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local anasthetics - mechanism of action
local administration
- mech= suppress pain by blocking inpulse (Na+ Channels)
- -Esters= (novacain) metab in bld
- -Amides- (lidocaine) metab in liver
- Locally admin= block small unmyelinated neurons BFORE larger myelinated
- =pain lost first, then temp, tounch, deep pressure
- = blocks both sensory and motor neurons
- If used centrally, excites then depresses the CNS and cardiac function
- **EPI is used to becuase of local vasoconstriction properties and to prolong anes. effects
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Epidural
- Spinal/subarachnoid(CSF circulation)
- Lumbar region
- SE= HypoTN-most sig. effect
- = fecal/urine incontinance or retention
- = Spinal headache
- => Place in supine position and apply a Blood Patch b/c CSF is leaking
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Cocaine
blocks NE reuptake, flooding the body with NE
-
4 general anesthesia types
- balanced
- gas
- volatile liquids
- IV-sedation
-
Pre-anesthesia- pain, anxiety, amnesia
Benzodiazapine-midozalam / Versed is DOC plus Opioids & NO2 for pain
-
Minimal Alveolar COncentration
Nitrous Oxide
- MAC
- [ ] that prodices immobility in 50% exposed to painful stimuilation
- **LOW MAC indicated HIGH potency (use less)
NO2= inhalation gas - not good to sedate, but is good for pain
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Sublimaze
Synthetic Morphine
100X potent
-
Isoflurane / Forane
- 2nd generation
- ***DOC for volatile lquids
- eliminated in exberation
- No SE
When mixed with Succs= Malignant Hyperthermia
-
Pentobarb, Midazolam / Versed
- Barbiturates, Benzodiazapines
- IV general anesth. for sedation
-
Propofol / Diprivan
- IV general anesth. for sedation
- conscious sedation
- change tubing q12 and glass bottle
***HypoTN and high risk for infection b/ of high lipid medium of drug
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Opioid analgesics
- Narcotics
- Activate Mu Receptors
- Morphine and synthetic drugs
- produce euphoria, constipation, urine retention, vasodlation, resp depresion
- increase intracranial pressure
- Physical dependence = not seem often w/ therapeutic clinical use
- = pt will have w/d if abruptly stopped
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3 things that determine cardiac output
- preload
- afterload
- contractility
-
preload
- 'the pool'
- amount of stretch created by the volume
-
afterload
- 'the pipes'
- resistance to outflow
- blood pressure
-
-
aldosterone saves h2o and Na+
but kicks out K+
aldosterone saves h2o and Na+
but kicks out K+
-
Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
Angiotensin II is a strong vasoconstrictor and signals release of Aldosterone
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Renin-Angiotensin-Aldosterone
Renin produced by_________in response to_____&______
Renin coverts Angiotensinogen to ________
A1 + ACE =A2
A2 causes______ and releases____
- Renin produced by Kidneys in response to decreased BP& flow
- Renin coverts Angiotensinogen to Angiotensin I
- A1 + ACE =A2
- A2 causes vasoconstriction and releases aldosterone
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ACE Inhibitors
- -PRILS
- given orally (except Vasotec IV)
- can be given with food (except Captopril)
- Pro-drugs= not activated until metab in Liver (except Lisinopril)
- Excreted by the Kidney
-
actions of ACE inhibitor
- Prevent Angiotensin II
- Vasodilation= Dec. BP
- Loss of Na+ and h2o and INCREASE K+= dec. bld volume
- Prevent and reverse cardiac remodeling
- A2 and Aldosterone
-
4 therapeutic uses of ACE Inhibitors
- HTN
- HF- from acute MI and Left Vent. dysfunction
- Diabetic and non-D nephropathy= Delay onset / slow progression of renal failure b/c of decrease in Kidney remodeling
- Prevent MI, stroke, death in pt's at high risk for CV events
-
Renal Artery Stenosis
#1 problem w/ ACE Inhibitors
constricts vessels, causing crappy blood flow
-
If we inhibit ACE/Kinase II...
promote the metabolic effects of Bradykinin (vasodilation and inc. permeability):
-
adverse effects of ACE inhibs
- 1st dose HypoTN
- angiodema
- cough
- hyperkalemia
- renal failure
- fetal injury
-
ACE preload and afterload
vasodilation witll cause both decrease
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Ca channel blockers
Therapeutic doses affect:
prevent contraction of smooth muscles
- T affect:
- peripheral arterioles and arteries
- cardiac muscle - decrease force of contract.
- SA & AV node - dec. impulse speed/conduction
- Coupling of cardiac Ca channels to Beta 1 receptors - Decrease force, rate, and conduction
-
activating B1 receptors will cause a 2nd messenger to open Ca++ channels
activating B1 receptors will cause a 2nd messenger to open Ca++ channels
-
the "-pines" drugs
vs
other blockers
- Ca++ blockers
- affects only the arterioles and NOT the HR
others= affect HR and atrerioles
-
Ca blocker that do not affect HR have a SE of Reflex Tachycaria
- can take Beta blocker to compete tachycard
Ca blocker that affects both HR and arterioles DOES NOT cause Reflex Tachycardia
- Ca blocker that do not affect HR have a SE of Reflex Tachycaria
- - can take beta blocker
Ca blocker that affects both HR and arterioles DOES NOT cause Reflex Tachycardia
-
Diltiazem / Cardizem
uses
SE
- Ca++ blocker
- affects arterioles AND HR
DOC for A-Fib and SVT to slpw HR enough for the heart to convert to nl rhythm
- -Peripheral arterioles= vasodilation
- -Cardiac arteries and arterioles= INc coronary bld flow
- -SA node= Dec. HR
- -AV node= slow myocardial conduction
- -Myocardium= Dec. force of contraction
- prevent angina
- HTN
- Dysrhyth
Se= same as previous Ca++ blocker
-
Nimodopine / Nimotop*
Special Ca++ blocker
Provides selective blocking of Cerebral blood vessels ONLY
Only used for rupture of Intracranial Aneurysm and used to prevent future vasospasm and re-bleed
-
Ca blocker and pre/afterload/force of contraction
- will decrease force of contraction
- will dec afterload
NO significant affect on preload
-
list of Vasodilators
1-4
- ACE inhibitors (prils)
- Angio II receptor blockers (sartens)
- Ca+ blockers (pines)
- Sympatholytics (alpha blockers)
- - prevent sympathetic vasocontriction
-
What vasodilators do...
- decrease the work load of the heart
- work on resistance vessels (arterioles)
- -reduce resistance to LV pumping
- -decrease afterload
- work on Capacitance vessels (veins)
- -reduce amount of blood return to the heart
- -decrease preload (and therefore BP)
-
SE of vasodilators
- Postural hypoTN
- -venous relaxation
- -blood pools in venous side
- Reflex Tachycarida
- -Central-sympathetic stimulation
- -Peripheral- baroreceptors
- Increase blood volume (over time)
- -decrease renal blood flow (RAA)
- -Na+ and h2o are reabsorbed
-
Sodium Nitroprusside / Nipride
Cyanide/Thiocyanide
- DOC for HTN Emegencies
- Arteriole and venous dilation
- Immediate effects and short 1/2 life
- Given very slowly IV push
- Need to protect from light
- thiocyanide is a metabolic by-product of use and can poison pt.
- Need to check levels is Nipride in use for >3 days
-
Beta blockers therp effects
- dec HR
- dec force of contraction
- dec velocity of impulse conduction
- dec BP but can also affect respers
uses: HTN, chest pain, HF, MI
-
2 types of beta blockers
after/preload
selective and non
- slightly reduce pre/afterload
- Reduce cardiac output
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