EXAM 2 - FULL REVIEW Flashcards
Autonomic nervous system
Systems not under conscious control, sympathetic/parasympathetic nervous system and enteric (gut with neurons?)
Sympathetic responses
increased HR/BP, dilated bronchioles, shunting to needed muscles. fight or flight bruh
Parasympathetic response
Rest and digest, conserve energy, shunt blood to endocrine, gi, urogenital.
Function of chain ganglia, and how they are similar to PNS plexi
sympathetic chain ganglia run along sides of spinal cord and transmit information for the sympathetic response.
PNS plexi help distribute parasympathetic response to specific organs
Sympathetic NS response, NTs, receptors, anatomy
originates from thoracolumbar region of spinal cord, short preganglionic fibers that release ach and long postganglionic fibers that release NE.
Uses receptors A1/2, b1/2/3
Paraympathetic NS response, NTs, receptors, anatomy
slow HR, promote digestion. Uses ach at both pre and post ganglionic neurons. Uses muscarinic and nicotinic receptors, and have long preganglionic fibers and short postganglionic fibers.
Sympathomimetic
drugs that mimic effect of sympathetic ns (epi)
Parasympathomimetics
drugs that mimic parasympathetic ns (acetyhlcholine)
Parasympathoplegic
drugs that inhibit parasympathetic (atropine)
Sympathoplegic
Drug that inhibit sympathetic ns (alpha and beta blockers)
Adrenergic (gQ, gI, gS) and their effects
alpha 1/2 and beta 1/2.
-Alpha 1 is gQ, and increases phospholipase C -> IG3/DAG
-Alpha 2 is gI, and decreases cAMP
-Beta1/2/3 are gS, increase cAMP
Cholinergic receptors
nicotinic: ligand-gated ion channels
muscarinic: g-protein coupled, varying subtypes (m1, m2, etc.
M1, 3 and 5 are excitatory (phospholipase C, gQ)
m2 and m4 are inhibitory, related to gI proteins to decrease cAMP
Where are alpha and beta receptors found? muscarinic and nicotinic?
alpha1 - blood vessels and eyes
alpha 2 - nervous system
beta-1 - heart
beta2-lungs and skeletal muscles (dilation for each)
muscarinic - heart and smooth muscle, glands
nicotinic - skeletal muscles and brain
6 classes of NTs and example
Esters - ACH
Monoamines - NE, serotonin, dopamine
Amino Acids - Glutamate, GABA
Purines - Adenosine, ATP
Peptides - Substance P, endorphins
Inorganic Gases - Nitric Oxide (NO)
Types of synpases
Electrical juntion, chemical synapse, and axodendritic synapse
Fate of NTs in synapse
Reuptake into neuron, degraded by enzymes, and diffusion
NE transport, storage, release and degradation
Synthesized from tyrosine into cell by CHT, combined by CHAT and stored in vesicles via VAT, and either taken back into presynaptic cell or degraded by monoamine oxidase (MAO)
Major uses of cholinomimetic agonists include
glaucoma (pilocarpine), urinary retention (bethanechol), diagnostic tool for MG (edrophonium)
Pharmacodynamic differences between direct acting and indirect acting cholinomimetic agents
direct acting bind directly to receptor to produce effects while indirect acting will inhibit things such as acetylcholinesterase to have more effect.
Difference between nicotinic and muscarinic
nicotinic are ionotropic and found at NMJ and autonomic ganglia, super fast
muscarinic are GPCRs found in heart and smooth muscles, glands, mediate slower and longer lasting effects.
Cholinomimetics effects in major organ systems
miosis and decreased intraocular prssure, decreased heart rate/contractility, increased GI motility/secretion, and increased bladder contraction
Types of glaucoma and drugs
open angle: increased intraocular pressure due to improper drainage, treated with pilocarpine to increase aqeuous outflow
closed angle: sudden blockage of drainage, acute pressure increase, emergency treatment
s/s of organophoshate poisoning
SLUDGE-M, resp failure, bradycardia.
s/s nictonic toxicity
N/V, muscle twitching, seizures/coma
effects on atropine across different organs
eyes: mydriasis and cycloplegia (dilation, dry eyes)
GI: decreases motility/secretions
Resp: reduces bronchial secretions
s/s atropine overdose and treatment
Dry mouth, blurred vision, tachycardia, hallucinations, hyperthermia (reduced sweating)
treatment: cholinesterase inhibitors such as physostigmine to reverse effects.
use of cholinomimetics in disease
MG (edrophonium to diagnose, stigmine to treat)
Glaucoma: pilocarpine
postop ileus: bethanechol to increase GI motility
clinical indications and contraindications for muscarinic antagonist
indications: bradycardia, motion sickness, reduce secretions for surgery
contraindications: glaucoma, urinary retention, obstructive GI diseases
Effects of two types of nicotinic antagonists
Ganglionic blockers and neuromuscular blockers
two types of muscle relaxants
depolarizing agents (sux) and non depolarizing agents (rocuronium)
catecholamine structure
consist of a benzene ring with hydroxyl groups at 3 and 4 position and amine group on the side chain. Removing hydroxyl groups (COMT), and MAO.
e.g. ephedrine is not degraded by these enzymes due to absence of OH groups
MOA of direct and indirect acting catecholamines
direct acting: (norepi and epi) bind directly to adrenergic receptors.
indirect-acting: (amphetamines) increase release or block reuptake of NE leading to prolonged affects
alpha-agonist, beta agonist, mixed agonist
alpha: phenylephrine - vasoconstrction, increased peripheral resistance, blood pressure
beta: isoproterenol - hr and contractility, reducing peripheral resistance.
mixed: epi - increase HR, contractility, vasoconstriction, increased BP
Nonselective alpha agonist
selective alpha 2
nonselective beta agonist
selective beta-1 agonist
selective beta 2 agonist
- epi
- clonidine
- isoproterenol
- dobutamine
- albuterol
tissues with alpa 1 and alpha 2 receptors
alpha 1 - blood vessels
alpha 2 - CNS and presynaptic nerve terminals
Tissues containing beta 1/2 receptors
beta 1 - heart
beta 2 - lungs
Major clinical applications of adrenoceptor agonists include
epi for anaphylaxis/cardiac arrest
dobutamine for heart failure
albuterol for asthma
phenylephrine for nasal decongestion/hypotension
triphasic effects of dopamine
low dose: D1 receptors, vasodilation in kidneys
mid dose: B1 contractility and hr
high dose: A1 vasoconstriction
common toxicities with sympathomimetics
CV toxicity: arrythmias, hypertension
CNS toxicity: anxiety, tremors, seizures
OTher: hyperglycemia, hypokalemia
Describe and compare the effects of an alpha blocker on BP/HR
cause vasodilation by inhibiting a1 receptors, reducing vascular resistance and lowering BP.
May lead to reflex tachycardia.
Effects of alpha blocker in presence/absence of agonist
absence: there is nothing to block and has little to not effect
presence (in presence of epi): prevents epi effects i.e. vasoconstriction Hr/contractility, may cause reflex tachycardia.
list the alpha and beta blockers described in class and their clinical uses
Alpha:
Phentolamine - used in pheochromocytoma and hypertensive emergencies
prazosin - used for hypertension and BPH
Beta:
propanolol - non selective, for htn, angina, arrythmias
metoprolol - beta 1 selective, used for heart failure and hypertension (not in end stage HF, need contractility)
labetalol - mixed alpha/beta, used in hypertensive crises
explain this sentence: phentolamine converts a pressor into a depressor
phentolamine is a competitive alpha blocker and it inhibits effects of epi on alpha receptors. By blocking these receptors, epi effects shift to beta-2 receptor mediated vasodilation, leading to a decrease in BP instead of increase.
Define the difference between selective and non selective beta blockers
selective beta blockers primarily block beta-1 receptors, which are found int he heart
non-selective beta blockers block both beta1 and 2, affecting heart rate as well as lungs causing bronchoconstriction (propanolol)
clinical indications and toxicities of beta blockers
indication: htn, angina, hf, arrythmias
toxicities: bradycardia, fatigue, bronchoconstriction, worsening of peripheral vascular disease.
clinical indications and toxicities of alpha blockers
indication: hypertension, BPH and pheochromocytoma
toxicity: orthostatic hypotension, reflex tachycardia.
regulators of BP
cardiac output (SV x HR) and PVR which is influenced by blood viscosity, vessel diameter, and vessel length.
anatomic control sites for BP
Heart (CO), blood vessels (PVR), kidneys (fluid balance, RAAS), and CNS (symp vs parasymp)
Non-pharmacological interventions for elevated BP
Dietary changes (DASH diet, reduced sodium intake)
Weight loss
physical activity
stress management
reduction of alcohol intake
Major groups of antihypertensive medications
diuretics (hydrochlorothiazide, furosemide, spironolactone)
beta blockers (metoprolol, propanolol)
calcium channel blockers (diltiazem, amlodipine, verapamil)
ACE inhibitors (lisinopril)
Renin inhibitors (aliskiren only one)
ARBs (losartan, valsartan)
Targets of centrally acting sympathoplegics
clonidine and methyldopa act on a2 receptors in CNS, specifically medulla oblongata, to reduce sympathetic outflow, lower BP, and decrease peripheral resistance.
major sites of action of peripheral sympathoplegics
beta receptors in heart (propanolol) and alpha 1 receptors (Prazosin)
doses for metoprolol, atenolol, and esmolol
metoprolol: 50-100mg/day (oral)
atenolol: 25-100mg/day (oral)
Esmolol: 50-300mcg/kg/min (IV infusion)
mechanism of action of vasodilator drugs and 4 classifications
work by relaxing vascular smooth muscle to reduce PVR
direct-acting vasodilators (hydralizine)
calcium channel blocker (amlodipine)
nitrates (nitoglycerin)
potassium channel openers (minoxidil)
compensatory response to vasodilators
tachycardia due to baroreceptor reflex and fluid retention due to RAAS
Major antihypertensive vasodilator drug and effects
Hydralazine (arterial dialation)
Minoxidil (Arteriolar dilation)
Sodium nitroprusside (arterial and venous dilation, used in hypertensive EMERGENCIES)
concerns with sodium nitroprusside and dosing
used in htn emergencies but may cause cyanide toxicity with prolonged use. 0.3-10mcg/kg/min
three classes of CBBs and major target
Dihydropyridines (peripheral vasculature, amlodipine)
Phenylalkylamines (Heart, verapamil)
Benzothiazepines (mixed heart/vessel, diltiazem)
RAAS pathway and treatment targets
Renin converts angiotensin to angiotensin I, ACE converts angiotensin I to angiotensin II, which increases BP by vasoconstriction and aldosterone release. Treatment targets ACE inhibitors such as lisinopril and ARBs (losartan)
There is one Renin inhibitor, called aliskiren
Differences between 2 angiotensin antagonists
ACE-I: block the conversion of angiotensin I to angiotensin II. (lisinopril)
ARBs: Block angiotensin II receptors (losartan)
MOA for pulm hypertension therapeutics
Prostacyclin analogs (epoprostenol), endothelin receptor antagonist (bosentan) and PDE-5 inhibitors (sildenafil)
Hypertensive urgency and hypertensive crisis (emergency)
Urgency: >180/100, no end organ damage (fix in hours to days)
Emergency: >180/110, with end organ damage, this is an emergency. (fix immediately)
Treatments for mild/mod/severe hypertension
mild: lifestyle mods and monotherapy
moderate: combination of two drugs (beta blocker + diuretic)
Severe/emergent: IV antihypertensives (sodium nitroprusside, cardene)
Differences in arterial, capillary, and venous tone
Arterial tone: controls BP
Venous: influences venous return and preload
Capillary: can completely shunt to bypass blood and make it go to more important parts of body.
Pathophysiology of effort angina and vasospastic angina
Effort: occurs with physical activity due to increased myocardial demand
Vasospastic: occurs at rest due to coronary artery spasm, determinants of oxygen consumption include HR, contractility and wall tension.
Coronary blood flow and diastole
directly related to duration of diastole because thats when the coronary arteries fill with blood.
Strategies for anginal pain relief
Drugs reducing oxygen demand such as beta blockers and nitrates, and increase oxygen supply (calcium channel blockers)
molecular pathways of vascular tone and drug targets
Pathways include nitric oxide, calcium, cAMP/cGMP, with targets like CCBs and nitrates.
Primary nitrates and nitrites
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
they cause vasodilation by increasing cGMP, used in angina and HF
Concerns with nitrate overexposure
Tolerance and methemoglobinemia (reduced oxygen binding) are major concerns with prolonged use of nitrates
Receptor differences in epicardial arteries
Alpha receptors cause vasoconstriction (reducing blood flow to heart and increasing BP, and beta 1 receptors cause increased heart rate and contractility.
Beta-2 receptors in the smaller vasculature of the heart can dilate smaller arterioles and increase blood flow to heart.
Targets of pFOX inhibitors and what drug?
Target fatty acid oxidation to reduce oxygen consumption in ischemic heart disease.
Drug is called Ranolazine and it acts on sodium channels to improve myocardial relaxation, not available in the US currently.
Therapeutic and adverse effects of nitrates, beta blockers, and calcium channel blockers
Nitrates reduce preload but cause headaches, orthostatic hypotension, and reflex tachycardia.
BB reduce heart rate but cause bradycardia, fatigue/depression, and bronchoconstriction.
CCBs reduce afterload but cause hypotension, peripheral edema, bradycardia.
Combination therapy for angina
combining nitrates with BBs or CCBs is more effective as it reduces oxygen demand and preventing reflex tachycardia.
Medical vs surgical therapy for angina
medical: drugs to manage symptoms
surgical: involves procedures like CABG, stent placement.
Define Heart failure and its pathogenesis
Heart is unable to meet myocardial demands of tissues, either due to systolic or diastolic dysfunction. Results in myocardial damage, high blood pressure, hyperthyroidism (and elevates myocardial demand). Congestion may occur, leading to pulmonary or peripheral edema.
Four factors of cardiac performance and how they are altered in HF
Preload: increased in HF due to fluid retention.
Afterload: elevated due to high blood pressure and vascular resistance
Contractility: Decreased due to damage or thinning of myocardium.
HR: increased as compensatory mechanism but exacerbates HF over time.
Define starling law
more the heart muscle is stretched, more forceful the contraction. In HF, excessive stretching leads to decreased contractility over time.
How ESV, passive filling, and atrial contraction contribute to EDV
End systolic volume is volume of blood left in ventricle after contraction
Passive filling occurs as blood flows into ventricle before atrial contraction, contributing to end diastolic volume
Atrial contraction adds a small additional volume to EDV, which is the total volume of blood before next contraction.
Strategies and drug groups for acute and chronic HF
Acute: diuretics, vasodilators, inotropes (dobutamine)
chronic: treat with ACE inhibitors, beta blockers, diuretics, aldosterone antagonists (ARBs)
Molecular mechanisms controlling normal cardiac contractility
Controlled by calcium entering cell, triggering calcium release from SR. This frees actin to interact with myosin, leading to contraction.
MOA of digitalis and major effects
digoxin inhibits na/k pump, leading to increased intracellular volume, enhancing contractility but also increases vagal tone, slowing heart rate.
Nature and mechanism of dig toxicity
Arrythmias, such as Vfib, due to calcium overload. Has a very narrow therapeutic index.
Positive inotropic drugs other than dig
dobutamine, dopamine, milrinone
Beneficial effects of non-inotropic drugs in HF
Diuretics reduce fluid overload
Vasodilators decrease afterload
ACE-I/ARBs decrease afterload
Rationale for BBs in HF
Reduce HR and myocardial oxygen demand, allowing heart to pump more efficiently.
Non-pharmacological interventions for HF
CABG, transplant, VADs. Lifestyle changes is crucial for managing early stages.
Neurotransmitter class - Esters examples
Acetylcholine
Neurotransmitter class - Monoamines example
NE, serotonin, dopamine
Neurotransmitter class - Amino acids example
Glutamate, GABA
Neurotransmitter class - Purines example
Adenosine, ATP
Neurotransmitter class - Peptides examples
Substance P, endorphins
Neurotransmitter class - Inorganic Gases example
Nitric Oxide (NO)
Original of Sympathetic NS fibers, length, location of ganglia
Thoracolumbar region of spinal cord, short preganglionic, long postganglionic, close to spinal cord.
Origin of fibers in Parasympathetic NS, length of fibers, location of ganglia
Brain and sacral spinal cord, long preganglionic and short postganglionic, in the visceral effector organs.
Autonomic feedback loop in blood pressure
Sympathetic/parasympathetic NS response (PVR, HR, Contractility, Venous tone)
Hormonal feedback lap in blood pressure
RAAS system pretty much
CHT, CHAT, VAT
CHT: choline transporter into neuron
CHAT: acetyl CoA + choline = ACh
VAT: Transports ACh into vesicle
Order of NE release in presynaptic neuron
Tyrosine gets into cell via Na+/Tyrosine channel, turns into tyrosine hydroxylase -> Dopamine -> dopamine -> into vesicle via VMAT -> Vesicle moves down to cell wall via SNAP and VAMP
Cholinomimetics - Alkaloids
Plants - Betel nut and muscarine, Nicotine
These all increase ACh
Cholinomimetics agents - Choline esters
ACh, Methanicholine, Carbechol, Methanechol
Are alkaloids and choline esters direct acting or indirect acting Cholinomimetic agents?
Direct acting
How does an Indirect-acting cholinomimetic work?
By inhibiting hydrolysis of ACh and inhibiting action of acetylcholinesterase. Both increase duration of ACh activity.
ADM in esters of choline
A: poor
D: poor
M: Varies
Use for ACh (in the eyes), Methacholine, Carbachol, Bethanechol
ACh: pupil constriction (miosis)
Methacholine: Diagnosis of asthma
Carbachol: Decrease intraocular pressure
Bethanechol: Bladder dysfunction, reflux disease
Which type of glaucoma is atropine contraindicated? Why?
Closed-angle/Narrow angle. Atropine relaxes the ciliary muscle and causes complete drainage obstruction of aqueous humor, may result in blindness.
Indirect cholinomimetic drugs
Simple alcohols: edrophonium (MG testing)
Carbamic acid esters of alcohols: Neostigmine
Organic derivatives of phosphoric acid: organophosphate
Myasthenia gravis diagnostic drug and dose
Edrophonium 2mg IV, check for neg reaction, then give 8mg IV, and if improvement lasts 5 minutes, boom, diagnosed.
Duration of action for tropicamide
4 hours
How to reverse cholinergic toxidrome
Atropine
Tx for organophosphate exposure
Atropine and Pralidoxime
Reversal for atropine
-stigmine
Nondepolarizing muscle relaxants have 3 categories
Short, intermediate and long acting
succinylcholine has how many phases?
phase 1 and phase 2
Reversal for non-depolarizing muscle relaxants
Neostigmine and pyridostigmine
sugammadex reverses steroid molecule curare derivatives
Indirect acting adrenergic agonists
Amphetamine and cocaine
Whats the one adrenergic agonist that is both direct and indirect acting
Ephedrine
Cardiac output equation
SV (70ml) x HR (75bpm) = 5250ml/min
Match these drugs to these receptors: Phenylephrine, Epinephrine, isoproterenol to Mixed, B agonist, A agonist
Alpha agonist: Phenylephrine
Beta agonist: Isoproterenol
Mixed: Epi
Norepinephrine receptors
alpha, B1, little B2
Isoproterenol receptors
Potent B agonist - vasodilator
Little effect on beta receptors, will increase HR/Contractility and reduce afterload/preload
Dopamine
D1, B1, and A1 depending on dose. Triphasic.
Dobutamine
B1 selective agonist – used in cardiac shock, acute HF
Non-catecholamine adrenergic agonists
Midodrine, phenylephrine, ephedrine, pseudoephedrine, amphetamines, methampethamines, cocaine, tyramine
Midodrine
alpha 1 receptor selective, primarily postural hypotension
Alpha antagonist drugs
Phentolamine (reversible) and Phenoxybenzamine (irreversible)
- used for treatment of pheochromocytoma
Prazosin - BPH and hypertension, highly selective to Alpha 1, tachycardia ABSENT
Beta blocking agents general characteristics
A: well absorbed orally, peak 1-3 and half life 3-10 hours
D: Rapid
M: Major first-pass metabolism - low bioavailability
E: Varied
Beta blockers effect on blood vessels
Acutely increases peripheral resistance, but chronically decreases peripheral resistance.
Beta blockers in eyes
Decreased IOP
Adverse affect with chronic use of beta blockers
Increased VLDL and decreased HDL
Propanolol characteristics
B antagonist, non selective.
Extensive 1st pass metabolism
Metoprolol and atenolol
Mainly B1 selective
Safer in COPD/asthmatics, diabetics
Labetalol
Has racemic mixtures
S,R isomer: potent alpha blocker, alpha 1 selective
R,R isomer: potent beta blocker.
Esmolol
Ultra short acting, Beta 1 selective, infusion. Terminated rapidly with D/C, safer in critically ill patients.
Hydraulic equation
BP = CO x PVR
4 types of antihypertensive agens
Diuretics: deplete sodium
Sympathoplegics: decrease PVR, Reduce CO
Direct vasodilators: relax vascular smooth muscle
Anti-Angiotensins: block activity or production
Drug used for pregnancy induced hypertension
Methyldopa! safe to cross placental barrier
Methyldopa
Acts alot like clonidine, analog of L-dopa, replaces NE in adrenergic nerve vesicles.
-Agonist at CNS alpha receptors.
General vasodilator mechanism
Relax smooth muscle of arterioles and veins: Nitroprusside and nitrates
-Best given in conjunction with other antihypertensive medications that combat reflex tachycardia induced by vasodilation
Minoxidil
Opens K+ channels in smooth muscles, less likely to contract and dilates arteries and arterioles. well absorbed orally/topically.
Hydralazine effects and toxicity
Dilates arterioles - Nitric oxide production MAYBE?
Toxicity: HA, Nausea, sweating, flushing
Sodium nitroprusside
HT emergencies, dilates arterial and venous vessels , rapidly lowers BP.
-INCREASES INTRACELLULAR cGMP
-cyanide accumulation after 48 hours causing arrythmias, acidosis, and death. Worse in renal insufficient pts.
Fenoldopam
Peripheral arteriolar dilator, HTN emergencies, post-op htn.
Agonist of D1 receptors for kidney perfusion.
Renin inhibitor
Aliskiren
ACE inhibitors
block angiotensin 1 from turning into angiotensin 2
captopril - can lead to severe cough from bradykinin accumulation.
ARBs
Block AT2 receptor to inhibit aldosterone secretion and therefore inhibit vasoconstriction, and decreasing sodium/water retention and decreased PVR
Losartan and Valsartan
Treatments for Pulm HTN
Endothelin receptor antagonists such as bosentan, which block endothelin (vasoconstrictor)
Prostacyclin analogs such as epoprostenol, promoting vasodilation and inhibit platelet aggregation.
Actions on Vascular smooth muscle by drug class: NO/nitrates, Beta-2 agonists, Beta blockers, CCBs
NO: increase cGMP
B2 agonists: increase cAMP - relaxation (dilation)
BB: Decrease demand
CCB: less total calcium - relaxation (dilation)
Types of heart failure
Systolic failure: Decreased CO, Decreased ejection fraction. typical of acute HF.
Diastolic failure: reduced filling. Decreased CO, normal ejection fraction.
HAlf life of nitroglycerin
2-8 minutes
Congestive heart failure results in
Increased LV pressure at end diastole
results in increased pulmonary pressure - pulmonary edema
Normal cardiac contractility
Trigger calcium enters cell
Binds to channel in SR, releasing stored calcium
Frees actin to interact with myosin
4 factors of cardiac performance
Preload, afterload, contractility, heart rate
CO = SV x HR
Heart rate is controlled by 5 things
CNS, ANS, Neural reflexes, atrial receptors, hormones
Stroke volume is made up of
Preload, afterload, contractility.
Left ventricle numbers that total end diastolic volume
Passive filling 75ml + Atrial contraction 25ml + ESV 50ml = 140ml total
Stroke volume = EDV - ESV
What is ESV?
ESV = 50ml
SV = 140ml - 50ml = 90ml
Altered preload
> 20-25mm HG = pulmonary congestion.
This is increased in HF, which increases blood volume and venous tone.
How to decrease preload
Salt restriction, diuretics, venodilation
Afterload: what is it and it increases as _______?
Resistance against which heart must pump blood
Increases as cardiac output decreases.
Digoxin
positive inotropic with narrow therapeutic index. The only oral pos inotropic for HF
Milrinone
PDE3 inhibitors - these are the enzymes that inactive cAMP and cGMP
causes inotropic effects, vasodilation.
Beta adrenergic stimulants
Dopamine and dobutamine: increase CO and decrease ventricular filling pressure
Active cardiac cell membrane (sodium activity and gates)
Influx of sodium, rapid closer of H gate and inactivation.
Explain the AP graph for cardiac action potentials
Sodium in as AP goes up, then at top of AP K+ and Cl- start flowing out, during plateau you got Ca++ coming in with K+ going out, and then on the downward line its K+ going out
Early and delayed afterdepolarization
Early: arises from the plateau, called re-entry circuits, common in torsades, exacerbated by drugs that prolong QT interval.
delayed: arises from the resting membrane potential. common in dig toxicity from elevated intracellular calcium.
These are both arrythmias
Four classes of antiarrhythmic agents
Class I: Sodium channel blockade
Class II: Sympatholytic
Class III: Prolong AP duration (K+ blockers)
Class IV: Block cardiac calcium channel currents
Class I antiarrhythmic
Class IA: Sodium channel blockade to prolong AP duration (APD)
e.g. quinidine, procainimide
Class IB: shorten APD
e.g. lidocaine
Class IC: slow dissociation, minimal effect on APD
e.g. Flecainide
Amiodarone
K channel blocker, prolongs APD
also dilates peripheral vasculature, and toxicity can cause bradycardia or heart block.
Half life of amio
13-100 days
Verapamil
CCB that blocks both activated and inactivated calcium channels
Prolongs AV node conduction while slowing SA node
hypotensive action
Miscellaneous agents that dont fit into 4 classes of anti-arrhythmics
Digoxin
Adenosine: enhanced K+ conductance, inhibition of cAMP induced calcium influx, 10 second half life.
Magnesium: dig induced arrythmias
Potassium: normalize k+ levels
Treatments for bradycardia
Underlying cause, D/C drugs, 1st line atropine, 2nd line epi/dopamine, and if chronic use pacemaker.
Treatments for heart block
initial: 1st degree not usually treated bc its asymptomatic
symptomatic: atropine, transcutaneous pacing
Chronic: pacemaker
Treatments for SVT
Assess cause, adenosine, and chronically treat with CCB and beta blockers
Treatments for sinus tach
Assess cause, adenosine, CCBs/cardioversion acutely, and chronically catheter ablation.
Treatments for vtach
amiodarone acutely and chronically, satolol chronically
Treatments for afib
Diltiazem, verapamil (CCBs) acutely and then beta blockers/amio chronically
Treatments for Vfib
CPR, defibrillation acutely. Amio/lidocaine chronically.
How does Botox work?
Blocks SNAPs in the neuron.
