what do antidysrhythmics do?
prolonging the AV node
increase or decrease conduction speed
altering ectopic pacemaker
group of cells that causes a premature heart beat outside the normally functioning SA node
altering the SA node
reducing myocardial excitability
inc Na, K can affect
lengthening the refractory period
resting period
stimulating the autonomic nervous system
vaughan-williams classification
sodium channel
class 1A, 1B, 1C
beta adrenergic
class II
potassium channel
class III
calcium channel
class IV
miscellaneous
class V
digoxin has pos. inotropic effects
all have neg. dromotropic & chromotropic effects
class 1A meds: sodium channel blockers meds
procainamide (short term)
for dysrhythmias at that moment
quinidine (long term)
had dysrhythmias and want to send this med home w/ them
class 1A meds: sodium channel blockers patho
slows conduction throughout the electrical system in the heart
slows down atrial and vent. pumps
delays repolarization
ses: SVT, vtach, afib, aflutter
class 1B: sodium channel blockers med
lidocaine
also used for anesthesia
class 1B: sodium channel blockers patho
dec electrical conduction & automaticity
increases rate of repolarization
class 1B: sodium channel blockers uses
short term for ventricular dysrhythmias like PVCs
if multiple = not good = bolus of lidocaine
class 1C: sodium channel blockers med
flecainide
class 1C: sodium channel blockers patho
this is conduction speed throughout the electrical conduction system
may also use the valsava maneuver
massage carotid
submerge hands in cold water
class 1C: sodium channel blockers uses
used for SVT
class II beta adrenergic blockers meds
propranolol
esmolol
class II beta adrenergic blockers patho
prevents SNS stimulation of the heart
decreases all kinds of things: HR, automaticity through the SA node, velocity conduction through the AV no, myocardial contractility, atrial ectopy
class II beta adrenergic blockers uses
afib
aflutter
PSVT
HTN
angina
PVCs
MI
class III potassium channel blockers meds
aminodarone
sotalol
class II and III properties
class III potassium channel blockers patho
prolongs action potential (electrical impulse) and refractory period of the cardiac cycle
reduces automaticity in the SA node, contractility and conduction in the electrical system, dilates coronary blood vessels
also use epinephrine
monitor K levels
class III potassium channel blockers uses
conversion of afib
vfib
vtach
aflutter
class IV calcium channel blockers meds
verapamil
diltiazem
class IV calcium channel blockers patho
depresses depolarization and decreases oxygen demand of the heart
decreases force of contraction, HR, slows conduction rate of the action potential
check bp before giving b/c may cause vasodilation
class IV calcium channel blockers uses
afib
aflutter
SVT
HTN
angina
class V
adenosine
stops the heart for a few seconds
have crash cart nearby
has a short half life <10 secs
digoxin
apical pulse for 1 min
postive inotropic effect
class V patho
decreases electrical conduction thru the AV node
class V uses
PSVT
SVT
class V complications
bradycardia
hypotension
lightheadedness
class V effectiveness
ECG normal
alertness
absence of symp.
better contraction
inc BP, CO
medications affecting coagulation
PO/parenteral anticoagulants/SQ
direct thrombin inhibitors
direct inhibitors of factor Xa
antiplatelet meds
thrombolytic agents
don’t give to pts with ulcers, Crohn’s, ulcerative colitis, women on menstral cycle
assess bleeding (ext. and int.)
bruising
blue distended abd.
tachycardia
PLT/CBC labs
lightheadedness
gum/nose bleeding
hematuria
bloody stools
dec bp
parenteral anticoagulants
heparin
inpatient med
monitor labs esp. if IV hep
determine if effective
enoxaparin (lovenox) (low molecular weight heparin)
outpatinet
less risk for blood clots
parenteral anticoagulants lab values
PTT/aPTT
IV
q6h
therapeutic level if 2x normal
PTT: 60-70
aPTT 20-39
inc if not therapeutic
dec if too much
maintain if stable and labs achieved
labs less freq. after 2x normal therapeutic level
RN can adjust dose based on results
subQ
no labs
PLT
can cause heparin induced thrombocytopenia (dec plts)
heparin uses
acute conditions (anything w/ clots)
stroke
PE
massive DVT
MI
heparin patho
low dose for prophylaxis DVT (prevents clot formations)
heparin protocol
monitor labs
change based on therapeutic level
administration: IV, SQ
IV if pt has clot
subQ to lower the risk
burns more than lovenox
antidote: protamine sulfate
slow IV: no faster than 20 mg/min or 50 mg in 10 mins
food interactions
herbal ginger
ginkgo biloba
feverfew
evening primrose oil increase bleeding risk
heparin complications
hemorrhage
HIT (heparin induced thrombocytopenia)
enoxaparin uses
prevent DVT prophylactically in the hospital setting
treat DVT and PE
enoxaparin
low molecular weight heparin (LMWH)
conjunction with warfarin
q24 hr dosing
longer half-life
longer to metabolize
antidote: protamine sulfate
slow IV: no faster than 20 mg/min or 50 mg in 10 mins
expensive
educating on self administration: enoxaparin
“bridge therapy”
enoxaparin for lower risk of clots but once a clot has formed then heparin used
use a small gouge needle for administration (25)
90 degrees
distance 2 inch from the umbilicus
burns and bruising can happen
pinch up an area and insert needle completely
do not aspirate
rotate sites
do not rub injection site
monitor for bleeding
pre-filled syringes: do not expel the air
inject entire contents (as ordered)
avoid aspirin, NSAIDs
inc risk for bleeing
use electric razor, soft toothbrush
warfarin (coumadin)
antagonize vit. k, preventing the synthesis of 4 coagulation factors: VII, IX, X and prothrombin
consistent intake of greens
NO DIET CHANGE
administration: PO
protein bound
med bounds to protein so don’t inc or dec
narrow TI
warfarin labs
PT/INR
PT: 9-12.5
INR: 1
therapeutic if 2x normal values
warfarin uses
venous thrombosis
afib
prosthetic heart valves
prevention of recurrent MI, TIA, PE and DVT
warfarin complications
hemorrhage
toxicity
administer vit. k as an antidote: IV, slowly and in a diluted solution
if vit. K is ineffective, administer FFP (fresh frozen plasma) or whole blood
warfarin contraindications
prior to surgeries or procedures
preg. risk X
heparin is better for preg. patients
pt with low platelet count
thrombocytopenic pts
interacts with many meds
contraceptives, anticonvulsant, etc
do med reconciliation
know drug interactions
foods in high in vit.K
spinach
canola oil
romaine lettuce
mayo
iceberg lettuce
broccoli
brussel sprouts
parenteral anticoagulants nursing considerations
heparin and warfarin
consistently take at same time
full therapeutic effect in 3-5 days
when discharging and the pt has schedules heparin and warfarin since they are going home with warfarin and not heparin, they would still take the heparin and the warfarin b/c warfarin takes 3-5 days to take full effect
PT/INR
2-3 (afib)
3-4.5 (heart valves)
advise pts to move around to avoid clots forming
use a soft-bristle toothbrush to avoid gum bleeding
direct thrombin inhibitors meds
dabigatran
bivalirudin
desirudin
dabigatran (pradaxa) patho
prevents thrombus from developing
advantage: less blood work monitoring
antidote: idarucizumab (praxbind)
dabigatran uses
prevents stroke from afib
treat DVT
prevent PE
dabigatran complications
bleeding
GI effects
bivalirudin patho
used to prevent blood clots during angioplasty
desirudin patho
used for pts having hip replacements
antidote for direct thrombin inhibitors
none
direct inhibitor of factor Xa meds
rivaroxaban (xarelto)
apixaban (eliquis)
direct inhibitor of factor Xa uses
afib
prevention of DVT and PE in pt undergoing hip or knee arthroplasty
direct inhibitor of factor Xa patho
prophylaxis for stroke and embolism in afib
monitor h&h, LFTs periodically
antidote: andexanet alfa (andexxa)
if starting to bleed
antiplatelets
antiplatelet/salicylic
antiplatelet/glycoprotein inhibitor
antiplatelet/ADP inhibitor
antiplatelet/arterial vasodilator
antiplatelet/salicylic med
aspirin
targets clot itself, destroys PLTs
antiplatelet/salicylic uses
prevention of
MI
reinfarction
stroke
TIA
antiplatelet/salicylic complications
GI upset: NSAIDs
prolonged bleeding time
tinnitus
hearing loss
ototoxicity
minimize use of other meds which enhance bleeding
one antiplatelet and one anticoag = don’t add more cause inc risk for bleeding
antiplatelet/glycoprotein inhibitor med
IV infusion
eptifibatide (integrilin)
antiplatelet/glycoprotein inhibitor uses
acute coronary syndrome
cardiac catherizations
cardiac specific
antiplatelet/glycoprotein inhibitor antidote
none
antiplatelet/glycoprotein inhibitor complications
hypotension
bradycardia
prolong bleeding time
antiplatelet/glycoprotein inhibitor nursing considerations
monitor cardiac catheterization access site; apply pressure
monitor for gastric bleed, bruising, petechiae, bleeding gums
antiplatelet/glycoprotein inhibitor patho
glycoprotein is given to connect the plts together therefore glycoprotein inhibitors prevent the connection of plts
antiplatelet/ADP inhibitor meds
clopidogrel (plavix)
pasugrel (effient)
antiplatelet/ADP inhibitor patho
ADP are receptors on the walls of plts that help plts stick together, ADP inhibitors prevent the receptors from binding to each other so glycoprotein will not form either
antiplatelet/ADP inhibitor uses
acute coronary syndrome
prevention of ischemic stroke
TIA
MI
re-infarction
usually, pts start after coronary angiography with stent placement
antiplatelet/ADP inhibitor complications
prolonged bleeding time
gastric bleed
thrombocytopenia
GI effects
antiplatelet/ADP inhibitor contraindications
pts with bleeding disorders
peptic ulcer disease
intracranial bleed
thrombocytopenia
use cautiously with other meds that enhance bleeding
stop 7 days before surgery
herbal supplements
ginger, ginkgo, biloba, feverfew, and evening primrose oil inc bleeding risk
antiplatelet/arterial vasodilator meds
pentoxifylline
enhances O2 cap. carry in RBCs
dipyridamole
antiplatelet/arterial vasodilator uses
commonly used for pts with PAD
intermittent claudification
cramping in leg caused by exercise
antiplatelet/arterial vasodilator complications
GI upset
thrombolytic meds
alteplase (activase)
aka TPA: tissue plasminogen activator
tenecteplase
reteplase
thrombolytic patho
dissolves clots
converts plasminogen to plasmin, which destroys fibrinogen and other clotting factors
thrombolytic uses
MI (when cath lab isn’t available)
massive PE
ischemic stroke
restore patency to central IV lines
PAD w/ embolic clots in different vessels
thrombolytic complications
serious risk of bleeding
thrombolytic nursing considerations
limit venipuncture and injections
apply pressure dressings to recent wounds
monitors for changes in patient’s condition
monitor h&h, aPTT, PT
thrombolytic contraindications
HTN
rupture of vessels = internal bleeding
if in the brain = hemorrhagic stroke
joint commission core measures for an MI
aspirin on arrival to ER/prescribed at discharge
BB at discharge
dec size of infarction
statin at discharge
LDL <100
ACE/ARB at discharge for LVSD
acute coronary syndrome (ACS) AHA
treatment of ACS involves the initial use of drugs to relieve ischemic discomfort, dissolve cots, and inhibit thrombin and platelets
oxygen
aspirin
nitroglycerin
opiates
morphine
sedative, anti-anxiety, pain
fibrinolytic therapy
heparin