-competetive, & is likely the main mediator of the analgesia found in — use.

ketamine

Metformin can accumulate with renal insufficiency. It is believed to cause — by promoting the conversion of glucose to lactate in the splanchnic bed of the small intestine. It also inhibits hepatic gluconeogenesis from lactate & pyruvate, which causes additional amounts of lactate.

lactic acidosis

metformin induced — almost always occurs in pts with renal or hepatic comorbidities or in the presence of sepsis or alcohol abuse. HF & any hypoxic or hypotensive states also increase the risk due to the increase presence of lactic acid.

lactic acidosis

metformin should be discontinued —hrs prior to surgery.

48 hours

— has been implicated in causing right vocal cord paralysis & laryngeal edema in a lupus-like syndrome (also known as drug-induced lupus erythematosus or DILE). Signs of drug-induced lupus erythematosus include arthralgias, fever, & development of rash on sun-exposed areas of skin.

Hydralazine

— is useful as an alkalinizing agent & given to pts at high risk for aspiration to quickly increase stomach pH, but also increases stomach volume.

Sodium citrate (Bicitra)

—or— which take significant time for the stomach pH to rise, sodium citrate provides immediate benefit.

proton pump inhibitors (omeprazole) or H2 blockers (famotidine)

— is a centrally acting alpha 2 agonist that works by presynaptically decreasing sympathetic output from the CNS.

Clonidine

Exaggerated responses to vasoactive medications may be seen in a patient taking — and under GA. Pts on this should not be administered —or—.

MAOIs ; meperidine or ephedrine.

— is an indirect thrombin inhibitor, forming a complex with AT III (antithrombin) causing deactivation of thrombin as well as factor Xa. It is the most efficacious drug to use in the treatment of pulmonary embolism.

Heparin

— mimics natural somatostatin by inhibiting serotonin release (carcinoid tumors release serotonin) along with the inhibition of gastrin, insulin, glucagon, & growth hormone. its actions in decreasing splanchnic BF.

Octreotide

— are rare, but are the most common GI neuroendocrine tumor. The ones that are local can be surgically resected, but others with metastasis require other therapy. Treatment of this syndrome is typically with octreotide, improving the symptoms of diarrhea & flushing in most pts. Extreme swings in BP with significant flushing, bronchoconstriction, dysrhythmias & altered mental status can last for hours or days.

Carcinoid tumors

— has some same side effects seen with all opioids, including causing nausea, vomiting & constipation. It is the opioid with antichoinergic effects. It causes orthostatic hypotension more so than other opioids, possibly due to alpha 2 agonism. Myocardial contractility is decreased by large doses. It causes an increase of HR rather than bradycardia that is typical of opioids. It can cause mydriasis (eye dilation) instead of miosis typically seen with opioids. Drying of secretions is also noted due to its anticholinergic effects.

Meperidine

—, a metabolite of meperidine, causes CNS effects including seizures in delirium – this is particularly seen in renal failure patients.

Normeperidine

The rate of absorption of any LA is dependent on the — of the location.

vascularity

The rate of absorption fastest to slowest w/ mnemonic:

In Time I Can Please Everyone But Susie and Sally Intravenous>Tracheal>Intercostal>Caudal>Paracervical>Epidural>Brachial Plexus>Subarachnoid, Sciatic, Femoral>SubQ

The risk of toxicity with LA is directly related to —.

potency

The max safe dose of lidocaine is —mg/kg when used without epi. Due to the local vasoconstriction caused by epi, with less drug entering the systemic circulation, epi combinations with lidocaine raise the safe threshold of administrable drug to —mg/kg. Risks of toxicity generally are heralded by neurologic symptoms including paresthesias (circumoral numbness), dizziness, blurred vision, & tinnitus, followed by slurred speech, drowsiness, seizures & obtundation. If toxicity is great, cardiac effects may be noted including heart block, bradycardia, ventricular arrhythmias & hypotension. The doses needed for cardiac toxicity are about 3x that needed for neurologic manifestations making them less likely to be noted without a preceding neurologic symptoms.

5 ; 7

The lateral femoral cutaneous nerve leaves the — roots & travels in a lateral/inferior direction anterior to the iliacus muscle.

L2-L3

Metoclopramide (Reglan) is contraindicated in — disease. Metoclopramide long term use is known to rarely cause tardive dyskinesia, which may not be reversable. Reports of tardive dyskinesia, neuroleptic malignant syndrome, hallucinations & harmful psychological effects have been reported in this disease pts who are administered it.

Huntington’s

Upon removal of the pituitary gland (hypophysectomy), the endogenous hormones secreted from it are also removed including —. Therefore, — is most likely condition to ensue. Replacement — will abate the side effects.

antidiuretic hormone (ADH) ; diabetes insipidus ; vasopressin (desmopressin)

— is released by the posterior pituitary along with oxytocin. —,—,—&— are all released from the anterior pituitary.

ADH ; Thyroid stimulating hormone (TSH), Adrenocorticotropic hormone (ACTH), Prolactin, & Growth Hormone (GH)

— is the only cerebral physiology that is increased by lidocaine administration. Lidocaine cerebrally decreases CMR, Cerebral blood flow, Intracranial pressure, & Cerebral blood volume.

Cerebral vascular resistance

A pH of >— is considered a good sign, & fetus with a pH <— is considered an abnormal sign & raises concerns of fetal well-being; fetal delivery should be done in an expedited fashion in this situation.

7.25 ; 7.20

— is added to increase the neutral, un-ionized fraction in order to quicken the onset of anesthesia.

Bicarbonate

— environments worsen the quality & prolong onset time of the anesthetic.

Acidic

All LA except for — are vasodilators, directly relaxing smooth muscle in arterioles.

cocaine

The greatest concern in pts having a vaginal delivery after a previous c-section (VBAC) is the possibility of —.

uterine rupture

— is the best means of detecting uterine rupture.

Nonreassuring fetal HR

Drugs that — variability of fetal HR include atropine, GA, magnesium, opiods, barbs, benzo, & ingested ethanol.

diminish

Terbutaline, a beta agonist tocolytic, — effect fetal HR variability. Other tocolytics such as nifedipine & nitroglycerine — alter fetal HR variability either, but magnesium as a tocolytic —.

does not ; does not ; does

— is the most common cause of bradycardia in the ped population. Other causes of bradycardia in the pediatric population include vagal stimulation, hypothermia, depression from anesthetic agent, and succ administration.

Hypoxia

The time from —mths is termed physiologic anemia of infancy, as it is a normal variant & is generally well tolerated by healthy term infants.

2-3

Soon after birth, erythropoietin synthesis greatly decreases & Hb levels slowly decrease. In 8wks, Hb reaches a low point of ~— mg/dL. In premature infants, this decrease also occurs more rapidly & will possibly fall as low as —mg/dL. Other factors, including frequent phlebotomy in sick neonates & the rapid growth of the infant compared to blood volume increases may also contribute to this anemia.

10 ; 7 or 8

After trachea, carina marks the — generation of the respiratory tree’s divisions. It then splits into bronchus (—) followed by the bronchioles (—).

1st ; 3rd ; 4th

— position is found during phonation or during effort closure, when the vocal cords are in an adducted position.

Midline

Expiration in humans is a — event that doesn’t require muscle effort.

passive

In pts that force expiration, the — muscles including —,—,— assist w/ forced expiration.

abdominal ; external & internal obliques & the rectus abdominis

The alveolar sac is the — generation (division) of the respiratory tree, which marks the end of the respiratory tree. This is the location where the alveoli begin. Actual gas exchange begins at generation — w/ the bronchioles.

23rd ; 17

Thyroid cartilage felt at — level. This cartilage forms the — wall of the larynx & provides anterior wall of the larynx.

C4-C5 ; anterior

— is the most potent coronary vasodilator volatile agent.

Iso

— has been shown to react w/ CO2 absorbents in anesthesia circuits to produce carbon monoxide. Baralyme that is dried (dessicated) is the most commonly implicated absorbent, however it can be seen w/ soda lime as well.

Des

Anesthesia hoses contain —L of gas in the adult circuit, & anesthesia absorbent containers hold —L of gas. An adult anesthesia bag can contain —L of gas, & ped bags can contain either —L of gas. The total wash-in volume of the anesthesia machine is —L.

2L ; 2L ; 3L ; 1 or 2L ; 7L

Cerebral vasodilation begins at >— MAC, at >1 MAC all modern volatile anesthetics actually begin to increase —.

0.6 ; ICP

— antiarrhythmic meds are the beta blockers. These meds work by antagonising sympathetic activity & slowing rate of SA or ectopic atrial discharges. They further slow conduction through primary 7 abberant accessory conduction pathways.

Class II

Lidocaine is a — antiarrhythmic drug

class IB

A QTc interval of >— seconds (— milliseconds) is considered prolonged.

0.45 ; 450

Most pts w/ a dissecting aorta will have a variation in BP of >— mmHg b/n arms. Pts may have a missing carotid pulse, depending on location of dissection.

In a pt w/ — syndrome, the incidence of having a dissecting aneurysm is greatly increased compared to the normal population.

Marfan’s

A pt in — is seen as having a progressively prolonged PR interval followed by a non-conducted (blocked) P wave. This condition can be due to a structural or electrical conduction problem, & is typically seen in pts w/ high vagal tone. If asymptomatic, no treatment is needed/indicated & the problem generally resolves itself. In symptomatic bradycardia (seen with a low atrial rate), atropine may be used temporarily & a permanent pacemaker may be indicated.

2nd degree AVB type I (Mobitz I/Wenckebach)

1 plt pheresis should raise plt count by — cells/microliter in a typical adult pt. 1 unit of plt concentrate should increase plt count by — mm3.

30,000-60,000 ; 5,000-10,000

A pheresis contains — the amount of 1 unit of plts.

The — test is the best test to determine renal functioning.

creatinine clearance

>— mL/min is considered normal renal function on lab testing, but true normal is —mL/min so significant renal function decline can occur before a drop in GFR is noted in lab work. Mild renal insufficiency seen at GFR of —mL/min, & mod renal insufficiency is from —mL/min. A GFR of <—mL/min is seen in overt renal failure, while a GFR of <—mL/min is seen in end stage renal disease.

120 ; 180 ; 40-60 ; 25-40 ; 25 ; 10

— disease: avoiding meds that stimulate SNS due to a potential for an exaggerated CV response under increased thyroid activity including HTN & tachycardia. Ketamine is one such agent.

hyperthyroid

— induction may be preferred as it has thyroid hormone blocking activity.

Thiopental

— is the fluid of choice for pts in RF. Giving a pt in RF any K+ containing fluids increases the incidence of hyperkalemia due to their inability to excrete K+. Glucose free fluids should be used when possible due to the glucose intolerance caused by peripheral tissue insensitivity to insulin in uremic pts.

NS .9%

NS .9% is —, — free & doesn’t contain —.

isotonic ; K+ ; glucose

Lithotomy position places the legs into stirrups most often implicated in damage to — nerve.

common peroneal

A minimum of —L/min is required to provide an FiO2 that will approximate a 1.0 FiO2.

Alfentanil is a — potent & — acting analogue of fentanyl.

less ; shorter

— failure, but not —, can prolong the action of Alfentanil.

Liver ; RF

—&— have been demonstrated to cause significant drops in BP when given the morning of surgery. These meds should be w/held at least 1 dosing cycle prior to surgery.

ACE-I (lisinopril) & angiotensin receptor blockers

— inhibit the H+/K+ATP-ase pump of the gastric parietal cell. This is the last stage of gastric acid secretion, reducing acid secretion by up to 98%. These meds can decrease the risk of morbidity in the event of aspiration by increasing stomach pH, but must be given time to work prior to induction–they should not be w/held prior to surgery.

Proton pump inhibitors (omeprazole)

— is a antiHTN w/ B1, B2 & A1 antagonism properties that is used frequently in pts w/ HF, HTN, & left ventricular dysfunction after MI. It also decreases HR & improves CO. It also has been shown to slow progression of CHF & decrease risk of death. This med shouldn’t be stopped the morning of surgery, as sudden cessation of this med or any beta blocker can greatly increase the risk of MI & sudden death.

Carvediol (Coreg)

— is commonly used for mod pain on an outpt & inpt basis. Any pt w/ a hx of mod to severe pain shouldn’t have their narcotics withdrawn unless specific indications are present. Pts should also be dosed w/ adequate analgesia prior to emergence from anesthesia & may have increased needs of analgesics due to down regulation of opioid receptors.

Percocet (combo analgesic consisting of oxycodone & acetaminophen)

— (alpha 1 antagonist) was used primarily as an antiHTN. Due to the incidence of side effects (orthostatic HoTN) & the availability of better antiHTNs, it is not used for this purpose as frequently any more. But, it has found popularity as a drug used to treat benign prostatic hyperplasia (BPH) due to the presence of alpha 1 receptors on the prostate gland. Antagonizing alpha 1 receptors on the prostate allows muscular relaxation & eases the symptoms. May be taken on the morning of surgery.

Terazosin

—: drug used to treat benign prostatic hyperplasia (BPH) due to the presence of alpha 1 receptors on the prostate gland. Antagonizing alpha 1 receptors on the prostate allows muscular relaxation & eases the symptoms.

Terazosin (alpha 1 antagonist)

Should Terazosin (alpha 1 antagonist) be taken on the morning of surgery?

Yes

Should ACE-I (lisinopril) & angiotensin receptor blockers be w/ held prior to surgery?

Yes, at least 1 dosing cycle

Should Proton pump inhibitors (omeprazole) be w/held prior to surgery?

Should Carvediol (Coreg) be stopped the morning of surgery?

Should Percocet (combo analgesic consisting of oxycodone & acetaminophen) be taken prior to surgery?

Yes

drugs that should not be given morning of surgery: 8

1. ACE inhibitors 2. ARBs 3. metformin 4. most insulins (or reduce dose) 5. oral antihyperglycemics 6. niacin 7. diuretics 8. NSAIDs (unless surgeon advises to take)

Drugs to take morning of surgery:10

1. Proton pump inhibitors 2. H2 blockers 3. pain med 4. beta blockers 5. alpha antagonists 6. other antiHTNs that are not ACE/ARBs/diuretics 7. steroids 8. lithium 9. antibiotics 10. anti-depressants including MAOIs and SSRIs.

Triamterene is a — diuretic

K+ sparing

The common peroneal nerve is — anesthetized by the psoas block bc the — nerve is spared.

NOT ; sciatic

The —,—&— of the thigh are anesthetized in a Psoas block.

femoral n., obturator n., & the lateral cutaneous n.

The — block is a useful block for anesthetizing the medial aspect of the leg from groin to ankle via blockade of the femoral nerve & its branches. It also provides anesthesia to the upper lateral aspect of the thigh.

psoas

The — nerve provides motor innervation to the hamstrings & to all muscles distal to the knee.

Sciatic

If you are performing a Sciatic nerve block & produce evoked contractions of the hamstrings then you are at the main trunk of the sciatic nerve & your position is correct. You want distal evoked contractions (Foot & Toes). The reason is that if you only have evoked contractions of the hamstrings you could be stimulating the —or—.

muscle itself or just a branch of the Sciatic nerve

— is the most cardiotoxic

Bupivacaine

— is a racemic LA mixture w/ a high lipid solubility & protein binding profile.

Bupiv

— competitively replaces NorE at the presynaptic terminal & is mostly used in pain management, not in surgical anesthesia.

Guanethedine

Intracranial HTN is defined as a pressure of >— mmHg, & ICP is typically <— mmHg.

15 ; 10

CO returns to the pt’s normal baseline w/in —wks after delivery of the fetus, assuming no cardiac pathology such as HF had developed during pregnancy.

2wks

— is contraindicated in pts w/ hypocalcemia or MG, due to its inhibition of acetylcholine release.

Mg+

— is renally excreted, so pts w/ RF should receive it very cautiously & serum levels should be monitored.

Mg+

Pts with MG should be administered little if any — meds. Certain other drugs also may worsen weakness in pts w/ MG. These drugs are —,—,—,—&—.

neuromuscular blockade ; beta blockers, lidocaine, opioids, aminoglycosides, & phenytoin

— antibiotics in particular, when given during surgery w/ neuromuscular blocking agents, increase the risk of postoperative respiratory depression.

Aminoglycoside

Spinal analgesia is useful in providing optimal conditions for cerclage placement, but must cover levels from — to ensure anesthesia of both the cervix & vagina. GA may be used & may be preferred when membranes are bulging through the cervix. Volatile anesthetics relax uterine smooth muscle which is beneficial during this procedure, however, this must be weighed against the risks of phsyiologic reflexes to intubation. Coughing & vomiting will raise intrauterine pressure & can herniate more of the fetal membranes through the cervix. No matter the method of anesthetic care, ensure abdominal pressure is kept to a minimum.

T8-S4

Pts w/ — may have the following anesthesia relevant abnormalities: endocardial cushion defects, atlanto-axial instability, hypothyroidism, macroglossia, narrow hypopharynx, subglottic stenosis, choanal atresia, obesity. Although hyperthyroidism does occur at a greater rate than the general population, they are far more prevalent to have a hypothyroid function.

Down syndrome

—&— have decreased brown fat stores, & thus have impaired ability to regulate their own temp.

Neonates & premature infants

— is highly vascularized & is innervated w/ beta sympathetic receptors. Stress created by a cold environment increases sympathetic nervous activity & the release of NorE, causing a breakdown of it & release of heat through increased metabolism. One quarter of the CO may be sent to it to directly warm blood. Decreased NorE stores are not the reason for decreased non-shivering thermogenesis.

Brown fat

During normal —, the following occurs: when NorE release is stimulated by sympathetic activity, free fatty acids & glycerol are released from triglycerides. The increase in O2 consumption due to increased metabolism allows an infant to double the normal thermogenic rate. A larger surface to weight ratio will increase radiant heat losses, thus making the choice about a smaller surface area to weight ratio incorrect.

nonshivering thermogenesis

Infants are born w/ low glycogen stores, & thus are more prone to dangerous —.

low blood sugars

Half of all deaths in pregnant pts are related to —. The next most common causes of death are due to —,—or—.

HTN ; infxn, hemorrhage, or embolic events

Failure to — is the leading cause of anesthesia related death.

secure an airway

— is a competetive antagonist of Ca+ at the motor endplate, reducing Ca+ influx into the myocyte.

Mg+

— decreases acetylcholine release at the neuromuscular junction & reduces sensitivity of the end plate to acetylcholine. It shares similar side effects to beta adrenergic tocolytic agents such as terbutaline (terbutaline stimulates beta2 adrenergic receptors causing smooth muscle relaxation). It’s side effects include chest pain & tightness, palpitations, HoTN, sedation, diplopia, nausea, flushing, muscle weakness, lethargy, AV conduction blocks & QRS widening can occur as well. Pulmonary edema & cardiac arrest have been reported. Neonatal side effects: lethargy, hypotonia, & respiratory depression.

Mg+

— is another tocolytic that has been compared to Mg+. Compared to it, Mg+ has less incidence of therapy failure than the drug group. In addition the drug group had to have therapy stopped more often than the Mg+ group due to HoTN.

Nitroglycerin

— is associated w/ polymorphic v-tach (Torsades de Pointes), which has been seen even at normal therapeutic levels of the drug.

Procainamide

— has a short DoA & seems to have a very low risk of pro-arrhythmic effects.

Lidocaine

— also has a very low risk of pro-arrhythmic effects Torsades de Pointes seen with its use is associated with low serum Mg+ levels.

Amiodarone