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
