PHAR100 exam

acetaminophen

Tylenol

MOA: inhibits the hypothalamic heat regulating center, has analgesic effects due to activation of descending inhibitory pathways in CNS

indications: fever, mild-moderate pain

contraindications: hypersensitivity, acute liver disease, severe hepatic impairment

adult dose PO: 975-1000mg to max of 4g a day, PR: 650mg q 4h no repeat

activated charcoal

MOA: absorbs toxic substances to prevent GI absorption

indications: acute poison ingestion

contraindications: GI obstruction, vomiting or unprotected airway, uncooperative patient, caustic ingestion

adverse reactions: GI; ABD distension, N/V, dental, and fecal discoloration, GI obstruction

dosage is 1g/kg to max of 50g

hydroxocobalamin

cyanokit

MOA: binds to cyanine ions and converts them to non-toxic forms for excretion

indications: cyanide poisoning

adverse reactions: increased BP, bradycardia, red urine, red skin and mucous membranes

adult dose: 5g over 15 minutes, IV infusion

acetylsalicylic acid

aspirin

MOA: inhibits COX1 and 2 to decrease prostaglandin precursors which inhibits platelet aggregation

drug interactions: thrombolytics, avoid aspirin for 24 hours

indications: acute coronary syndrome/chest pain with cardiac features

contraindications: hypersensitivity to NSAID’s

adverse reactions: bleeding, worsening of active GI ulcer

adult dosage: 160mg chewed and swallowed

dextrose

MOA: source of calories and fluid

classification: antidote, monosaccharide

indications: hypoglycemia

contraindications: hypersensitivity to corn products, hyperglycemia

adverse reactions: phlebitis, hyperglycemia, dehydration

adult dose: 25 grams q 10 min prn PO, 0.5g/kg or 10 grams reassess BGL to a max of 25 grams IV/IO

dimenhydrinate

gravol

MOA: competes with histamine for H1 receptor sites in GI tract, blood vessels, and respiratory tract

classification: H1 antagonist, antiemetic

drug interactions: may potentiate CNS depressant effects of opiates, barbiturates, ethanol and other sedatives. may potentiate the effects of tricyclic antidepressants

indications: motion sickness, N/V, vertigo

contraindications: hypersensitivity, MOA inhibitors within 14 days, prostatic hypertrophy, children < 2

adverse reactions: tachycardia, dizziness, drowsiness, excitation

adult dose: 1mg/kg to max of 50 mg over 2-3 min dilute in 10ml SIVP, 50mg in mini bag over 20 minutes infusion

epinephrine

adrenaline

MOA: stimulates alpha1 and beta 1 and 2 adrenergic receptors to relax muscle of bronchial tree, stimulate cardiac output, large dosage may produce constriction of skeletal and vascular smooth muscle

indications: cardiac arrest, anaphylaxis, severe asthma, croup, symptomatic bradycardia, hypotensive shock refractory to fluid resuscitation

adverse reactions: cardiac arrythmias, hypertension, nausea, vomiting

drug interactions: incompatible - sodium bicarbonate

glucagon

MOA: stimulates glycogenolysis and gluconeogenesis in the liver, raising blood glucose levels. Extra effects include the relaxation of the smooth muscle of the stomach, duodenum, small bowel, and colon

classification: antidote, antihyperglycemic agent

indications: hyperglycemia, beta/calcium channel blocker OD

contraindication: hypersensitivity, pheochromocytoma

adverse reactions: nausea, increased BP, hypoglycemia

adult dosage: 1mg q 15 min max 3mg IM/SC, 2.10mg bolus IV

ibuprofen

MOA: reversibly inhibits COX1 and 2 enzymes, decreasing formation of prostaglandin precursors, also antipyretic properties

classification: analgesic, nonopioid, nonsteroidal anti-inflammatory NSAID

indications: mild to moderate pain, fever

adverse reactions: decreased hemoglobin, epigastric pain, heartburn, increased bleeding time, dizziness

adult dose: 200-400 mg q 4-6 hours up to 3200mg PO/PR

drug interactions: aminoglycosides, caffeine, digoxin and vancomycin clearance may be reduced, corticosteroids may increase risk of intestinal perforation

ipratropium bromide

MOA: blocks the action of acetylcholine at the parasympathetic sites in bronchial smooth muscle

classification: bronchodilator, anticholinergic

indications: asthma exacerbation, COPD with bronchospasm

contraindications: hypersensitivity

adverse reactions: headache, nausea, dizziness

ketorolac

Toradol

MOA: decreases the formation of prostaglandins by inhibiting COX 1 and 2 enzymes, has antipyretic, analgesic, and anti-inflammatory properties

classification: analgesic, nonopioid, nonsteroidal anti-inflammatory NSAID

indications: moderate - severe pain

contraindications: hypersensitivity, active GI bleeding, severe hepatic impairment, hyperkalemia, serious bleeding

adverse reactions: headache, GI pain, indigestion and nausea, burning at injection site

adult dose: 10-15mg IM/IV

drug interactions: anticoagulants, heparin , diuretics, ACE inhibitors< selective serotonin reuptake inhibitors all may increase bleeding risks

naloxone

narcan

MOA: competes and displaces opioids at the opioids receptor site

classification: antidote, opioid antagonist

indications: respiratory depression associated with opioid OD

adverse reactions: agitation, body pain, irritability, shivering

adult dosage: 0.1-0.4mg titrate to effect IV/IO, 0.4-2mg IM, 1-2mg IN

nitroglycerin

nitrostat

MOA: reduces cardiac oxygen demand by decreasing payload; may reduce afterload; dilate coronary arteries and improves collateral flow to ischemic regions

classification: antianginal, vasodilator

indications: ACS and acute cardiogenic pulmonary edema

contraindications: hypersensitivity, systolic BP <90mmHg, HR <50bpm, recent use of phosphodiesterase inhibitors

adverse reactions: headache, dizziness, hypotension, syncope

dose: 0.4mg q 3-5min titrate to effect SL

nitrous oxide

nitronox

MOA: general CNS depressant action

indications: pain

contraindications: hypersensitivity, inability to follow commands, intoxication, chest trauma

adverse reactions: dizziness, headache, nausea, vomiting

dose: PRN titrate to effect inhaled

drug interactions: may potentiate effects of other CNS depressants such as opioids

may not work in low temps, monitor SpO2

ondansetron

MOA: blocks serotonin on vagal nerve terminals and in chemoreceptor trigger zone

classification: antiemetic, selective 5-HT3 receptor antagonist

indications: acute, sever nausea and/or vomiting

adverse reactions: headache, burning at site drowsiness

adult dose: 4mg SIVP over 2-5 min every 4-6 hrs max 8mg dilute in 10ml IV, 4mg, max 8mg IM

ECG monitoring recommended in patient with electrolyte abnormalities, CHF, or bradycardia arrythmias, crosses placental barrier

oral glucose

MOA: source of calories and fluid

classification: antidote, monosaccharide

indication: hypoglycemia

contraindications: hypersensitivity to corn products, hyperglycemia

adverse reactions: electrolyte imbalances, hyperglycemia, local pain at site

oxygen

MOA: reverses hypoxemia, necessary for cellular metabolism

class: gas

indications: hypoxia, signs of inadequate tissue perfusion

adverse reactions: drying of mucus membranes

dose: 2-15 ppm titrate to effect

pharmacokinetics: onset immediate, lasts less than 2 min

oxytocin

MOA: stimulates uterine contraction by activating G-protein-coupled receptors that trigger increases in intracellular calcium levels in uterine myofibrils. decreases local prostaglandin precursors which stimulates uterine contraction.

class: uterotonic, oxytocic agent

indications: postpartum hemorrhage, to produce uterine contractions during third stage of labour

contraindications: hypersensitivity, second fetus, uterine inversion placenta previa, abrupto placenta

adverse reactions: tachycardia, premature ventricular contractions, nausea/vomiting

dose: 10 units I, 20 units in 1000mml NS or LR IV infusion then 500ml bolus titrate drip to control bleeding IV (ACP)

pharmacokinetics: onset 3-5 min, duration 2-3 hours IM

drug interactions: concurrent use of dinoprostone

methoxyflurane

penthrox

MOA: effects on substance P and beta-endorphin

classification: analgesic, non opioid

indications: pain

contraindications: hypersensitivity, renal failure, hemodynamics instability, respiratory impairment, altered LOC, malignant hyperthermia

adverse reactions: dizziness, headache, drowsiness

dose: 3ml max 6ml per day

drug interactions: may potentiate CNS depressants such as opioids or ethanol

pharmacokinetics: onset <5min, duration 60 minutes intermittent inhalation

MUST BE ABLE TO SELF ADMINISTER

salbutamol

Ventolin

MOA: relaxes bronchial smooth muscle by action on beta2 receptors with little effect on HR. redistributes and induces a transcellular shift of K

classification: bronchodilator, beta2 agonist

indications: bronchospasm, hyperkalemia

contraindications: hypersensitivity, tachyarrythmias

adverse reactions: excitement, nervousness, tremor, tachycardia

dose: 5mg titrate to effect PRN nebulized, 10 inhalations with aero chamber PRN MDI

pharmacokinetics: onset <5 min, duration 3-6 hours

drug interactions: MAO inhibitors or tricyclic antidepressants: effect on vascular system may be potentiated

use with caution in patients with glaucoma

six rights of medication

right patient, medication, dose, route, time, PCR

percutaneous, enteral, and parenteral

percutaneous: applied and absorbed through skin or mucous membranes; transdermal, sublingual, buccal, pulmonary

enteral: GI tract, usually oral; oral, per rectum

parenteral: everything else; IV, IO, IM, SQ

solid drug forms

extract: drug in solution and evaporating excess solvent

powder: pulverized form

capsule: gelatin container enclosing dose of medication

pulvule: non gelatin capsule

tablet: powdered drug pressed into small disk

suppository: drug in firm base designed to melt at body temp

ointment: semisolid designed for external application

patch: medication on the surface of a patch

liquid drug forms

solution: one or more chemicals dissolved in water

suspension: supplied as powder add water

fluid extract: concentrated drug from dissolving drug in fluid

tincture: dilute alcoholic. extract of a drug

spirits: volatile substance dissolved in alcohol

milk: aqueous suspension of insoluble drug

emulsion: one liquid dispersed in another

liniments: lotion for external use

clinical trials phases

animal testing occurs before; testing in at least 2 species is required by law

phase I: drug tested in healthy volunteers to compare with animal results

phase II: trials are performed in homogenous groups of patients and one group receives a placebo to determine safety, efficacy, and dosage

phase III: drug is made available to a larger group of patients

phase IV: drug company submits new drug submission to the HPFB for marketing approval

controlled drugs and substances act

schedule I: narcotics

schedule II: cannabis

schedule III: stimulants and hallucinogens

schedule IV: anabolic steroids, barbiturates, benzodiazepines

schedule V: phenylpropanolamine

schedule VI: precursors that can be converted into controlled substances

schedule VII: limits associated with application of cannabis - related penalties, cannabis 3kg

schedule VIII: defines limits with application of cannabis - related penalties, cannabis 30kg

canadian food and drugs act

three major classifications of drugs: non prescription, prescription, restricted

allows the government to withdraw drugs that are found to be toxic

regulation of over the counter drugs

absorption

the transfer of a medication from its site of administration to specific target organ or tissue

factors affecting rate of absorption: solubility, concentration, pH of body, site, surface area of site, blood supply to site, bioavailability (how much of med is active upon reaching target)

distribution

how a drug moves through the body, its form and its concentration in the tissues influences the effect it will have. Adequate blood circulation is required.

Plasma protein binding is an important mechanism of distribution. Drugs are bound in variable degrees to proteins or become stored in fatty tissues. These are referred to as bound drug. Only those drug particles that are not bound can be active in the cells. These are referred to as free drug.

Drugs can also be stored in other body tissues such as fat and muscle for gradual release

albumin

plasma protein that is too large to diffuse out of the bloodstream which binds to meds making them ineffective

biotransformation (metabolism)

takes place mostly in liver, how the body metabolizes meds

occurs in 2 ways: transforming med into a metabolite or by making med more water soluble

only free drugs can be biotransformed

phase 1: liver enzymes oxidize the drug or bind it with oxygen molecules. may also hydrolyze it either way its more water soluble

phase 2: medication molecules combine with chemical found in body to form conjugates that are more easily excreted

excretion

occurs primarily through the kidneys in three ways:

glomerular filtration: passive process where blood flows through glomeruli of kidneys, forcing waste into a capsule where it is transported for excretion via urine

tubular secretion: active transport process where medications are bound to transporters who aid in their elimination

partial reabsorption: some amount of the drug is reabsorbed after being filtered

four mechanisms of medication action

1. bind to receptor site

2. change physical properties of cells

3. chemically combine with other chemicals

4. alter normal metabolic pathway

agonist vs antagonist

agonist stimulates as normal

antagonist blocks receptor or inhibits its action

partial agonists produce only a moderate effect

therapeutic index

ratio of a drugs lethal dose for 50% pop to its effective dose for 50% pop

unpredictable med responses

idiosyncrasy: rare unique response for a specific person

tachyphylaxis: rapid development of tolerance to med

iatrogenic response: adverse condition inadvertently induced in a patient by treatment given (UT infection after catheter)

accumulative vs summation vs synergism vs potentiation

accumulative: increased effect from several successive doses

summation: additive effect, two medications give combined effect equal to the sum of their individual effects

synergism: combined effect greater than sum of individual effects

potentiation: when one med enhances the effect of another

ADME process

pharmacodynamics vs pharmacokinetics

pharmacodynamics is study of the drugs effects

pharmacokinetics is the study of drug absorption, distribution, metabolism, and excretion

how many sites need to match for a cell to be receptive

3

efficacy vs potency

efficacy is the maximal effect a drug produces irrespective of concentration (dose)

potency is the amount needed to produce an effect

preganglionic vs postganglionic

preganglionic neurons originate in the CNS, through spinal cord, and synapse in ganglia. release acetylcholine

postganglionic neurons innervate target organs. primarily release norepinephrine, sometimes ACh

sympathetic nervous system (meds)

sympathetic nerves have origins in thoracic and lumbar regions of the spinal cord

primary chemical messengers are norepinephrine and epinephrine and catecholamines

two types of receptors:

1. adrenergic

   1. alpha1

   2. alpha2

   3. beta1

   4. beta2

2. dopaminergic (cause renal, coronary, and cerebral artery dilation)

sympatholytic: interfering or inhibiting the effect of impulses from SNS

sympathomimetic: stimulates adrenergic receptors

parasympathetic nervous system (meds)

principle neurotransmitter is acetylcholine; cholinergic receptors (nicotinic and muscarinic)

parasympathetic nerves have origins in the brainstem and sacral segments of spinal cord. nerves from brainstem pass through 4 of the cranial nerves: ocularmotor III, facial VII, pharyngeal IX, and vagus X

cholinergic receptors

ound in CNS and PNS nicotinic are triggered by ACh but opened by nicotine. nicotinic effects are the same as sympathetic overactivity; tachycardia, hypertension, dilated pupils. muscle twitching, muscle weakness

found in CNS and ANS muscarinic are triggered by ACh and muscarine. muscarinic effects result in parasympathetic overactivity; bradycardia, miosis, sweating, blurred vision, excessive lacrimation, excessive bronchial secretions, wheezing, SOB, urinary and fecal incompetence. atropine reverses effects of muscarinic overstimulation.

alpha beta 1 and 2

1 heart

2 lungs

A B C D

ac: alpha constricts

bd: beta dilates

alpha 1: located on peripheral blood vessels

• peripheral vasoconstriction

• mild bronchoconstriction

• increased metabolism

• sweat glands

alpha 2: located on nerve endings

• control release of neurotransmitters

beta 1: located in cardiovascular system

• increased HR

• increased conduction

• increased contraction

beta 2: located on bronchial smooth muscle

• bronchodilation

• peripheral vasodilation

analgesics

affect CNS

medications that relieve pain

most common are opioid agonists which bind to opiate receptors preventing pain signals

nonopioid analgesics alter the production of prostaglandins and COX

• salicylates

• NSAIDS

• para-aminophenol derivatives

opioid antagonists reverse the effects of opioids (narcan)

opioid agonist-antagonists have agonistic and antagonistic properties. are preferred because decrease pain without diminishing respiratory system or leading to dependence or addiction

anaesthetics

affect CNS

medications intended to induce loss of sensation to touch or pain

systemic anaesthesia is usually done via inhalation and is used for operating room

regional anaesthesia focuses on a particular portion of the body

local anaesthesia focuses at a specific spot on the body where a procedure is about to take place

can slow the functioning of the respiratory system, CNS and cardiovascular system

anti anxiety, sedative, and hypnotic medications

affect CNS

benzodiazepines are sedatives most commonly used to prepare for invasive procedures. they enhance the affinity of GABA binding sites which causes brain activity to slow

barbiturates: increase the affinity between receptor sites and GABA as well however they have significant side effects

nonbarbituate hypnotics: also the same MOA, less side effects

anticonvulsants

affect CNS

work by inhibiting the influx of sodium into cells, enhancing GABA A system, reducing excitatory glutaminergic neurotransmission, and reducing activity in calcium channels

opioid antagonists

affect CNS

MOA: attach to opioid receptors and displace the narcotic

pure: competitive, occupy receptor so narcotic cannot

partial: bind with receptor sites and produce weak narcotic like effects

may cause worsening of respiratory depression

non narcotic analgesics

affect CNS

MOA: provide analgesia by blocking prostaglandin stimulation in CNS, fever reduction by affecting hypothalamic center, increase sweating and peripheral blood flow to increase heat loss. some can reduce inflammation by stabilizing cell membranes

inhalation anesthetics

affect CNS

stage 1: analgesia. cerebral cortex is inhibited, decreased response to pain, euphoria, unconsciousness

stage 2: involuntary movement. cerebral cortex completely depressed, hypothalamus takes over, absence in sympathetic tone cause increased HR, BP, resp, and muscle tone

stage 3: surgical anesthesia: hypothalamus is depressed, cardiac and respiratory function return to normal, spinal reflexes blocked, muscles relax

stage 4: medullary paralysis. medulla is paralyzed, cardiac and respiratory centres are effected, death may occur

cholinergic medications

affect PSNS

stimulate cholinergic receptors of the PNS

excessive cholinergics can cause SLUDGEM

anticholinergic medications

affect parasympathetic NS

work in opposition to the parasympathetic NS by blocking cholinergic receptors

muscarinic cholinergic antagonists: block ACh at the muscarinic receptors

nicotinic cholinergic antagonists: block ACh at nicotinic receptors which disables the ANS so they are almost never used

neuromuscular blocking agents

bind to to somatic ACh receptors at neuromuscular junction

depolarizing: stimulate depolarization of muscle cells (causes muscle twitches) then produces continuous stimulation of the muscle cell

nondepolarizing: bind in a competitive but nonstimulatory manner to part of ACh receptor (no muscle twitches), but have long onset and DOA

sympathomimetics/adrenergic agonists

stimulate adrenal medulla to release epinephrine and norepinephrine

stimulation of dopaminergic receptors: dilation of renal, coronary, cerebral arteries

adrenergic receptors: cause various effects alpha beta 1 and 2

non selective adrenergic agonists stimulate both A and B receptors

bronchodilators

b2 agonists

• act on sympathetic NS

• fit and act at b2 receptors in lungs

• bronchodilation, decreased resp secretions

• short acting <12hrs, long acting >12hrs

anticholinergics

• act on parasympathetic NS

• block action of ACh on bronchial smooth muscle

• brinchodilation, decreased resp secretions

• best treatment for COPD

xanthines

• act directly on respiratory muscle

• most commonly oral

• narrow therapeutic range

antianginal agents

nitrates: relax smooth vascular muscle, vasodilation results in decreased preload, after load, and work meaning less oxygen is required

• prevent angina attacks

• decrease BP

• nitroglycerin

• alcohol potentiates

beta blockers: block beta 1 receptors in heart decreasing HR and contractility reducing oxygen demand

• post myocardial infarction

• bradycardia, reduced AV conduction, reduced contractility

calcium channel blockers: block calcium channels in arterioles which causes arteriolar dilation

• angina

• can cause hypotension and tachycardia

anticoagulants and platelet inhibitors

anticoagulants: prevent production of fibrin by disrupting the coagulation cascade

• can cause bleeding gums, nosebleeds, easy bruising

platelet inhibitors: decrease the ability of platelets to stick together by inhibiting TXA2 or ADP

• effective for preventing arterial thrombosis

• ASA

• prevention of myocardial infarction, thrombotic stroke

• increases risk of bleeding

uterotonics

stimulate uterine contractions and compression of maternal blood vessels at rheumatoid arthritis placental site to induce labor and control postpartum hemorrhage

• oxytocin

• ergometrine is contraindicated by hypertension, pre-eclampsia or heart disease

vitamins

vit A: enables retinal rods to adapt to dim light

vit D: regulates serum calcium levels as well as parathormone and calcitonin

vit E: grevants formation of toxic metabolites, maintenance of RBC membranes

vit K: synthesis of blood clotting factors

vit B: cell reproduction and maturation

vit C: formation of catecholamines, steroids, and conversion reactions

antihypoglycemic agents

either

• break down glycogen stores from liver

• supply usable glucose to bloodstream

used for hypoglycemia

antimicrobials

antibiotics: prevent cell wall synthesis (penicillins), block synthesis of folic acid (sulphonamides), interfere with protein syntheses (tetracycline, macrolydes, amnuglycosides) interfere with DNA synthesis (quinolones)

• can cause bacteria to become resistant

antivirals: prevent the virus from replicating, inhibit revers transcriptase used by RNA viruses, inhibit protease used by RNA viruses, prevent virus from incorporating into host cells

• treats herpes

• decrease HIV virus production

• can cause nausea, headache, dizziness, drowsiness

antifungals: inhibit ergosterol synthesis in fungal cell membranes inhibiting fungal cell membrane synthesis

antidotes and neutralizing agents

they:

• compete and displace drug from receptor sites

• use different cellular mechanism to overcome poison

• prevent biotransformation

• bind and inactivate the poison

antiemetics

5-HT3 receptor antagonist: blocks the effects of serotonin

• most effective in controlling N/V with simulation of the CTZ

H1 histamine antagonists: blocks the effects of H1 histamine and blunts vestibular inputs

• effective in treating N/V with stimulation of vestibular system

iv formuler

V x S = T x R

vestibular

immediate transfusion reactions

acute hemolytic transfusion reactions: usually due to incompatible blood, fever, chills. hypotension, hemoglobin in urine, flank pain, SOB. discontinue and keep open with saline

febrile reactions: fever during transfusion due to

• destruction of RBCs or WBCs

• bacterial contamination of blood

• reaction to proteins

discontinue and keep open with saline

allergic reactions: urticaria (hives) are not serious unless accompanied by other signs of anaphylaxis. discontinue and keep open with saline. when anaphylaxis occurs, discontinue, keep open, provide high flow 02

transfusion associated circulatory overload: fluid overload and pulmonary edema. causes SOB, hypertension, dyspnea, lumbar pain. discontinue and keep open, high flow O2, sitting position

chills and hypothermia: discontinue and keep open with saline

delayed transfusion reactions

include hepatitis, sepsis, iron overload, delayed hemolytic reaction, post transfusion purpura, transfusion associated graft-versus-host disease

rights of transfusion

patient, product, amount, rate, time

blood product monitoring guidelines

• patient must be stable for 30 min before transport

• reassess vitals after 15 minutes of initiation

• repeat vitals every 30 min wth temp

• only normal saline can be infused via same line as blood

• tubing must changed every 2-4 units of blood

needle sizes

SQ: 24-26 gauge, 1.27-2.5cm needle

IM: 21 or 22 gauge, 2.5cm or 5cm

rates of absorption

oral 30-90 minutes

rectal very rapid

subcutaneous slow onset and prolonged duration

intramuscular is faster than SQ

intravenous: fastest onset

endotracheal/inhalation: 2-3 minutes

transdermal: slow, sustained release

sublingual/buccal: very rapid

alarm system infusion pump

end of infusion

occlusion (blockage)

air in line

battery low

bad tubing

excessive pressure

signs of dehydration and over hydration

dehydration: decreased LOC, tachypnea, dry mucus membranes, tachycardia, poor skin turgor, flushed dry skin

over hydration: SOB, puffy eyelids, edema, polyuria (excessive urination), moist crackles, acute weight gain

electrolytes

sodium: water regulation, nerve and muscle function. high levels: edema, lethargy, weakness. low levels: pulmonary or cerebral edema

potassium: nerve and muscle function. low levels: decreased skeletal muscle function, GI disturbances, arrhythmia. high levels: hyperstimulation of neural cell transmission leading to arrhythmias and cardiac arrest

calcium: bone formation, heart function, nerve transmission, blood clotting. too low: muscle cramps, abdominal cramps, hypotension, vasoconstriction. high levels: weakness, lethargy, lack of coordination, cardiac arrhythmia, vasodilation, flushed skin

magnesium: metabolism of protein and carbs, neuromuscular activity, myocardial function. low levels: weakness, irritability, tetany, delirium, convulsions, anorexia, nausea, emesis, cardiac arrhythmia. high levels: hypotension, weakness, N/V, altered mental functioning

bicarbonate: determine acidosis or alkalosis in body

chloride: strongly liked to sodium, formation of stomach acids, fluid balance, Ph. low levels: muscle spasms, metabolic acidosis, shallow respiration, hypotension, tetany. high levels: lethargy weakness, metabolic acidosis, rapid deep breathing

phosphorus: component of ATP

macro vs micro drip set

macro: 10, 15 or 20 gtts/ml

micro: 60 gets/ml

IV fluids

D5W: 5% dextrose in 100ml of water. not used for fluid replacement

ringers lactate: isotonic solution containing chloride, lactate, potassium, and calcium that remains in the vascular space. good for trauma patients. volume expander

normal saline: isotonic solution of 0.9 sodium chloride. close to body fluid in density and osmotic pressure. good for hemorrhage, fluid loss due to burns, peritonitis, or diarrhea. volume expander

local IV site reactions

infiltration: escape of fluid unto surrounding tissue causing edema, cold skin. discontinue, apply cold packs early, hot packs later, re-establish IV at another site, physician

thrombophlebitis: inflammation of the vein due to the presence of a clot, red skin, swelling, palpable cord along course of vein. discontinue, war packs, physician

phlebitis: inflammation of the vein, edema, redness, hot skin. discontinue, apply warm packs, notify physician

occlusion: physical blockage of vein or catheter.

vein irritation: observe closely for allergic reaction, discontinue and reestablish in another extremity

hematoma: accumulation of blood in surrounding tissue. discontinue and apply pressure

systemic IV reactions

circulatory overload: too much fluid in the intravascular compartment, rapid pulse, venous distension, increased BP, coughing, SOB, increased resp, syncope, shock, pulmonary edema - dyspnea, cyanosis. slow to TKO, administer O2, sitting position, physician

air embolism/catheter embolus: air or a piece of the catheter enter the circulatory system causing shock, chest pain, cyanosis, tachycardia, resp distress, rapid loss of consciousness. close adjustment valve, clamp off tubing, patient on left side with head down, administer O2, initiate IV, physician

discontinuing IV

1. shut off flow valve

2. remove tape

3. hold cotton swab or 4×4 above entry site

4. remove catheter, check its in tact while applying pressure

5. apply band aid

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