Principle Flashcards
Pharmacokinetics
The action of the body on a medication.
Pharmacodynamics
The action when a medication is administered, it begins to alter a function or process of the body.
Processes of pharmacokinetics
Liberation Absorption
Distribution Metabolism
Excretion
When a medication binds to a receptor site, what 4 possible actions will occur.
- Channels permitting the passage of ions in cell walls may be opened or closed.
- A biochemical messenger becomes activated, initiating other chemical reactions within the cell
- A normal cell function is prevented.
- A normal or abnormal function of the cell begins.
Two types of medications/chemicals directly affect cellular activity by binding with receptor sites on individual cells.
Agonist
Antagonist
Agonist medications
Initiate or alter a cellular activity by attaching to receptor sites, prompting a cell response
Antagonist medications
Prevents endogenous and exogenous agonist chemicals from reaching cell receptor sites and initiating or altering a particular cellular activity.
Affinity
Is the ability of a medication to bind to particular receptor sites.
What two properties determine the number of receptor sites bound by a medication?
Affinity and concentration.
The minimum concentration needed to initiate or alter cellular activity is known as the?
Threshold level
The concentration of medication required to initiate a cellular response is known as?
Potency
Efficacy
The ability to initiate or alter cells activity in a therapeutic or desired manner
Dose response curve
Illustrates the relationship of medication dose(or concentration) and efficacy.
Agonist effects on
Alpha 1
Vasoconstriction of arteries and veins
Agonist effects on
Alpha 2
Insulin restriction
Glucagon secretion
Inhibition of NE release
Agonist effects on
Beta 1
Increased heart rate(chronotropic effect)
Increased myocardial contractility (inotropic)
Increased myocardial conduction(dromotropic effect)
Renin secretion for urinary retention
Agonist effects on
Beta 2
Bronchus and bronchiole relaxation
Insulin secretion
Uterine relaxation
Arterial dilation in certain key organs
Agonist effects on
Dopaminergic
Vasodilation of renal and mesenteric arteries
Numerous receptor subtypes exist
Agonist effects on
Nicotinic
Present at neuromuscular junction,allowing ACh to stimulate muscle contraction
Agonist effects on
Muscarinic 2
Present in the heart, activated by ACh to offset sympathetic stimulation, decreasing heart rate, contractility, and electrical conduction velocity.
Antagonists can either be
Competitive or non competitive
Competitive antagonists
Temporarily bind with cellular receptor sites, displacing agonist chemicals.
Efficacy of competitive antagonist is directly related to?
It’s concentration near the receptor sites.
As the concentration of of a competitive antagonist increases near the receptor sites,it is able to?
Prevent a greater number of agonist chemicals from reaching the receptor.
As the competitive antagonist concentration falls or when the concentration of agonist chemicals increase…
A greater number of agonist chemicals bind with receptor sites and continue or resume cellular activation.
The efficacy of a competitive antagonist is related to its affinity compared to?
The affinity of the agonist chemicals present
Noncompetitive antagonists
Permanently bind to the receptor sites and prevent activation by agonist chemicals
Effects of noncompetitive antagonists continue till
New receptor sites or new cells are created
Efficacy of competitive antagonist is directly related to?
It’s concentration near the receptor sites.
Partial agonist chemicals
Bind to the receptor site, but do not initiate as much cellular activity or change as do other agonists.
Partial agonists effectively lower?
The efficacy of other agonists that may be present at the cells.
What are the three primary types of body substances that medications distribute through?
Water
Lipids
Protein
If a medication is water soluble higher weight based doses will be administered to?
Infants rather then adults or elderly.
Lipid soluble medication requires higher doses for?
Elderly people
What types of medication may require increased initial doses to overcome widespread distribution?
Water and lipid soluble
Medication metabolism in the liver is affected by?
Cytochrome P-450 system
A decrease in liver or kidney function requires doses to be?
Decreased due to impaired elimination from e body.
What is paradoxical medication reactions and who are prone to it?
Pts clinical experience effects opposite from the intended effects of e medication. Pts at extremes of age.
Formula for ideal weight for men
Kg=50+2.3 times the pts height in inches over 5 feet
Ideal weight for women
Kg=45.5+2.3 times pt height in inches over 5 feet
How does fever affect drug metabolism?
Initially it will increase metabolism of drugs in the liver due to tachycardia and reducing the amount of drug returned to circulation by the liver.
*fever also suppresses function of the cytochrome p450 system, ultimately decreasing rate of metabolism in certain classes of medications.
Special consideration with
Pulmonary hypertension
May have acute decompensation when vasopressors are used
Special consideration with
Glucose 6 phosphate dehydrogenase deficiency
Salicylate meds such as Asa may precipitate hemolysis
Special consideration with
Sickle cell
Adequate hydration and intravascular fluid volume and diuretic medications or vasoconstrictors may fatally complicate sickle cell
Pregnant pts have better renal function while?
Supine
FDA pregnancy category classification
A
Controlled studies fail to demonstrate risk to fetus in first trimester(no evidence of a risk in later trimesters) and possibility of fetal harm is low.
FDA pregnancy category classification
B
Either animal reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women or animal studies have shown an adverse effect(other then a decrease in fertility) at was not confirmed by studies in women in first trimester(no evidence in of risk in later trimesters
FDA pregnancy category classification
C
Either animal studies revealed adverse effects on fetus and no controlled studies in women or studies in women and animals not available
Drugs should only be given if potential benefit justifies the potential risk to the fetus
FDA pregnancy category classification
D
Positive evidence of human fetal risk but benefits from use in pregnant women may be acceptable despite the risk (life threatening)
FDA pregnancy category classification
X
Fetal abnormalities
Evidence of fetal risk
Risk of drug in pregnant women outweighs any possible any possible benefits. Contraindicated in women who are or may become pregnant.
Administering multiple doses of the same medication to obtain a desired response or continuous administration demonstrates?
Cumulate action
Adverse effects are also known as
Untoward effects
Idiosyncratic medication reactions are when
Adverse effects occur that are completely unexpected and not previously known to occur with a particular medication
LD50
Median lethal dose,Weight based dose that causes death in 50% of animals tested
TD50
Median toxic dose,for particular adverse effect of medication 50% of animals tested had toxic effects at or above this weight based dose
ED50
Median effective dose, for particular use or indication
Therapeutic index
Is the relationship between the ld50 td50 and ed50
Tolerance of a medication is
Certain medications known to have decreased efficacy or potently when taken repeatedly by a pt
Down regulation
Mechanism that reduces available cell receptors for a particular medication causing tolerance
Cross tolerance
Repeated exposure to a medication with a particular class has the potential to cause tolerance to other medications in the same class.
Tachyphylaxsis
Repeated doses within a short time rapidly causes tolerance making medication virtually ineffective.
Habituation
Repeated exposure to certain medication or chemicals, abnormal tolerence to adverse or therapeutic effects associated with a substance
Medication Interference
Undesirable medication interactions
Pharmacokinetic values of medication
Onset
Peak
Duration
Onset and peak of a medication are generally related to?
Absorption and distribution
Duration of effect is generally related to?
Medication metabolism and elimination
Bioavailability
Is the percentage of unchanged medication that reaches circulation
Medication interaction
Addition or summation
Two meds w/ similar effect combine to produce a greater effect than that of either medication individually
Medication interaction
Synergism
Two meds w/ a similar effect combine, and resulting effect is greater then the sum of the medications (ie,1+1=6)
Medication interaction
Potentiation
The effect of one medication is greatly enhanced by the presence of snore medication, which does not have the ability to produce the same effect.
Medication interaction
Altered absorption
The action of one medication increases or decreases the ability of another medication to be absorbed by the body.ie medications at increase or decrease GI pH or modality may increase or decrease the absorption of other medications that are taken orally.
Medication interaction
Altered metabolism
The action of one medication increases or decreases metabolism of one medication within the body.
Medication interaction
Altered distribution
The presence of one medication alters the area available for distribution of anywhere medication, which becomes important when both medications are bound to the same site.if proteins are already occupied by one medication
Toxic levels of the other medication may develop
Medication interaction
Altered elimination
Medications may increase or decrease the functioning of the kidneys or other route of elimination,influencing the amount of or duration of effect of another medication in the body
Medication interaction
Physiologic antagonism
Two medications, each producing opposite effects are present simultaneously, resulting in minimal or no clinical changes.
Medication interaction
Neutralization
Two medications bind together in new body creating an inactive substance
GI medication absorption
GI motility
Ability of medication to pass through GI tract into the bloodstream
GI medication absorption
GI pH
Perfusion of the GI system (may be decreased during systemic trauma or shock)
GI medication absorption
Presence of foods, liquids, or chemicals in the stomach
Injury or bleeding in the GI system(both can alter GI motility, decreasing e time that oral medications can be absorbed)
IO site/ vein
Proximal tibia
Popliteal vein
IO site/ vein
Femur
Femoral vein
IO site/ vein Distal tibia(medial malleolous)
Great saphenous vein
IO site/ vein
Proximal humerous
Auxiliary vein
IO site/ vein
Manubrium
Internal mammary and azygos veins
What type of medication molecules easily pass through the phospholipid bilayer?
Nonionic(not charged)
Lipophilic(lipid loving)
Lager medication molecules use
Pinocytosis
Facilitated diffusion
When medications bind to carrier proteins
Requires no energy
Active transport is used to move medication molecules
Across a gradient
Three anatomic barriers that prevent passage of medication through openings in capillary walls
Blood brain
Blood placenta
Blood testes
Plasma protein binding
Significantly alters distribution of certain medications within the body, medication molecules temporarily attach to proteins in blood plasma
As a medication undergoes bio transformation it becomes
A metabolite
Metabolite can become either
Active or inactive
Active metabolizes
Remain capable of some pharmacologic activity
Inactive metabolite
No longer possess the ability to alter cell process or body function
4 effects on medications through bio transformation
- inactive substance can become active
- An active metabolite can be changed into another active medication
- an active medication can be completely or partially inactivated
- A medication can be transformed into a substance that is easier for the body to eliminate.
Two patterns of metabolism and excretion
Zero order elimination
First order elimination
Zero order elimination
A fixed amount of a substance is removed during a certain period of time.
First order elimination
The rate of elimination is directly influenced by plasma levels of the substance.
In essence, the more substance in the plasma, the more the body works to eliminate the substance.
First order elimination is quantified as a medication’s
Half life
Half life
The time needed in an average person for metabolism and excretion of 50% of a substance in he plasma
Anhelmintics
Treats intestinal parasites
Affects GI
Anticoagulants
Reduce the efficacy of clotting factors present in the blood
Antiemetic
Treat or prevent nausea and vomiting
Affects CNS and GI
Antihistamine
Bock histamine receptors, dry mucus membranes, inhibit immune response in allergic reactions
Antihyperlididemics
Decrease blood cholesterol,sequester cholesterol chemicals in bite
Barbiturates
Reduce or prevent seizures, provide sedation
Calcium channel blockers
Reduce heart rate and bp
Cardiac glycosides
Decrease heart rate and improve contractility
Cholesterol sysntheisis inhibitors
Prevent cholesterol conversin in the liver
Cholinergics
Activate secretory glands in eyes and GI,improve muscle weakness in myasthenia gravis
Corticosteroids
Decrease inflammation,immunosuppressant
Glucocorticoids
Replacement or maintenance therapy, treat systemic inflammation, numerous other uses
Glycoprotein IIb/IIIa inhibitors
Deactivate proteins involved in platelet aggregation
Histamine-2 receptor antagonists
Block histamine receptors, including those responsible for gastric acid secretion
Immunomodulators
Inhibit or enhance functioning of the immune system
Immunosuppressant
Prevent rejection of transplanted organs and tissues, treat rheumatoid arthritiis
Insulin
Positive inotropic effects, allows cellular glucose uptake, treat hyperkalemia
Mineralocorticoids
Promote sodium and water retention
Mucolytics
Assist with elimination of mucous in the respiratory tract
Mydriatics
Dilate pupils for ocular diagnostic and treatment procedures
Narcotic analgesics
Relieve pain and relieve or suppress cough
Nasal decongestant
Decrease upper airway mucous secretion
Neuromuscular blocking agents
Provide paralysis in incubated and ventilated pts
Phophodiesterase inhibitors
Treat erectile disfunction
Protein pump inhibitors
Suppress activity or parietal cell acid secretion
Selective serotonin reuptake inhibitors SSRI
Treat depression, anxiety, and related conditions
Tocolytics
Decrease or eliminate uterine contractions during preterm labor
Tricyclics antidepressant
Treat depression, neuropathy, and chronic pain syndromes
Xanthines
Bronchodilation
Etomidate
Onset, peak, duration
30 to 60 sec
Peak in 60 sec
Lasts 5 mins
What can happen if multiple doses of etomidate are given?
Adrenal suppression
Klonopin
Clonazepam
Restoril
Temazepam
Benzodiazepines have what qualities?
Potent anti seizure
Anxiolytic
Sedative properties
At high doses benzos can cause
Hypotension
Prehospital benzos are pregnany class?
D
Neuromuscular blockers antagonize ACh at what receptors?
Nicotenic
Succylcholine
Onset, duration
Onset 30 to 60 sec
Duration 3 to 8 min
Rocuronium
Onset
Duration
1 to 3 min
15 to 60 min
Beta2 receptor sites on bronchial smooth muscle causes
Muscle relaxation, and bronchial dilation when antagonized by beta 2 agonits
Two varieties of beta agonists
Selective, and nonselective
How does albuterol effect potassium in the body?
Promotes cellular uptake of potassium
Can be used as a temporary treatment for hyperkalemia
How is levabuterol different then albuterol?
It is structurally similar but without many of the reported beta 1 effects
Ipatropium bromide antagonizes what receptors?
Muscarinic receptors
Corticosteroids are administered in respiratory emergencies to?
Reduce airway inflammation, and ultimately improve oxygenation and ventilation
Antidysrhythmic medication target
Cells within the heart or suppresses ectopic foci
Antidysrhythmics are grouped by what classification scheme?
Vaughn williams
Cardiac phases in order
4,0,1,2,3,4
Cardiac cycle begins at what phase
4
Phase 4
Cardiac cells are at rest
Waiting for spontaneous impulse from within(automaticity) or transfer of an impulse from an adjacent cardiac cell
Coincides with diastole of the heart.
Phase 0
Begins with rapid influx of sodium ions through channels in the cardiac cells, potassium ions slowly begin to exit the cell, and depolarization occurs, altering the electrical charge present in the cell.
Phase 1
Sodium influx decreases while potassium continues to exit the cell slowly.
Phase 2
Begins the movement of calcium into the cell while potassium leave the cell
Phase 3
Calcium movement ceases with continued outflow of potassium
Depolarization and myocardial contraction are occurring through phase 2 and 3
Absolute refractory period
Effective refractory period
During phases 0,1,2, and 3
No additional depolarization may occur because of external stimuli.
Limits the potential the maximum heart date by ensuring that a certain amount of time elapses between myocardial contraction.
Immediately after the absolute refractory period the brief period where an unusually powerful stimulious can initiate depolarization known as
Relative refractory period
Class 1 anti dysrhythmic
Slow the movement of sodium brought channels in certain cardiac cells
Procainmide
Lidocaine
Antidysrhythmic class 1a
Suppresses activity of ectopic foci and slow conduction velocity. This has the potential to prolong QRS and QT interval.
Effective for a variety of atrial and ventricular dysrhythmias,
Antidysrhythmic class 2b
Blocks sodium channels in the purkinje fibers and ventricle, effectively resolving various ventricular dysrhythmias and suppressing ectopic foci.
Quickly metabolized by the liver.
Use caution with pts with kidney or liver disease
Class II antidysrhythmic
Beta adnergic blocking agent
Beta blockers competitively inhibit catecholamine activation of beta receptors
Precautions/toxic effects of beta blockers
Toxic effects include bradycardia,hypotension,conduction delays, and a variety of cardiovascular effects.
Use extreme caution in pts with reactive airway disease
Also may cause massive conduction abnormalities when given simultaneously or other medications that slow av node conduction.
Metoprolol MOA in ami and ischemia
Reduces rate during myocardial ischemia and certain atrial tachycardias w/ modest drop in BP
Reduces rate resulting in lower myocardial oxygen consumption
Class III antidysrhythmic
Increases duration of phases 1,2, and 3 of the cardiac cycle by extending the cellular action potential, these medications prolong the absolute refractory period, treating atrial or ventricular tachycardias.
Class III antidysrhythmic amiodarone
Useful in treating atrial and ventricular tachycardias
Controversial uses in treatment of wow
Widely distributed throughout the body.
Class IV antidysrhythmic
Calcium channel blockers
Reduce BP and control hr and may increase myocardial oxygen delivery during periods of ischemia.
May be used to inhibit uterine contractions during preterm delivery, long term management of migraines, and treatment of cardiomyopathy.
Class IV MOA
Slow conduction through the av node, decrease automaticity of ectopic foci within e heart, and decrease the velocity of the heart.
Cardiac workload and oxygen consumption are decreased by lowering PVR(afterload) while simultaneously reducing cardiac output.
Class IV antidysrhythmic in prehospital use
Diltiazem verapamil
Control of heart rate in pts with a flutter or a fib.
Class V antidysrhythmic
Adenosine
Psvt
Adenosine decreases cardiac conduction velocity and prolongs the effective refractory period, producing a several second pause in cardiac activity.
Alpha blockers
Prevents endogenous catecholamines from reaching alpha receptors, primarily in smooth muscle of blood vessels
In general these medications lower bp(diastolic primarily) and decrease systemic vascular resistance.
Nonselective blockade of alpha 2 receptors causes
A reflex tachycardia by allowing an increase of NE secretion by the sympathetic nervous system
Pts taking alpha blocking medications are prone to?
Postural hypotension and tachycardia
Alpha adnergic receptor antagonists re prescribed for pts with?
Hypertension, an enlarged prostate gland, and glaucoma
Clonodine catapres is primarily
Alpha 2 receptor agonist often given for emergency treatment of HTN
By activating alpha 2 receptors clonodine suppresses the release of NE, causi vasoconstriction
Labatalol (trandate)
Alpha 1,beta 1, and beta 2 antagonism properties
IV form has far greater effect on beta 1 and 2 then alpha 1
Pts at risk for Unopposed alpha stimulation, such as pheochromocytoma or cocaine overdose should…?
Receive another alpha adnergic antagonist before receiving labatolol for HTN crisis.
In this case the decreasing CO due to beta 1 antagonism prompts secretion of endogenous catecholamines potentially causing uncontrolled hypertension.
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
Vagus nerve releases ACh that acts on…?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
Excessive activation of Muscarinic 2 receptors by ACh causes…?
Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.
AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by
Atropine sulfate
Atropine is classified as an
Competitive muscarinic receptor blocker
During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not…?
Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
Vagus nerve releases ACh that acts on…?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
Excessive activation of Muscarinic 2 receptors by ACh causes…?
Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.
AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by
Atropine sulfate
Atropine is classified as an
Competitive muscarinic receptor blocker
During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not…?
Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
Vagus nerve releases ACh that acts on…?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
Excessive activation of Muscarinic 2 receptors by ACh causes…?
Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.
AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by
Atropine sulfate
Atropine is classified as an
Competitive muscarinic receptor blocker
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
Vagus nerve releases ACh that acts on…?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
Excessive activation of Muscarinic 2 receptors by ACh causes…?
Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.
AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by
Atropine sulfate
Atropine is classified as an
Competitive muscarinic receptor blocker
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
Vagus nerve releases ACh that acts on…?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
Excessive activation of Muscarinic 2 receptors by ACh causes…?
Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.
AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by
Atropine sulfate
Atropine is classified as an
Competitive muscarinic receptor blocker
Atropine is used for bradycardia when
Vagal stimulation of maucarinic-2 receptors is suspected
When atropine is administered for bradycardia ACh activation is
Prevented of muscarinic 2 receptors is prevented allowing underlying sympathehtic stimulation to predominate.
Atropine is unlikely to be effective for treatment of bradycardia caused by
Blocked cardiac conduction such as in second and third degree AV blocks
Pts exposed to pesticides and nerve agents (AChE inhibitor toxcitity)are to
Receive atropine continuously until respiratory and hemodynamic status improves regardless of total dose required.
In AChE inhibitor exposure atropine does not
Bind to nicotinic receptors so it will not improve muscle weakness, fasciculations, or paralysis from cholinergic poisoning.
Catecholamines
Are naturally occurring chemicals in the body that stimulate receptor sites in the sympathetic nervous system.
Two structures of catecholamines
The catechol group
The monoamine oxidase group
Endogenous catecholamines include
Epinephrine , norepinephrine , and dopamine.
These chemicals stimulate alpha, beta, and dopaminergic receptor sites.
Catecholamines are rapidly metabolized by?
Catecholamines are rapidly metabolized by monoamine oxidase and catechol O-methyltransferase( an enzyme), resulting in brief duration of action after admin
Sympathomemtic chemcicals are not
Found naturally in the body
Sympathyomemetic mimic
Catecholamines and do not undergo the same metabolism as catecholamines thus allowing longer duration of action.
Epinephrine stimulates
Alpha, beta 1 and beta 2 receptors causing potent vasoconstriction, a marked increase of inotropic ,dromotropic , and chronotropic,CO and powerful bronchodilation.
Epinephrine infusion drips are used for
Profound hypotension, shock, and refractory bradycardia.
Norepinephrine
Stimulates beta 1 amped alpha receptors causing increase in BP, contractility(inotropic), and chronotropic (heart rate)
Vasoconstrictor(alpha effects) are usually greater then cardiac (beta1 effects )
Dopamine has an affinity to
For dopaminergic receptor sites that is greater than the affinity for beta receptor and a greater affinity to beta receptors the alpha sites.
Dopamine activation by dose
Dopaminergic receptors are activated at 2.5 to 5 causing mesinteric and renal artery vasodilation
5-10 activates beta 1 causing inotropic and chromotropic effects
10-20 alpha 1 effects predominate(dopaminergic receptors not activated)
Dobutamine
Synthetically manufactured catecholamine similar to dopamine.
It activates beta1 and to lesser degree beta 2 and alpha1 receptor sites. Dopaminergic receptors are not activated.
Slight +chromotropic, while providing significant +inotropic
When combined with a vasodilator medication, dobutamine for cardiogenic shock…
Increases inotropic while decrease in afterload, resulting in improved cardiac output
Neo synephrine (phenylephine)
Almost pure alpha 1 agonist
Minimal beta 1 effects
Potent vasoconstrictor w/ longer duration the. Catecholamines
May cause reflex tachycardia, and tachyphylaxis
Vasopressin(pitressin, ADH)
Has emerged as a potent vasopressor medication recommended in ACLS
Secreted in response to plasma hyperosmolerity(elevated concentration of glucose and plasma proteins) or intravascular volume depletion.
Clinically is administered for treatment of GI bleeding, diabetes insipidus, shock,and cardiac arrest.
