Page Summary Flashcards
Which nerve is responsible for the larynx?
Vagus
2 nerves for motor of larynx?
External superior laryngeal and recurrent laryngeal
Where is external superior laryngeal nerve responsible for with motor?
Cricothyroid
Stimulation of which nerve causes laryngospasm?
Superior laryngeal nerve
Which 2 nerves are responsible for sensory of larynx?
Internal superior laryngeal and recurrent laryngeal
Where is internal superior laryngeal nerve responsible for with sensory?
Above vocal cords and cords
Where is recurrent laryngeal nerve responsible for with sensory?
Below vocal cords
Posterior cricoarytenoid movement?
Abduct
“You take it out back”
Lateral cricoarytenoid movement?
Adduct
“You bring it in from the side”
Cricothyroid does — to vocal cords
Tenses
Thyroarytenoid does — to vocal cords.
Relaxes
Which 2 nerves are responsible for pharynx?
Spinal accessory and glossopharyngeal
Which nerve controls motor in pharynx?
Spinal accessory
Which nerve controls sensory in pharynx?
Glossopharyngeal
Laryngeal cartilages from superior to inferior (6)
Epiglottis
Thyroid
Cuneiform
Corniculate
Arytenoids
Cricoid
Normal P50 value?
26-27mmHg
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
6 causes of right shift in oxyhemoglobin dissociation curve?
Increase PCO2
Increase H+
Decrease pH
Increase temp
Increase 2-3 DPG
Sickle cell anemia
Right shift — O2 from blood
Unloads
Right shift of oxyhemoglobin dissociation curve=
Release
Left shift — O2 affinity
Increases
Left shift of oxyhemoglobin dissociation curve=
Locked
PaCO2 affects oxyhemoglobin dissociation curve
Bohr effect
PaO2 affects CO2 dissociation curve
Haldane affect
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
+1
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?
- Age
- PP vent
- PE
- 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?
E
Jackson-Reese minimum — L/min (2.5-3xMV)
5
Bain circuit is which mapleson circuit?
D
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
4L
Normal FVC
5L
Normal FEV1/FVC
.8
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:
- Physically dissolved (5%)
- Carbonic Acid (<1%)
- Bicarbonate ion (HCO3-, 90%)
- 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?
- Short,muscular neck
- Receding mandible
- Protruding maxillary incisors
- Unable to visualize uvula
- Limited TMJ (<40mm)
- 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?
- Acute intrinsic (ARDS, aspiration, or CHF)
- Chronic intrinsic (sarcoidosis, drug induce)
- Chronic extrinsic (obesity, ascites, pregnant; “big bellies”)
- 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
1
<20kg LMA
2
20-30kg LMA
2.5
> 30kg LMA
3
Normal adult LMA
4
Large adult/men LMA
5
Crazy large LMA
6
Sterilization temperatures:
275F & 135C
Aspiration steps:
- head down (#1)
- disconnect circuit
- Suction
- examine w/ bronchoscope
- x-ray
- abx (debatable)
- 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
30
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:
- Hypokinesis (less than normal wall motion)
- Hyperkinesia (greater than normal wall motion)
- Akinesis (absence of wall motion)
- 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
20
Swan-ganz catheter: RV depth
30
Swan-ganz catheter: PA depth
45
Swan-ganz catheter: PCWP depth
45-50
— is never higher than PADP
PAWP
When can PAWP be higher than PADP (3)
- MS
- Increase alveolar pressure
- 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)
1
Arterial wave number: dicrotic limb: blood flow to periphery
2
Arterial wave number: dicrotic notch: aortic valve closure, coronary artery perfusion
3
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
20
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
V5
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
- Liver dysfunction
- 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”
3
CN: Inferior rectus- infradduction “look down”
3
CN: Medial rectus- adduction “look in”
3
CN: Lateral rectus- abduction “look out”
6
CN: Supeiror oblique- look in & down
4
CN: Inferior oblique- look out and up
3
— 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
8%
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:
- Dehydrate brain w/ Mannitol (0.25-1g/kg) or Lasix 2. Give steroids- slowest but may restore BBB
- Hyperventilate PaCO2 25-30 mmHg (1/2 life 6hr)
- Restrict fluids
- Elevate HOB to 30degrees
- Administer cerebral vasoconstrictor (pentathol, etomidate)
- 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?
No
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
- Hypocalcemia
- Hypomagnesemia
- Hyponatremia
- 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:
- Hypotension due to sympathetic blockade
- 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=
- Hypervolemia = CVP > 10 mm Hg, PCWP = 12-20
- Hypertension = SBP 160-200 mm Hg
- 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
- Notify surgeon so they can flood the field or pack
- Turn off N2O
- Administer 100% O2
- Aspirate central venous catheter to remove air
5.↑CVP (Valsalva maneuver) - CV drugs to support circulation
- Bilateral jugular vein compression
- PEEP
- Position- left lateral decub w/ 15 degree head down tilt
CSF pathway: (10)
- Choroid plexus
- Lateral ventricle
- Foramen Monroe
- 3rd ventricle
- Aqueduct of Sylvius
- 4th ventricle
- Foramen luschka & foramen magendie
- Subarachnoid space
- Brain
- Arachnoid Villi
4 main sources for circle of Willis:
- R internal carotid
- L internal carotid
- Basilar artery
- 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
Mu
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
no
— – 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:
- Decrease Cerebral perfusion secondary to hypotension, decrease PaCO2, increase ICP
- Cerebral hypoxia
- Hypothermia (MOST)
- Hyperthermia
- 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:
- Femoral - saphenous
- 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 —
L1
The origin of the scapular spine corresponds with —
T3
The most protuberant cervical vertebra is at the level of —
C7
The tip of the scapula corresponds with —
T7
level of the posterior superior iliac spine —
S2
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:
- Pruritus (most common)
- Urinary retention
- N & V
- Respiratory depression
4 common side effects of epidural opioids:
- urinary retention (bup/morphine)
- pruritus (morphine)
- weakness of hands
- 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
C8
— = numbness @ middle fingers
C7
— = numbness @ thumb & index finger
C6
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
T6
Procedures & Level of Block:
Kidney
T10-L1
Procedures & Level of Block:
Uterine and cysto
T8-T10
Procedures & Level of Block:
C section
T4
Procedures & Level of Block:
Tourniquet
T8
Procedures & Level of Block:
Upper abdominal
T4
—: 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)
- Preexisting neurological dz
- Back disorder (Ankylosis)
- Heart Disease
- Surgery above umbilicus
- Failure to obtain free flow
- Sepsis
- Mobitz type I or II
- 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
10
Ticlodipine – — days
14
Clopidorgrel- — days
7
GPIIb/IIIA – hold for — weeks post operative
4
↑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
3
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
- Blood solubility
- Cardiac output
- Alveolar ventilation
- Inspired concentration
Three ways to increase speed of equilibrium:
- Increase Inspired anesthetic concentration
- Second gas effect
- Increase Alveolar ventilation
Two most important factors for increase alveolar partial pressure:
- Inspired concentration
- 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:
- Increasing age
- Hypothermia
- CNS depressants
- Acute ethanol intoxication
- Alpha-2 agonists (Clonidine)
- Pregnancy
- Decrease Levels of CNS neurotransmitters
Five factors that increase MAC:
- Hyperthermia
- Hypernatremia
- Increase Levels of CNS neurotransmitters
- Young
- 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
2
N2O is metabolized to N2 in the intestine by — metabolism.
reductive anaerobic
Five contraindications to the use of N2O:
- Venous air embolism
- Ear surgery (middle ear)
- Closed pneumothorax
- Potential pneumocephalus
- Bowel obstruction
Four adverse side-effect of N2O:
- Aplastic anemia
- Congenital anomalies
- Spontaneous abortion
- 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:
- Decrease RBF
- Decrease GFR
- 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
- Oxidation
- Reduction
- 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:
- Barbiturates
- Opioids
- Benzodiazepines
- Amide LA’s
- Tricyclic antidepressants
- 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
- Arterial vasospasm with intense pain down the arm
- Blanching of the skin with loss of distal pulses
- 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:
- Suppression of adrenocortical response to stress 2. N & V
- Decrease Plasma cortisol concentration
- 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 </= sufent < meperidine < fent
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.
Mu
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:
- Decrease Breathing rate
- Decrease Minute ventilation
- Decrease Response to CO2, secondary brainstem depression
- 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:
- d-Tubocurarine
- Metocurarine
- Atracurium
- 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:
- Succinylcholine 2. Atracurium
- Cisatracurium 4. Mivacurium
Three NDMRs not significantly excreted by kidneys:
- Atracurium
- Cisatracurium 3. Mivacurium
— is primarily eliminated by renal (70%) and secondarily by biliary (20%).
Pipecurium
What 5 things can augment NMB:
- Hypermagnesium
- Hypocalcemia
- Hypokalemia
- VA : des > sevoflurane > iso > N2O/fentanyl
- Hypothermia
Eleven possible complications of Succinylcholine administration:
- Hyperkalemia
- Bradycardia (@ ♥ SA Node)
- Increase HR and/or BP
- Skeletal muscle myalgia
- Allergic reaction
- Triggering of MH
- Sustained masseter muscle contraction
- Myoglobinuria
- Increase IOP (NOT prevented with defasculating dose)
- Increase Intragastric Pressure (prevented with defasiculating dose)
- 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:
- Unhealed third-degree burns
- Denervation of skeletal muscle
- Severe skeletal muscle trauma
- Upper motor neuron injury (head injury, Parkinson’s, CVA)
- Muscular dystrophy
- Renal Failure w/ hyperkalemia
- Severe Sepsis
- Duchennes
- Guillian Barre
11 clinical manifestations of MH:
- Hypercarbia
- Tachycardia
- Tachypnea
- Hyperthermia
- Hypertension
- Cardiac dysrhythmias
- Acidosis (metabolic)
- Hyperkalemia
- Skeletal muscle rigidity
- Myoglobinuria
- 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:
- Discontinue inhaled agents & Sux
- Hyperventilate with 100% O2
- Administer Dantrolene
- Treat acidosis with NaHCO3 (1-2 mmoles/kg)
- Decrease Body temp to 38C
- Replace anesthesia circuit and CO2 absorber
- Monitor ETCO2 & ABGs
- 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:
- Reoccurrence
- DIC
- Myoglobinuric renal failure
- Skeletal muscle weakness
- 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 —%
10
—: 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:
- Tricyclic antidepressants (imipramine)
- Opioids (especially Demerol)
- Indirect acting sympathomimetics (ephedrine)
- 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)
- Anticholinergic effects (dry mouth, blurred vision, tachycardia)
- Orthostatic hypotension
- Sedation
Tricyclic antidepressants interact with: 5
- Anticholinergics (atropine, scopolamine)
- Sympathomimetics (ephedrine)
- Inhaled anesthetics (increase dysrhythmias)
- Antihypertensives (rebound HTN)
- 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
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
- isolated coagulation factor deficiencies
- reversal of Coumadin
- liver dz- reverse coagulation issues
- after massive transfusion and still bleeding
Max allowable EBL = equation
EBV x [(Hbi-Hbf)/Hbi]
Hct = — x Hbg
3
Hct of PRBC = —
75
PRBC replacement= equation
[(blood loss - MABL) x desired Hct]/Hct of PRBC
Estimated Blood Volume (EBV):
Premie (<term)
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)
75
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)
LR
Too much of this fluid = metabolic alkalosis
LR
— : Na = 154 meq/L = Isotonic (osmol = 308)
NS
Too much of this fluid = hyperchorlemic acidosis
NS
—: Hypotonic (osmolality 252 mOsm)
D5
—- 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:
- Pulmonary edema and Cardiac decompensation
- Rebound increase ICP
- Hypovolemia
- Hyperkalemia
- Hyponatremia
Virchow Triangle:
- endothelial injury
- stasis or turbulent blood flow
- 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
- hypo- and hyperthermia
- acidosis
- mild degrees of hypoxemia
- hypotension
- hypovolemia
- 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:
- Chemotherapy or unrecognized cancer
- Liver disease and splenomegaly
- DIC
- Pre-eclampsia
—: Metabolic d/o affecting biosynthesis of heme = thick blood
Porphyria
Porphyria Signs & Symptoms: 3
- Acute abdominal pain, N & V
- Neurotoxicity: confusion, SIADH, difficulty swallowing, HTN & tachycardia
- 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:
- Laryngeal edema
- Bilateral cord paralysis
- Hematoma formation
- Hypocalcemia secondary to hypoparathyroidism
Six hormones of the Anterior Pituitary: (Adenohypophysis) (Blood flow through Hypothalamic-Hypophyseal Portal System)
- Adrenocorticotropic hormone (ACTH)
- Thyroid stimulating hormone (TSH)
- Growth hormone (GH)
- Prolactin
- Leutinizing hormone (LH)
- 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:
- Subtotal lobectomy of thyroid
- Goiter
- Autoimmune disease (myxedema)
- 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
- Airway obstruction
- Laryngospasm secondary hypocalcemia
- Bilateral recurrent laryngeal nerve damage
- 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
- ECG changes (prolonged Q-T interval)
- 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:
- Depressed neuronal activity (coma)
- Cerebral vasodilation (increase CBF, increase ICP)
- Decrease Cerebral perfusion pressure (cerebral ischemia)
- 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:
- Ketoacidosis
- Lactic acidosis
- Renal failure
- Toxic dose of salicylates
Three causes of Metabolic Alkalosis:
- Vomiting
- NG suctioning
- 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++:
- Action potentials in smooth and cardiac muscle
- Blood coagulation
- Bone formation
- Muscle contraction
- Membrane excitability (Ca++ controls threshold)
- 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:
- Prolonged QT interval
- Increase ST segment duration
- Flat or inverted T-waves
7 Functions of Magnesium:
- Functions as a cofactor in many enzyme pathways
- Regulates the Na+/K+ pump
- Regulates adenylate cyclase
- Regulates slow Ca++ channels
- It antagonizes Ca++ (an endogenous Ca++ channel blocker) = vasodilatation
- Controls the threshold potential (membrane stabilizer)
- 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:
- Arrhythmias
- Hypotension
- Pulmonary edema
- Mental changes
- Muscle cramps
- Weakness
- Myoclonia
- 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:
- Alkalosis
- Insulin
- Beta-2 adrenergic stimulation
Seven ways to treat Hyperkalemia:
- Give calcium gluconate
- Give glucose/insulin
- Give sodium bicarbonate
- Give diuretics (to increase excretion)
- Give kayexalate (potassium exchange resins)
- Use hemodialysis
- 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
I
MEN — = medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism (type IIa) or multiple mucosal neuromas (type IIb or type III)
II
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
67
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:
- Glomerulus
- Proximal tubule
- Descending LOH
- Ascending LOH
- Distal tubule
- 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
40
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
- Primary on collecting ducts in the nephron = passive water reabsorption
- 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:
- Decrease Renal perfusion pressure
- Hyponatremia
- 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:
- Polyuria, > 2-15 L/day- HALLMARK
- Hypernatremia (plasma hyperosmolality)
- 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
- Decreased plasma osmolality (< 270 mOsm/kg)
- Increase urine [Na+] (> 100-150 mOsm/kg)
- Hyponatremia d/t retention of H2O
SIADH: Tx: —4
remove underlying cause, Limit H2O , 3% Saline, demecolcine
Liver: —% CO
25
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:
- Storage and filtration of blood (500ml)
- Metabolic functions such as carbo, fat, and protein metabolism
- Secretion of bile
- Storage of vitamins
- Blood coagulation
- Storage of iron
- 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:
- Obesity
- Pregnancy
- Opiods
- Diabetes mellitus
- Trauma
- Pain
- Anxiety
Drugs that ↓ LES Tone: (↑ risk of aspiration)
- Anticholinergics
- Dopamine
- Thiopental
- Opioids
- Propofol
- Tricyclic antidepressants
- Sodium nitroprusside
5 Patients who benefit from antiemetics:
- Eye surgery patients
- Gynecological patients
- Obese patients
- History of vomiting
- 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 — )
pH
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:
- Cimetidine (Tagamet)
- Ranitidine (Zantac)
- 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:
- Cutaneous flushing
- Bronchospasm
- Diarrhea
- Large BP swings
- 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
- Malnutrition
- Abnormal liver FX
- ETOH WD (alcoholism frequent cause of pancreatitis)
Symptoms of pancreatitis: 4
- Dehydration
- Hypocalcemia
- Hyperglycemia
- ARDS
Alcoholism is a frequent cause of pancreatitis.
5 “F’s” of Cholelathiasis:
- Fat
- Female
- Fertile
- Forty
- 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 = — %
6
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
20
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
- Hypotension
- Tachycardia
- Hypoxemia, decrease SpO2
- Bronchospasm
- Hypocapnia, decrease ETCO2 (1st sign d/t dead space ventilation)
- PVR > 300
- +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
1
ASA class: mild systemic disease- HTN, DM, Anemia, age, obesity, chronic bronchitis
2
ASA class: severe systemic disease- Cardiac dz with limiting activity, Uncontrolled HTN, DM w/vascular issues, MI or Angina
3
ASA class: incapacitating systemic dz – CHF, persistent angina, advanced kidney or liver dz
4
ASA class: moribund pt. – Not expected to live 24 hours after surgery- PE, AAA, cerebral trauma
5
ASA class: brain dead- organ procurement
6
ASA class: not elective- i.e appy
E
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:
- Pheo
- Recent MI (4-6 wks)
- CVA <3mos
- recent intracranial surgery- <3mos
- Intracranial mass lesion
- 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)
40
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
2x
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 <—
60
Hypotension: SBP 1year <—
70
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
60
Elective surgery: at least — weeks post conception
60
—: 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
- Decrease PVR and increase pulmonary flow
- Increase SVR = increase L vent = increase LAP
MOA of ductus arteriosus: 2
- Increase PaO2 and decrease prostaglandins
- 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
- Hypoxia
- Hypercarbia
- Acidosis
- Hypothermic
- 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:
- Large single ventricular septal defect
- Aorta that overrides the right & left ventricles
- Obstruction to right ventricular outflow
- 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
- Hyperchorlemic metabolic alkalosis- ↓Cl, K, Na, Ca
- ↑ Aldosterone secretion
- 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
- Difficult intubation: use small than usual ETT
(Large tongue Short neck Small mouth) - Neck flexion- Cervical spine dislocation- antlanto-occipt (Instability & Weak ligaments)
- 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:
No
Omphalocele presence of sac:
Yes
Gastroschisis presence of sac:
No
3 concerns with gastroschisis:
Infection, hypothermia, and hydration
Omphalocele and gastroschisis: steps 4
- Decompress stomach with tube
- No nitrous
- Hydrate 8-16ml/kg/hr
- 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
4
Tonsillectomy: 3 complications:
bleeding, laryngospasm & emesis
NPO Guidelines: Solid Food
8
NPO Guidelines: Commercial Formula/Milk
6
NPO Guidelines: Breast Milk
4
NPO Guidelines: Clear Liquids
2
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
- CPAP- 10-15cm H2O
- atropine 0.02mg/kg
- 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
CO
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
14
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
BP
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:
- Fetal trophoblasts
- Cytotrophoblasts
- Syncytiotrophoblasts
Placental Transfer of Drugs: 4
- Concentration gradient
- Molecular weight of drugs – MW < 500 = easier transfer
- Lipid solubility- lipids soluble drugs = easier crossing
- 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 —)
1
Late Decelerations (Type —)
II
—:
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
20
—:
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
45
—:
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
25
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
T4
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
- 2.5mg diazepam up to 10mg IV
- Fentanyl 1μg/kg IV
- 40% N2O
- 0.25mg/kg ketamine IV
- 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
- Repetitive late decelerations
- Loss of beat to beat variability associate w/ late or deep decels
- Sustained FHR < 80 BPM
- Meconium-stained amniotic fluid
- Oligohydramnois
- Fetal Scalp pH < 7.2
- 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
38
—: 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:
- BP 160/110
- Proteinuria increase 5 g/day
- Oliguria, < 500 ml/day
- Pulmonary edema
- Hepatic tenderness or HELLP syndrome
- 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:
- Thrombocytopenia
- Prolonged PT
- Prolonged PTT products
- Decrease Serum fibrinogen, increase Fibrin split
DIC is associate with 3 OB problems:
- retention of dead fetus
- Placental abruption
- 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
30
Geriatrics: A-A gradient: >/= —
20 (normal 8)
Geriatric System Changes
Cardiac: fx declines —% (20-80 y.o)
50
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
70
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.
50
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
70
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
T8
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.
13
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
PE
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
- Major crush injury
- thermal/electrical injury
- Acute muscle ischemia d/t arterial occlusion
- Acute muscle injury 2nd prolonged immobilization
- Compartment syndromes
- MH
- Extreme lithotomy
- 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:
- Pupillary response to light
- Corneal reflex
- Oculocephalic reflex (dolls eyes)
- Oculovestibular reflex (caloric response)
- Gag & cough reflex
- 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
- Hypocapnia
- Vasodilators
3.VA - High or low pulmonary artery pressure
- High or low mixed venous partial pressures
- 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
- Clonidine
- Physostigmine
- Serotonin antagonists
- 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
16
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
25
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)
- Ventilator power inlet
- pipeline inlets, check valves, pressure gauges
- flow meter valves
- oxygen pressure- failure devices
- oxygen second stage regulators
- flush valve
Components of the low-pressure system of AM: 16 psig (4)
- flow meter tube
- vaporizers
- check valves
- 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
D
Mapleson — only one w/o reservoir bag
E
Mapleson — = Jackson Reese - peds d/t ↓ WOB but heat loss
F
Forced Air Warmer:
Maximum temp —C
Average contact —C
48 C ; 46 C
Blood Salvage Contraindications: 5
- Infection 2. malignant cells 3. Urine 4. bowel contents 5. Amniotic fluid
Blood Salvage Contraindications: 5
- 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.
40
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
40
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
47
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
25
— #- 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
- Stop ventilation
- Stop O2 Flow
- Extubate patient
- Extinguish the fire
- Mask ventilate
- 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
- Risks
- Benefits
- Complications
- 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.
XI
— 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
1
ASA —-A pt w/ mild systemic disease w/o functional limitation. (Smoker, Pregnancy, Controlled Diabetes)
2
ASA —-A pt w/ severe systemic disease. (Morbid obesity, ESRD with regular dialysis)
3
ASA —-A pt w/ severe systemic disease, constant threat to life. (Recent (< 3mths) TIA or MI, ESRD not on regular dialysis)
4
ASA —-A moribund pt who is not expected to survive w/o the operation (Massive trauma, ICH with mass effect)
5
ASA —-A declared brain-dead pt whose organs are being removed for donor purposes.
6
— 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.
Mu
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 —.
BP
— 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.
B
Sympathetic — fibers are attenuated 1st so the sympathectomy is the 1st sign of the LA starting to work.
B
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.
20
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.
20
Intracranial HTN is defined as a sustained increase in ICP >— mmHg
15
— 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.
50
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
no
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.
C
Category — drugs are ones that controlled studies have shown no risk.
A
Category — drugs show no evidence of human fetal risks. These are typically animal reproduction studies w/o performing controlled studies in pregnant women.
B
Fetal abnormalities have been clearly demonstrated w/ administration of category — drugs, & these drugs shouldn’t be given in any pregnancy situation.
X
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).
D
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:
- FFP for prolonged PTT
- cryoprecipitate for fibrinogen levels <100 mg/dL
- 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.
SV
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.
75
— 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.
C3
— 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).
17
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.
2
Type — pneumocytes are tight junction cells that prevent passage of materials into the alveolar sacs.
1
— 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.
17
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.
J
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.
20
— 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.
1
Hypokalemia may lead to prominent - waves.
U
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.
20
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.
6x
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.
10
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?
No
Should Carvediol (Coreg) be stopped the morning of surgery?
No
Should Percocet (combo analgesic consisting of oxycodone & acetaminophen) be taken prior to surgery?
Yes
drugs that should not be given morning of surgery: 8
- ACE inhibitors
- ARBs
- metformin
- most insulins (or reduce dose)
- oral antihyperglycemics
- niacin
- diuretics
- NSAIDs (unless surgeon advises to take)
Drugs to take morning of surgery:10
- Proton pump inhibitors
- H2 blockers
- pain med
- beta blockers
- alpha antagonists
- other antiHTNs that are not ACE/ARBs/diuretics
- steroids
- lithium
- antibiotics
- 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
