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369 Cards in this Set
- Front
- Back
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goal of antibiotic therapy
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cure
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thrush
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white, yeast patches in mouth
pain with swallowing |
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infection
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microbe invades and multiplies
-pathogenic will have s/s |
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nosocomial
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hospital acquired
-can be endogenous from pt -tends to be more severe and resistant |
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superinfection
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result of antibitoics
aka secondary vaginitis thrush diarrhea |
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colonization
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can have no s/s of infection
issue with MRSA (nasal passage) |
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inflammation
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protective response
-exudate |
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sepsis
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infection at worst
multiple organ involvement |
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acquired resistance
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bacteria could be destroyed by antibiotics and now they can't
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sterile areas
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blood
CSF urine synovial fluid lower respiratory musculoskeletal |
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iatrogenic
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result of a procedure
(IV) |
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contributing factors to bacteria resistance
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-widespread use of antimicrobial drugs
-interrupted tx, didnt finish course -increased # of high risk patients -location |
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high risk patients for bacteria resistance
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malnourished
immunosuppressed organ transplants chronically ill invasive lines mechanical ventilators |
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bacteria resistance ex
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MRSA (methicillin resistant staph aureus)
-VRE: vancomycin resistant enterococcus -MDR-TB: multi drug resistant TB |
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factors that impair host defense
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1. breaks in the skin
2. impaired blood supply (edema, swelling) 3. malnutrition (chronic alc, end state HIV, cancer) 4. poor hygiene 5. suppression of normal flora 6. suppression of immune system 7. chronic disease 8. advanced age |
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allergic/hypersensitive rxn and tx
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-can occur w/ all antimicrobial agents
Treatment: -antihistamines (benadryl) -epinephrine -corticosteroids (prednisone) |
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mild allergic rxn
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pruritis
use benadryl |
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sensitization
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can occur with antibiotics over time
-present in salad bars, meats |
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anaphylaxis
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use epi to open airway with corticosteroids that will decrease inflammation of airway
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systemic infection characteristics
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tend to run a fever
increased HR and RR fatigue anorexia n/v high WBCs (>10,000) normal is 5-10,000 |
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assessments for allergic rxns/antibiotics
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-current or potential infection
-drug allergies -renal and hepatic fxn -factors that increase patients risk for infection |
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therapeutic/ADE of antibiotics
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fatigue
self care deficit activity intolerance diarrhea altered nutrition-less than body requires risk for injury risk for infection knowledge deficit |
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broad spectrum antibiotics
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antibiotics, bacteria are gram meg and positive
-may need to change after culture |
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narrow spectrum antibiotics
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only do gram positive or gram negative
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beta lactum ex and what you need for them to work
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penicillin
cephalosporin *ring must be intact to work |
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penicillin prototype
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penicillin G
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penicillinase
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from bacteria, can destroy B-lactum ring so you need penicillinase resistance drugs
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types of penicillins
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-penicilin V
-penicilinase resistance -ampicilins extended spectrum -penicillin/beta lactamase inhibitors |
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what constitutes an empty stomach
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1 hour before eating or 2 hours after a meal
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penicillin assessment
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-C&S
-Allergies -K+ level -Na+ level -Superinfection -Rena and liver fxn |
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is PCN bacteriocidal or static
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cidal
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interventions for PCN
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-emergency equipment
-benemid -empty stomach -IM in a large muscle or PO -observe for ADEs -prev. superinfection -increase fluids -pt teaching -syphilis and upper airway probs |
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how is PCN excreted
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by kidneys
mostly unchanged |
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PCN is drug of choice for what
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streptococca infections, esp with vaue probs (murmur) or congenita (hx of endocarditis)
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benemid
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not an antibiotic
-increases serum K by decreasing renal excretion so PCN can hang longer |
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cephalosporins prototype
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keflex (PO)
kefzol (IM or IV) |
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cephalosporins uses
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-surgical prophyaxis: 30 min-2hrs pre-op
-complete 30 mins pre-op -treatment of infection |
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what types of infections do cephalosporins treat
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respiratory tract
skin and soft tissue bones and joints bloodstream urinary tract |
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what type of spectrum are cephalosporins
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broad
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are cephalosporins bacterocidal or static
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cidal
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how are cephalosporins excreted
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by kidney
mostly unchanged |
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what is the benefit of cephalosporins over PCN
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-can give with food, milk so its easier to coordinate
-similar in chem structure, mechanism, excret and sensitivity |
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contraindication for cephalosporins
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-pregnant/lactating because it can cross placenta into breast milk
-category B teratogen: animal studies show no risk |
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cephalosporins assessment
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-C&S report
-allergy: ceph & PCN -IV site: red? pain? swollen? -renal and liver fxn -superinfections -given w/ lasix or aminoglycosides--kidney damage |
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what types of infections do you not treat with cephalosporins
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brain...it can't cross BBB
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after how long do you need another cephalosporin dose in the OR
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3 hours
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ways cephalosporins can be given
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PO
IM in lg muscle group IV |
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biggest uses of cephalosporins
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infection
surgical prophylaxis |
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issue with cephalosporins and aminoglycosides
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synergists for nephrotoxicity
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aminoglycosides prototype
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garamycin or gentamycin
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lasix/cephalosporin prob
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lasix is a diuretic and can dehydrate you
-increase ADE from cephalo -don't take w/ alc or you'll get an antabuse effect |
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aminoglycoside uses
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-serious systemic infections
-TB -bowel prep -Tx of hepatic coma or hepatic encephalopathy |
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why do you give aminoglyco for bowel prep
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for resection or opening the bowel
PO decreases # of pathogens in bowe |
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what type of bacteria are aminoglycosides used for
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gram negative
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why do you use aminoglycosides in conjunction with PCN
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it works within the cell wall so give PCN first to hep destroy cell membrane of bacteria and amino can then get inside
-give 2 hours apart because PCN could inactivate amino |
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aminoglycosides used as tx for hepatic coma
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prob with liver caused the coma, issue is the liver can't deactivate ammonia and it builds up causing CNS probs
-give aminogyc PO and the bacteria making ammonia are killed |
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contraindications for aminoglycosides
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-when you can use a less toxic drug
-take blood levels -initial: highest level after 30-60min correlates w/ toxicity -1/2 hr before next dose is lowest level |
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ototoxicity
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permanent damage to CN VIII
tinnitus, lose high pitch sounds amino deposits around ear IRREVERSIBLE |
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nephrotoxicity with aminoglycosides
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shows kidney fxn
look at creatinine levels (.6-1.4 is norm) -therapeutic levels are close t toxic levels |
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how do aminoglycosides potentiate anesthetic neuromuscular blockers
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immediately post op can reactivate and lose ability to breathe
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are aminoglycosides bactercidal or static
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cidal
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assessment for aminoglycosides
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C&S
hearing fxn renal fxn post op respiratory rate |
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nursing dx/PT eval for aminoglycosides
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-potential for sensory perceptual alteration
-potential for alteration in urinary elimination |
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interventions for aminoglycosides
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-force fluids
-monitor creatinine -refrigerate drug -IV: 30-60 min -2 hrs apart from PCN |
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elderly and aminoglycosides
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give low dose
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contraindications for aminoglycosides
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pregnancy
kids? avoid diuretics |
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floroquines prototype
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ciprofloxacin (cipro)
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floroquines uses
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Tx of infections of respiratory
GU GI bones joints skin soft tissue -TB -Anthrax |
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assessment for floroquines
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C&S
allergies ADEs |
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interventions for floroquines
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empty stomach
IV over 60 mins |
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what type of drug is floroquines?
synthetic/natural cidal/static broad/narrow |
synthetic
cidal broad |
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liver/kidney role in floroquines
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liver metabolizes floro a little
-kidney excretes ~60% unchanged |
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how are floroquines usually given
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PO
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patient teaching for floroquines
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-avoid Al, Mg, Fe, Zn
-increase fluids -avoid sunlight -avoid high impact exercise because of tendon rupture |
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contraindications for floroquines
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kids
antacids diet supplements w/ Fe, Zn kidney crystals |
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tetracyline prototype
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tetracycline (achromycin)
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uses for tetracyline
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-rarely for systemic infections
-rocky mt spotted fever -prostitis -PID, STD -Acne |
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tetracyline is static or cidal
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static
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tetracyline is broad or narrow spectrum
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broad
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contraindications for tetracyline
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renal failure
during pregnancy children up to 8 years old lactating women |
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excretion with tetracyline
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about 60% excreted by kidney
-decrease % by liver |
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why don't you take tetracyline with pregnancy
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-hepatic necrosis in mom
-effects bones and teeth in fetus...gets deposited in formation of teeth, brown and mottled and decreases bone growth |
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exp date with what drug
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tetracyline,...gets stronger after expiration
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tetracyline assessment
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-C&S
-Allergies -Pregnancy -Lactating -Renal fxn -Age |
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nursing.pt eval for tetracyline
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potential for injury
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interventions of tetracyline
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-increase fluids
-N/V/D, renal and liver fxn - |
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patient teaching for tetracyline
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-Avoid Fe, Ca, Mg, Al
-Full glass of water -avoid sun -report s/s of superinfection |
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sulfonamides prototype
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sulfamethoxazole-trimethoprim
(bactrium, septra) |
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uses for sulfonamides
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-not for systemic infections
-UTI: excreted by kidneys -ulcerative colitis -topically: vaginal infection, dermatitis, burns |
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contraindications for sulfonamides
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-late pregnancy--kernicterus
-lactating women -< 2 months old -history of allergies to sulfa meds -renal failure |
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are sulfonamides static or cidal
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static
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kernicterus
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increased bilurbin in brain of newborn, gets damaged
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history of allergies to sulfa meds with sulfonamides, explain
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-thiazide diuretic (HCTZ)
-antidiabetic sulfonylureas -diabetics |
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sulfonamides assessment
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C&S
Allergies Pregnancy Lactating Pts ability to take large amts of fluid Renal fxn Taking oral hypoglycemics |
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interventionfs for sulfonamides
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large amts of water
ADEs |
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sulfonamides...why is it impt to know about oral hypoglycemics
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sulf can decrease blood sugar A LOT
s/s of hypoglycemia |
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sulfonamides are given how? and pyridium?
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-PO: urinary antiseptics
-pyridium: + sulfa, decrease pain w/ urination until sulfa can work, can change urine to be orange or red |
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macrolides prototype
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erythromycin
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how is vancomycin given
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only via IV
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vancomycin uses
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severe infections (MRSA)
helps w/ C. diff |
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why is there resistance with vancomycin
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MOs resistant because of frequent use in ICU
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specific guidelines for vancomycin
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slowly over 1-2 hours to avoid red man syndrome from histamine release
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metronidazole (flagyl) used for
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tx of prophylactic colorectal area surgical patients
-c. diff. in colon can overpop and cause diarrhea |
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contraindication for macrolides
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liver disease
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macrolides uses
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community acquired infection
(pneumonia, bronchitis) |
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macrolide metab/excretion
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metab by liver to some extent
mostly excreted in bile |
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sub for PCN allergy
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macrolides
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dosing. ade with macrolides
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less frequent
GI irritation |
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viruses cause
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herpes
flu common cold AIDS and other diseases |
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ADE of antiviral drugs
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anorexia
n/v hallucinations seizures |
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tx for herpes virus
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zovirax, treats s/s but no prevention of reoccurrence
-can give PO, topically, or IV for severe cases -prolonged repeated use ---drug resistant virus |
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meds for HIV, AIDS
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Viracept, ACT
-inhibit enzymes for viral replication, use in combo -4-6 different types |
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viruses
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intracellular parasites, must be in living cell to reproduce
-difficult to kill virus, w/o killing host cell |
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purpose of antiviral meds
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inhibit viral reproduction
DONT ELIMINATE viruses |
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meds for influenza
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symmetrel, flumadine
-prophylactic use -w/in first 24 hours to shorten duration |
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drug abuse
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self administered drug(s) to the point of physical and/or psycholgoical dependence
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IV use probs
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increase infection
hepatitis HIV |
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CNS depressents
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ETOH
antianxiety/sedative-hypnotic narcotics or opiates |
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CNS stimulants
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amphetamines
coke nicotine |
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physical dependence
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physiological adaptation to chronic use to avoid unpleasant s/s if the drug is stopped
-if you stop use you see s/s of withdrawal -rapid tolerance built -often dependent on more than 1 drug |
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psychological dependence
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feelings of satisfaction and pleasure
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sober
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.05% or less
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impairment in general with alcohol
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.051-.149%
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impairment in vt
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.08%
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unquestion intoxication
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>.15%
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rate of alcohol metabolism
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120 mg of ethanol/1 kg of body weight
OR 10 mL/hour |
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rate of alcohol metab is the amt in
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2/3 oz whiskey
3-4 oz of wine 8-12 oz of beer |
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alcohol dehydrogenase
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women have less
-women ~30% more ETOH absorbed -rate our body can metabolize alc is consistent hour after hour |
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alcohol effects
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-drug and a poison
-crosses BBB: increased lipid content allows this -lowers inhibition -impairs reasoning and judgement |
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alcohol effects on lower brain
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-false feeling of freedom & emotional stimulation
-can kill: liver, brain, kidney and other tissue |
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alcohol effects on upper brain
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interrupts chemical balance
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alcohol effects on urinary system
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produces more urine because ADH is suppressed
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alcohol effects on reproductive system
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decreased sexual performance
preg= miscarry, FAS, LBW |
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alc effects on endocrine system
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blood sugar swings
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alc effects on skeletal system
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dec muscle coordination
ataxia staggering |
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circulation effects from alc
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increased HR
vasodilate--heat loss from body cardiomegaly w/ chronic use CV collapse |
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alc effects on respiratory system
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small doses raises RR
-large can dramatically decrease it |
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alc effects on NS
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relax, lower inhibition
sedation severe: lose gag reflex, vomit--lungs, brain damage, seizures depression |
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alc effects on digestive system
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increased secretion
increased appetite in small dose high dose: GI bleed, ulcer -increased fatty deposits in liver -pancreatic disease -n/v, malabsorption of nutrients with long term use |
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alc effects on hematological system
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suppresses bone marrow
Pancytopenia: lower RBC's, platelets, WBC's |
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liver damage and alc
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difficult to predict where pt is on spectrum
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ethanol uses
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beverage
dilutant base=elixir destroy nerve fibers-inject at site to decrease pain appetite stim: elderly, debilitated astringent and antiseptic |
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methanol uses
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antiseptic: rubbing alc, no PO
sponge baths: ETOH competes at receptor, give via IV w/ excess |
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enzyme induction with alcohol
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liver changes, more enzymes for detoxification but reaches a point where liver cells are destroyed by alc
=fatty deposits and you can't break it down or tolerate it |
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Meds/EtOH
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acute intoxication
can't metabolize meds and may have exaggerated.toxic effect -chronic: breaks down med faster adn you don't get full effect |
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s/s of alcohol withdrawal
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agitation
anxiety tremors sweating nervousness tachypnea fever hyperreflexia postural hypotension convulsions and delirium |
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most serious s/s of alc withdrawal
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dilerium tremors
-confused, disoriented, visual hallucinations s/s of acute psychosis |
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meds 4 alc withdrawal
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benzodiazapenes, anticonvulsant
-librium and ativan are longer acting |
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tx of acute intoxication
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control environment
sedate restrain coma...intibate adn give meds for BP etc |
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tx of benzodiazapene abuse
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romazicon
-short acting, may need repeated dose -if you give, throw into withdrawal so be careful, breathe or increase? |
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treating alcohol addiction
|
antabuse
-increased flusing -vasodilation -hyperventilate -copious vomitting |
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benzodiazpene as tx for alc withdrawal,,,
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rhohyphenol
w/ alc...no odor or taste 10-20 mins you feel dizzy, difficulty moving or speaking and pass outwith no memory |
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crystal form of amphetamines
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ice, crystal, glass
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powder form of amphetamines
|
speed
meth crank |
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MDMA/Ecstasy
|
synthetic drug, cheap
-lasts 3-4 hours, more of a prob than heroin -long term: brain change like Parkinsons **marked increase in temp |
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actions of amphetamines
|
SYMPATHOMIMETIC
-reduces fatigue -depress appetite -increase aggressiveness -increase competitiveness -increase alertness -enhance self confidence -increase HR, BP, BMR, T -decrease libido -dilated pupils -paranoid schizophrenia -masks pain |
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increased BMR with amphetamines
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breakdown of muscle mass and damages kidneys and CV system
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mydriasis
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pupil dilation...amphetamines
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paranoid schizophrenia type with amphetamines
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persecution type, voices
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withdrawal of amphetamines
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depression
irritable |
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therapeutic uses of amphetamines
|
narcolepsy
weight loss hyperactive kids: ritalin depression |
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abuse potential for amphetamines
|
schedule 2
high abuse potential |
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main concern with amphetamines...type of dependence
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concerned with OD
don't produce physical dependence so no s/s |
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long term use of amphetamines causes what kind of dependence
|
psychological
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cocaine effects
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reduces fatigue
depress appetite increase aggressiveness increase competititveness increase alertness enhance self confidence increased energy increased HR, BP, BMR,T dilated pupils masks pain increaed euphoria |
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issue with coke
|
more powerful than amphetamines
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cocaine causes what to be released? with what effects?
|
NorEpi and dopamine released
-stims brain activity -blocks reabsorption of it so it has a longer lasting effect |
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assessment of coke addict
|
nasal congestion
weight loss w/o diet declining social status behavior changes mood swings: depression to apathy needle tracts |
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nasal congestion with coke
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chronic snorting so mucous membranes BV's are killed because coke is a vasoconstrictor
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therapeutic use of coke
|
great topical anesthetic
-ENT surgery and eye for potent vasoconstriction -rhinoplasty (coke strips on nose) |
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cardiac complications with coke
|
-increased HR and BP
-myocardial ischemia and infarction -HTN crisis=CVA -crack heart -sudden death |
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BP increase with coke and HR
|
esp systolic, increased oxygen demand of tissues
HR = 120-160 BP= 250/150 hTN crisis |
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crack heart with coke
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cardiomegaly, toxic effect on muscle
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suddent death with coke is due to
|
arrythmia
vent. tachycardia |
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respiratory complication of coke
|
pulmonary hemorrhage
crack lung decreased lung capacity chronic inflamed throat chronic cough pneumonias |
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crack lung with coke
|
toxic to lining of lungs
chronic bronchitits -irreversible lung damage from smoking it |
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neurological complications of coke
|
seizures
CVAs subarachnoid bleeds -lose sense of smell -burns from free blasting -hyperthermia -sexual deficiencies |
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nursing care of cocaine OD...type of addiction
|
no antidote
treat symptomatically can give alcohol to lessen crash -not physically addicting but severely psychological |
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coke OD tx for:
-HTN and tachycardia -Effects of concomitant narcotics -Dehydration |
HTN: inderal, beta blocker
-narcan -dehy: IV fluids |
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fever tx for coke OD
|
hypothermia blankets
cold IV fluids sponge bath cold NG levage |
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nicotine type of addiction
|
physically
psychologically |
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whats in a cig
|
4,000 chem
200 known poisons 8-9g of nicotine |
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coke oD looks like
|
exaggerated version of expected response
|
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effects of nicotine
|
-CNS: increase alert, stim, decrease appetite, tremor
-CV: increase HR and BP -GI: more HCl, motility, n/v, diarrhea, aggravates ulcers -Respiratory -Cancer -Death |
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nicotine withdrawal
|
anxiety
irritability restlessness diff concentrating headache increase appetitie sleep disturbance cravings |
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nicotine tx
|
patches...combine with behavior modifications, change routine, be careful of kids
zyban: anti depressant |
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LSD effects
|
psychic distortion
increase HR, BP, T extreme panic to euphoria very potent flashbacks, reliving hallucinations years later 8-12 hours to metabolize |
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LSD risk
|
injury from uncontrolled behavior
|
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tx for LSD
|
no antidote
quiet envt talk and act calmly reassurance keep your body between patient and the door open |
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marijuana effects
|
dreamlike
confused detached, aloof relaxed, inner focused no sense of time dose-related |
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withdrawal of mariuana
|
headache
anxiety restless -tolerance deveops |
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thereapeutic use of marijuana
|
intraocular P for glaucoma
n/v with chemo increases appetite |
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chronic weed use
|
lung and airway damage
1 joint is a pack of cigs? |
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flumadine is used on what type of patients
|
those with chronic illness that can't get flu shot, get this anti viral to shorten the duration
|
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contraindications for the flu vaccine
|
fever
immunocompromised egg allergy mercury allergy guion-beret disease |
|
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inotropics
|
increase the force of myocardial contraction
|
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cardiotonics prototype
|
digoxin
|
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fxn of cv system
|
-transport supplies to the cell
-remove waste products |
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systole
|
when the heart is contracting
|
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diastole
|
ventricles opening
heart fills with blood |
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SA node normals and what it does
|
pacemaker of heart
60-100 bpm |
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av node bpm
|
40-60 bpm
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ventricles bpm
|
20-40 bpm
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explain pacemaker of the heart and who can take over etc..order of command
|
normal chain is
SA,AV then ventricles -any cell within the heart can take over as pacemaker, whichever beats the fastest so ventricles could overpower SA |
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explain dosage with digoxin
|
-digitalize or "loading dose" =
.75 mg - 1.0 mg into 3 doses, 6-8 hours apart to get blood level where it needs to be, 1st pass so give more PO and less if with IV |
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|
what is digoxin dependent on?
|
normal electrolytes:
-K-if it drops then dig toxicity -Ca..high levels increase dig toxicity -Mg...low levels toxic |
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action of digoxin
|
-increased contractility: + inotropic
-increases CO -decreases HR, - chronotropic -antiarrhythmic, only atria -indirect diuretic |
|
|
efficiency of cv system is dependent on
|
-hearts ability to pump determines efficiency
-quality of blood (healthy RBCs and Hb) -quantity of blood |
|
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digoxin therapeutic level
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.5-2
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digoxin uses
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-CHF
-Atrial arrhythmias -sinus tachycardia from sa node |
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contraindications for digoxin
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Vtack
Vfib heart block (2nd or 3rd degree) -won't help after SA node |
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ADEs of digoxin
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N/V
Anorexia Blurred vision Diploplia Halos Bradycardia Tachycardia PVC:premature ventricle contractions |
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metabolism and exretion of digoxin
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metab: 40% by liver
excretion: 60% |
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s/s of digoxin toxicity
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N/V
Confusion Blurred vision Bradycardia*** PVCs |
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treatment of dig toxicity
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-stop dig
Tx symptomatically: -KCL -Antiarrhythmias -Atropine for bradycardia -Digibind |
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at risk for dig toxicity??
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1. hypokalemia...add IV or supp
2. Renal or liver failure 3. Large loading dose 4. Large maintenance doses 5. Infants and aged..lower fxn and immature liver 6. hypothyroidism -lower BMR 7. Hypoxia 8. Ca Channel Blockers because high Ca is bad |
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indirect diuretic
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more efficient heart
increases CO perfuses kidneys better and removes fluid |
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plasma fxn
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albumin exerts osmotic P that helps hold fluid intravascularly (w/Na and glucose)
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HCT and HGB levels
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HCT: % of RBCs
HGB: carries O2 Ratio should be 3:1 of HCT: HGB |
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wbc fxn
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produce antibodies, short life (hrs to days)
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rbcs life
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120 days
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thrombocytes and platelets fxn
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1st to injury to form and unstable clot until others reach the area
-come from bone marrow with RBCS and WBCs |
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extreme dig toxicity tx
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digibind, binds in CV and can excrete it
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digoxin assessment
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allergies
HR Dig level S/s of toxicity K+ level |
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nursing dx/PT eval for digoxin
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1. pot for injury: toxicity
2. Pot for sensory perception alteration (halo,diplopia) 3. pot for altered metab 4. altered tissue perfusion: cardiac, neuro, renal, periph 5. activity intolerance (brady 6. self care deficit: fatigued |
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digoxin interventions
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1. K+ . don't want on k sparing diet
2. explain med regimine 3. administer with meals or water instant coffee has K |
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pt teaching for digoxin
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check pulse daily, hold if <60/min
don't skip a dose or double report ADEs |
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drug for outpatient tx of CHF
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milirinone (primacor)
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Na/K pump and 3 stages for impulse to be propagated
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1. Polarized/Resting or Read State:
-Na, Ca extracellular and K intra 2. Depolarization or Discharge state -Na and Ca move intra and K extra -P wave and QRS 3. Repolarization or Recovery: -Na and Ca move back extra, K intra -T wave |
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QRS part of wave
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thru AV, systole, vent contract
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T part of wave
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when k goes back in and Na out
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class I of antiarrhythmics
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Na Channel Blockers
-IA: Quinidine, phase 2 slows -IB: Lidocaine -IC: flecanide (tambor) |
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prototype for all Na channel blockers
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quinidine
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antiarrythmic meds are referring to
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vent tachy
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class II antiarrythmics
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Beta adrenergic blockers
proto: Inderal/propranolol -block SNS, MI kicks SNS in for life threatening arrythmia |
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class III antiarrhytmics
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K Channel blockers
-Amiodarone (Cardarone) |
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class IV antiarrhythmics
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Calcium Channel Blockers
-Verapamil (calan) |
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Na/Ca Channel blockers do what
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slows movement of Ca in and therefore Na too
-decreases HR |
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non-pharmacological tx of arrhythmias
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1. treat underlying disorder
2. valsalva or carotid a. massage 3. defibrillate 4. pacemakers, AICDS-shock heart 5. ablation |
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underlying disorders that could cause arrythmias
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MI
dehydration hypoxia hypoTN |
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valsalva or carotid a. massage for arrythmias
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forced air on closed glottics increases vagus tone
-PSNS take sover to decrease HR -Holding breath like a BM -Innervates vagus n with massage |
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ablation for arryhthmias
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destroys cells
map out conduction in elcrophys, EPS lab |
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causes of arrythmias
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-something changes rate
-conduction pathway block -combo of both **HYpoxia **Ischemia of heart: leading cause of death from MI -hyper and hypokalemia |
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4 different types of arrhythmias
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1. sinus: from SA node, basic brady and tachycardias
2. Atrial: fibrillation, flutter, digoxin tx 3. Nodal: AV node or jxnal 4. Ventricular: tachy, fibrillation meds for |
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bradycardia tx
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epi
atropine, anti-chol |
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ventricular arrhythmias
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-mechanism for meds: decrease rate
slow conduction myocardial depressants |
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arrhythmias assessment
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-V/S frequently (1-5min)
-Breath sounds -N/Headaches -Continuous cardiac monitor b/c BP can fall -mental status -normal CO, get disoriented and restless -Mental satus - |
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nursing dx/pt eval for arrhythmias
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-pot for decreased CO
-Alt in comfort -Fear, anxiety -Alt tissue perfusion -Activity intolerance -Self care deficit -FVE -Noncompliance |
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arrhythmias intervention
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1. IV pump, closely monitored
2. Resuscitation equip: life threatening 3. check pt freq: 24 hr care 4. explain procedures to pt: restless, disoriented, rails up, low bed 5. Safety |
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antianginal meds used for
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plaque build up
trickle of blood or vessels spasm and decreases teh amt of blood to an area of the heart -substernal pain in left arm and jaw |
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non-pharm tx for angina
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stop and rest
stop smoking wt loss decrease fat in diet relaxation stress management |
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3 classifications of antianginal meds
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1. organic nitrates
2. beta adrenergic blockers 3. ca channel blockers |
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organic nitrates prototype
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nitroglycerine
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what do organic nitrates do for antiangina
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-dilates veins: decreases preload or P in veins
-dilates coronary a. : increases myocardial flow -dilates arterioles: decreases afterload |
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what makes nitroglycerine a good drug for angina
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-decreases myocardial demand for O2
-increased blood supply to myocardium because it can affect smooth muscle |
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angina
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when you have an increased demand for O2 and you can't get it
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what can also cause angina besides lack of O2
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exercise
cigs stress anxiety cold weather |
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beta adrenergic blocker prototype
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inderal, given PO can have nitro too
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beta adrenergic affect on angina
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-decreases HR, - chronotropic, - inotropic
-lower BP, decrease myocardial worload and O2 demand -can use long term for angina to lower severity -increase exercise tolerance - |
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ADE of beta adrenergic inderal
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hypoTN
lower HR (bradycardia) bronchoconstriction w/ no lung disease |
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angina v MI
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angina subsides in a few minutes with treatment or rest...less than 10
-MI: if you stop doing or treat and pain stays |
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calcium channel blockers prototype
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verapamil
calan |
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Ca channel blockers action on angina
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slows the movement of extracellular Ca into the cell
-coronary & periph art. dilation= lower afterload -lower myocardial contraction= - inotropic -conduction sys is depressed = neg dromotropic .treats HTN too |
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ADE of nitro
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hypoTN
headache tachycardia dizzy |
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teaching pt when to call 911 with angina etc after taking nitro
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-take nitro dose w/ pain and then rest
-5 min later still pain: 2nd dose -another 5 min: still pain take 3rd dose and call 911 |
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nitro patch pt teaching
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wear gloves
can be absorbed quickly headache put on a non-hairy area, rotate sides -tolerance: 1st thing in morning and take off at bedtime |
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assessment for nitro
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-want baseline vitals
-sitting/laying for 1st dose -bed if IV -systole <90, hold nitro so you don't drop further -infusion pump -check vitals freq -need wet mouth for sublingual dose -teach importance of spacing doses |
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thiazides prototype
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chlorothiazide
(diuril) |
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contraindications for thiazides
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-bad if allergic to sulfas
-mild vasodilation -not if you need immediate diuresis |
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thiazides lose
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water
K Na/Cl |
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thiazide risk and what its good for
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risk of hypokalemia
-2-4 hours moderate activity good for ROUTINE use |
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uses of thiazides
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HTN
edema CHF |
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loop diuretics prototype
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furosemide (lasix)
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loop diuretics lose
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water
K Na and Cl |
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uses of loop diuretics
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HTN
edema CHF renal diuresis **Immediate diuresis |
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when you see results with loop diuretics
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IV in 5 min
PO 30-60min |
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K+ sparing diuretic prototype
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spironolactone
(aldactone) |
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K+ sparing diuretic uses
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HTN
liver disease |
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K+ sparing diuretics lose and gain
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lose water and na and cl
gain K |
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contraindications for K+ sparing diuretics
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Renal disease
K supplements -Aldosterone agonist, makes body retain water and Na...so blocks this |
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osmotic diuretic prototype
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mannitol
(osmitrol) |
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osmotic diuretic loses
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water
K Na Cl |
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uses of osmotic diuretics
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to increase ICP with traumatic brain in jury
-glaucoma -oliguria: <400ml in 24 hrs -anuria <100 ml in 24 hrs -short term IV use |
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HTN increases the risk for
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MI
CHF CVA and hemorrhage Renal disease |
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regulation of arterial Bp
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1. CO (systolic P)
2. PVR (diastolic P) 3. nervous and hormonal sys 4. renal sys |
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difference between NS/hormonal sys and renal sys with arterial BP
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NS/hormonal are fast acting and renal is slow
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cardiac output (systolic P) with arterial BP
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CO= HR x SV
stroke vol is amt of blood ejected with each beat./systole 60-90ml of blood -increased HR means you can;t adequately fill ventricles |
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PVR (diastolic P)
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peripheral vascular resistance
-vascular tone -determined by constriction and dilation -constriction: increases tone and P -dilation does opp, w/ dec resistance |
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bodily response to hypotension
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-lower BP->baroreceptors -> SNS stim
-lower renal blood flow->SNS stim -renin is released, ang I-->Ang II -constriction of arterioles = high PVR = high BP and afterload |
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what does renin do with aldosterone in response to hypoTN
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renin makes it secreted
-kidneys hold on to Na and water -increases blood vol increases CO and BP increases preload |
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HTN values of systole and diastole
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systolic >140 mm HG
diastolic > 90 mm Hg |
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primary/essential HTN
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no direct cause
makes up 90-95% of cases |
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secondary HTN
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renal, endocrine or CNS disorder
-drugs they're on (sympathomimetic) -usually result of lifestyle choices -find cause and will cure 5-10% |
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issue with HTN control
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less than 30% of cases are
-compliance prob ADE, cost, remembering, asymptomatic |
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diuretics assessment
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-monitor BP because of lower fluid
-Na: 135-153 K: 3.5-5.5 Cl: 95-110 -Weigh daily bc pitting edema is subjective 1L=2.2 lbs -intake/output sheet -orthostatic hypoTN -preg/lactating risk benefit |
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hypertension,...whats going on
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-increased cardiac workload
-arteriosclerosis: a. thickening -lumen of vessels narrows and decreased blood to tissues -increased risk of thrombosis -can lead to hypertrophy of myocardium..compensatory -m. can fail because it works continuously w/ workload - |
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s/s with HTN
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ASYMPTOMATIC
-don't see whyt hey need meds -usually undetected until MI, CVA etc |
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HTN treatment
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stepped program
1. lifestyle modifications: if pt is asymptomatic in pre HTN phase 2.diuretics: 140/90 or s/s of HTN, start meds immed and lifestyle changes 3. antiadrenergic : add 2nd drug if it doesnt work 3rd...max drug dosage 4. direct acting vasodilators 5/ angiotensin convering enzyme inhib (ace inhib) 6. ang II receptor blockers 7. Ca channel blockers |
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antiadrenergic drugs
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alpha 1 blockers
alpha 2 agonists alpha beta blockers beta blockers |
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alpha 1 blockers prototype and describe
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cardura
-peripheral, a. dilate and dec vasc resistance -prob w/ 1st dose, orthostatic hypoTN -cardiac palp, syncope, pass out -1-3 hrs after -give at bedtime -easier for men with BPH to pee |
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issue with alpha 1 blockers
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long term cause of Na./H20 retention
need to use with diuretic |
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alpha 2 agonists prototype
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methyldopa or aldomet
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alpha beta blockers prototype
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coreg
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beta 2 blocker
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lung bronchodilators
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direct acting vasodilators prototype and action
|
hydralazine
-on smmooth muscle BV's to vasodilate and decrease BP |
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ACE inhibitor prototype and action
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captopril
-blocks enzymes for ang I- II use with CHF and diuretic -vasodilate and decrease P decreases afterload -decreases aldosterone production so you can rid Na and water =decreased preload (***total decrease in hearts workload |
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ADE of ace inhibitors
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10-20% of pts get persistent dry cough
-prob with sleep and daily fxn sexual dysfxn not as effective with blacks |
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ace inhibitors are good for
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diabetics, preserve kidneys
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angiotensin II receptor blockers prototype and uses
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losartan
-stops from going to receptor site -cant vasoconstrict so it dilates -decreases BP and periph vasoconstriction -use for CHF too -no cough combine with diuretic |
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chf caused by
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MI
HTN anything that decreases pumping ability or increases the workload of the heart...decreasing CO |
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compensatory mechanism for CHF
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lower CO but increases initially
1. increased sympathetic activity = higher workload, myocard contract 2. activation of renin-ang-ald system = high afterload, preload 3. ventricular hypertrophy |
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CHF, what happens with increased preload, afterload and workload
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initially effective: myocardium diseases eventually
-LV stops fxning properly Eventually: -lower BP and higher HR -lower periph. perfusion -crackles, tachypnea -pulm congestion/edema -FVE -cardiomegaly |
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nursing dx/PT eval of CHF
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-impaired gas exchange
-altered tissue perfusion r/t decrease in CO (cardiac, cerebral, renal, peripheral) -decrease in CO r/t arrythmias -FVE -Activity intolerance -Self-care deficit -Noncompliance -Knowledge deficit |
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why impaired gas exchange with CHF
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bc of venous congestion/fluid accumulation in lungs
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decrease in CO and arrhythmias in CHF reason
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increased hypoxia increases risk
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FVE in CHF
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because aldosterone retains Na/water
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chf noncompliance because
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long term drug tx
|
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goal of drug therapy for CHF
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1. improve myocardial fxn - make heart more effective pump to increase CO
2. alter compensatory mechanisms |
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drug therapy for CHF
|
1. ace inhibitor
2. diuretics 3. cardiotonics 4. beta blockers 5. vasodilators |
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diuretics for CHF
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quick lasix
dec blood vol excretes na/h20 dec preload |
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alpha blockers suppress
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SNS
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vasodilators for CHF
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1. venous dilators: nitrates...dec preload
2. arterial dilators: hydralazine -decrease afterload |
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outpatient treatment for CHF
|
inotropics IV, vasodilate
to decrease preload and afterloads -sit up in chair -4 hrs/ 2x a week -dec # of hospitalization increases quality of life |
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anticoagulant
|
prevents venous clots
|
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antiplatelet
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prevent arterial thrombus
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thrombolytic
|
lyse thrombus
|
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anticoagulant drugs
|
1. heparin: lab PTT
2. Fragmin & lovenox 3. Coumadin-lab PT/NR |
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heparin antidote
|
protamine sulfate
|
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coumadin antidote
|
vitamin K
|
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anticoagulant prototype
|
heparin
|
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coumadin use
|
long term to prevent and treat clots
-DVT, atrial fib, post mech heart values |
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contraindications for coumadin
|
bleeding ulcers
severe liver or kidney disease HTN recent surgery on eye, SC, brain |
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dosing of coumadin
|
depends onf PT/INR
PT= 12-13 s normal want to 1.5x increase so aim for 18 s INR: 2-3 -initially check PT/INR daily and then once regulated every 2-4 weeks test |
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PTT draw with IV and subq
|
IV = draw anytime
subq - draw 1 hour before next dose |
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how is heparin given and coumadin
|
hep is IV or sub q
coum is oral |
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PTT values
|
25-35s is normal, prlong it though
1.5-2x norm so 38-70s is therapeutic time |
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antidote signif with heparin
|
protamine sulfate
short duratin about 2 hours os give frequently |
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what does coumadin do when do you go on it
|
when you go home off heparin but stay on heparin because it's not effective for 3-5 days
-acts in liver to prevent synthesis of vit K |
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when does heparin take effect with IV and subQ
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IV is immediate
subq is 20-30 min |
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perk of heparin
|
preg or lactating can take it
doesnt go into milk |
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when would heparin be prescribed
|
-bed rest more than 5 days
-prophylactically to prevent clots -history of thrombophlebitis, DVT, pulmonary embolism -major ab or orthopedic surgery |
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fragmin and lovenox signif
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low molecular weight heparin
perk is you dont have to watch PTT come pre made in syringe |
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antiplatelet drugs
|
asa, nsaid
ticlid, plavix glycoprotein IIb/IIIa Receptor antagonists **fxn is to interfere with platelet adhesion |
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asa/nsaid signif with platelets
|
nsaid is only as long as the drug is in circ
-asprin is in there for the life of the platelet and binds irreversibly with a single dose |
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ticlic plavix are often prescribed for
|
ppl who can't take aspirin
|
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glycoprotein IIa etc prototype and use
|
aggrastat
-inhibits platelets from binding -use with heparin -IV to prevent thrombus or treat a thrombus within an a. |
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contra for glycoprotein IIb
|
low platelet count
major surgery trauma active bleeding |
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thrombolytic drugs are used to treat
|
acute-severe thromboembolic disease
-MI -pulm embolism -clot in a. |
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thrombolytic prototype
|
activase
|
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goal of thrombolytics
|
re-establish blood flow and prevent tissue damage
|
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antidote for thrombolytics activase
|
amicar
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tx with thrombolytics, specifications and guidelines
|
MI: time = tissue, re-est perfusion in less than 30 mins
- cant treat after 4 hours from onset of s/s like chest pain |
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ade of thrombolytics
|
bleeding: internal, gi, cranial, UG
ext: IV, puncture |
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contraindications for thrombolytics
|
bleeding
CNS surgery stroke trauma within last 2 mos |
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normal v high chol
|
norm is less than 200
high is >240 |
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hyperlipidemia
|
modifiable risk factor for atherosclerosis
can reduce morbidity from CAD by dec lipids |
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|
management of hyperlipidemia/how to treat
|
-stop meds that increase lipids : roids, b-blockers
-low fat diet -increase soluble fiber, oats-f+v -lose weight (10%) -exercise (30 min 5x) -stop smoking |
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|
atherosclerosis/hyperlipidemia major cuases of
|
ischemia
HD MI stroke PVD angina death |
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|
drug therapy for hyperlipidemia
|
statins: lipitor
bile acid sequestrants: questran fibrates: lopid niacin: nicotinic acid |
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|
statins/lipitor effect
|
decrease chol made
-lowers chol, LDL, TGs -2-6 weeks for max effect -decrease CAD risk by 25-60%, death by 30% -dec risk of angina, stroke, PAD< angioplasty and open heart |
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|
drugs to treat hyperlipidemia,..guidelines
|
6 mos trial of lifestyle changes before if they are asymptomatic for CAD
-immediate if diabetic or smoker -can prevent/delay or promote regreggion of already |
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bile acid sequestrant actions
|
binds bile acids in intestines and is excreted in feces
|
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|
fibrates action and ade
|
lower TGs
high TGS >1000 is indication for use ADE-GI discomfort |
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niacine and ade
|
OTC
lowers chol and TGs -need high doses which means more ADES |
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|
where does chol come from
|
1. synthesized in liver2
2. diet |
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|
serum chol is responsible for
|
atherosclerostic plaques in BV linings..narrows them, get MI and stroke
-correl with high sat fat, trans fats, lack of exercise and stress |
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TG normals
|
<200
stored in adipise stress, diab, obesity, diet, high alc use increase |
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|
HDL norms etc
|
>60 norm
<35 is bad -not directly affected by diet -increase with exercise, mod alc intake -dec with obesity, diab uncontrolled, smoking, roids |
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ldl norms etc
|
<100 norm
high sat fat will increase -high LDL, tgs and chol linked with cvd |
