Exam 3- Cardiac, diuretics, anticoagulants, thrombolytics Flashcards
Flow of blood through the heart and
systemic v pulmonary circuit
inferior/sup vena cava R atria tricuspid valve R ventricle pulm semilunar valve pulm trunk pulm arteries lungs
reoxygenated blood into heart via pulm veins L atria mitral valve L ventricle aortic semi-lunar valve aorta ascending aorta body
pulmonary circuit- pulmonary arteries to veins (lungs)
systemic circuit- aorta-vena cava (body)
electrical stim pathway of heart
top to bottom
SA node, AV, apex, Purkinje fibers, ventricles (contraction starts at bottom)
primary pacemaker of heart- signal from atria to ventricles
stimulated by bradycardia (sympathetic ns) function- depolarize sinoatrial node (in uppr prt right atrium)
transfer signal via AV
beta 2 v beta 1 receptors
beta 1- stimulate AV node= inc heart contractility
can contribute to vent remodeling w/ pt that have heart failure
beta 2- stimulate sympth nervous system= bronchodilation
L v R sided heart failure
L- blood backs into pulm system, hypertrophy/ overstretched L ventricle= dec SV= dec CO
“congestive heart faliure” s/s hypoxia and trouble breathing
R- blood backs into venous system= inc p pulm arteries= pulm edema, jugular venous distention, ascites
alpha 1 receptors
cause vasoconstriction and sm musc contraction
s/s heart failure
dec cardiac output= fatigue, exercise intol
FVO- crackles (L HR), pulm edema, inc rr, SOB, distress dec o2
(R HR)- distended jugular veins, periph edema
systolic v diastolic HF (b/ left sided)
systolic- dec contractility- hF w/ reduced ejection fraction
diastolic- shortened filling/relaxation time- HF w/ preserved ejection fraction
classification of HF- AHA stage v NYHA functional
aha- structural- A-D *need to know ejection fraction to test structural changes
A= high fisk but no structural changes of s/s
B-=structural changes, no s/s
C= structural changes w/ prior or current s/s
D= changes and s/s at rest- need specialized interventions
functional- s/s I-IV (based on pt ability to function, and complete ADL) I-asympt II-symptom w/ mod exertion III- sympt w/ minimal exertion IV- symtom at rest
heart failure def + causes
dec tissue perfusion
abnormal heart function
cause- CAD, HTN
cardiac output
hr x stroke vol min/mL amnt blood pumped/min normal 3-7 L/min dec heart rate or sv= dec co
stroke vol
mL/contraction x # beats/min
dec sv=dec co
contractility
(inotropy) strength of muscular contraction of the heart
dec contractility = dec co
inc contractility= inc sv=inc co *till a certain point (if too stretch myosin fibers have no leverage)
preload- def and causes of inc/dec
amnt stretching of ventricular cardiac musc before a contraction begins
dependant on vol fluid in ven
heart failure= inc preload
inc vol= inc preload= inc contractility (until certain point)
dec vol= dec preload= dec stroke vol= dec contractility= dec co
ideal is btw 8-12
causes dec= hemorr shock, dehydration= dec contact btw actin and myosin fibers (too srunched)
inc= fluid overload= dec contact of fibers
ejection fraction
percent of blood in LV leaving w/ e/ contraction
dec contractility= dec EJ
afterload
resistance against which LV has to work to push blood into arteries
factors- SVR (p in arteries) can inc w/ vasoconstriction
inc svr= inc afterload (P)
inc svr + additional V fluid from heart failure (preload) w small valve opening = inc p/workload= L ventricular remodeling
purpose of measuring bp
tells us lvl resistance
diastolic- resting state
systolic= CO
MAP= afterload
pathway of hf
dec EF- dec contractility- dec CO- inc sympathetic activation- stimulation of beta 1 recep. (vasoconstriction, fluid retention)- inc hr and contractility- alpha 1 recep activation (inc pvr and inc afterload P)- inc myocardial workload- dec co- dec renal perfusion- inc renin secretion- inc angiotensin 1- angiotensin 2 (vasoconstriction, fluid retention and inc bp) *also cardiotoxic at high lvls can cause v remodeling
fluid retention bc- inc aldosterone (na and h2o retention- further inc preload- L HF-pulm edema and R HF- peripheral edema)
natrietic peptides
stimulated by hypertrophy LV
anp/bnp- natural diuretic/vasodil
goals of pharmacologic therapy in hf
improve QOL and dec mortality/morbidity
by inc contractility
dec afterload, elevations in preload, ventricular remodeling, peripheral (R) and pulm edema (L)
classes meds to trt hf
ace inhib angiotensin recep neprilisyn inhib (ARNI) cardiac glycosides diuretics beta blockers
ace inhib- types, action and indications
lisinopril, enalapril, captopril, benazepril
action- dec conversion from ang 1 to ang2= dec preload and afterload
indications- hf, htn, dec mortality and morbidity after MI, prevn diab nephropathy (dec p and therefore damage of glomerular basement mem)
need to take if EF < 50% or s/s HF bc can dec prel, afterload and vent remodeling while improving EF
ace inhib- containdications, pharmacokin
coindiated- preg/lactation, hypersen (angioedema), renal impairment
pharmacokin- Po, duration 24h, 100% renal elimination
ace inhib- ae
hypotension (dec ang2= dec ability vasoconstrict)
watch after 1st dose! and espec if FVD (dehydration)
persistant dry cough- if block converting enzyme= inc bradykinin= inc dry cough
angioedema- inc risk as inc bradykinin (swelling of throat, feeling fullness, something stuck in throat)
hyperkalemia- flip btw na and K, dec ang 2= dec aldosterone= dec fluid retention= inc K 3.5-5 can result in vent tachy- cardiac dysrhyth
angiotensin II receptor blockers (ARBs)- types-action and indication
Valsartan, Losartan, Candesartan
block effects ang 2
so same effect as ace just different chemical process (not acutally inhibit converting enzyme so no inc bradykinin)
therefore no inc problems w/ dry cough and angioedema
angiotensin II receptor blockers (ARBs)- pharmacokin v ace i
valsartan- liver metab, majority excreted via feces
losartan- extensive liver metab, excreted by kid as active metab
candesartan- prodrug- excreted in urine and majority in feces
** more liver metab, less kidney excretion worry
relationship btw vasodil and afterload
and aldosterone and preload
inc vasodil= dec SVR= dec constriction= dec afterload (P)
dec aldosterone= dec fluid retention= dec preload
Angiotensin recept- Neprylisin inhib (ANRI)- type, action, indication
ARB (valsartan) combo w/ neprylisin inhib (sacubitril) Entresto
neprylisin enzyme inactivates natrietic peptides (respon diuretic/vasodil)
inhibiting enzyme will inc anp/bnp= inc diuresis= dec preload and vasodil= dec afterload
preferred med if not taking anything to control HF
if switching to this frm acei need to stop taking acei or arb for 36h or high risk for angioedema
trial- improved HR s/s, dec hospitalizations and reduced mortality
nursing considerations for acei, ARB and ANRI
monitor bp (hypotension), incl orthostatic changes
monitor angioedema (esp w/ acei or switching)
monitor bun, cr, K+
renal bc acei fully excreted via kidneys, risk for hyperkal in acei
pt education- change position slowly, avoid salt sub w/ acei (already high ris k for inc K due to dec aldosterone)
cardiac glycosides (Digoxin)- action, indication
trt a-fib and control hr
action- inc contractility by inc Ca into musc cells= stronger contraction and enhance parasympath ns (vagal influences)= dec onduction via AV node frm artrial to ven= dec hr aka “rate ventricular contracting”
cardiac glycosides (Digoxin)- containd, route, pharmacokin
contraind- av heart block (rhythm abnormality delays conduction thru AV) so adding digoxin can exacerbate block
WPW- abnorm conduction pathway otherthan AV, so if shut off main pathway can overstim alt pathways
hypokalemia
renal impairment, acute MI (inc contractility= inc o2 demand= ae of MI)
trt MI before admin
route- Po or IV
pharmacokin- unchanged by kid
cardiac glycosides (Digoxin)-ae and inc risk
ae- bradycardia**
n/v, anorexia, abdom discomfort earliest s/s
blurred vision, green/yellow aura (halo arnd lights)
inc risk w/-
hypokalemia (K and med compete for same cardiac cell recep so if K is depelted med has more room to be activated and therefore cause toxicity)
extremes in age (inc sensitivity)
use loading doses
give inc dose so drug reaches theraputic range faster but can overshoot this and cause toxicity)
hypoxia (inc contract= inc o2 demand)
impaired renal function
cardiac glycosides (Digoxin)- nursing considerations
monitor apical pulse 1 min- hold if <60
continuous EKG for IV admin
assess therapeutic effect (should hold hr and stop afib)
geriatric consdier (ink risk falls if bradycardia bc dec sv=dec co= dec perfusion= syncope)
monitor labs (cr, bun, gfr, K+)
pt ed- how assess own pulse
hold med if <60
s/s dig toxicity (GI, visual changes, bradycardia)
test for pt w/ possible digoxin toxicity
K, bun, cr, gfr labs
akg
continuous heart monitor
if comes back positive- dig lab lvl
hold med
k supplement
temporary pacemaker (external transcut or transvenous)
types diuretics
loop
thiazide
aldosterone antagonists
loop diuretics- types, moa, indication
bumetanide (Bumex) po oriv
furosemide (lasix) po/iv *can dev resistance
torsemide (Demadex) iv only
moa- act on ascending loop to dec na and h20 resorption= inc excretion
indications- edema, s/s HF (dec vol= dec P on vessles= dec afterload), renal dis, hepatic cirrhosis, HTN
loop diuretics- pharmacokin, ae
absorbed in GI tract
onset po- 1h, IV 5-10 min
ae- electrolyte depletion (K)
s/s- weakness, dizziness, leg crmps, vomiting, confusion, dysrthmias
need K replacement -always check!
Gi disturb- diarrh, anorexia, stomach pain/cramping
hypotension- hold if <100
ototoxicity w/ IV admin if push too fast!
impaired glucose tol (might need inc insulin)
FVD or s/s overdiuresis- dry muc mem, dec urine output
reflected in labs- dec blood vol= dec LV supply= dec preload= dec sv= dec co= dec kidney function
=inc Cr, BUN, gfr (rapid)
loop diuretics- interactions
digoxin- toxicity/ hypokalcemia
corticosteroids- hyperglycemia and hypokalemia
warfarin- inc anticoag effect
inc hypotension w/ o/ antihtn meds
aminoglycoside antib “gentamicin”- ototoxicity
thiazide diuretic- type, moa, indication
hydrochlorthiazide (HCTZ)
moa- block na and cl reabsorption in distal tubule
indications- htn,
edema-HF, renal dis, cirrhosis, corticosteroids, estrogen therapy
thiazide diuretic- pharmacokin and contraindications
pharm- po, excreted unchanged by kidneys
contraind- allergy to sulfonamides. impaired renal function, lactation, pregnancy (jaundice/thrombocytopenia)
thiazide diuretic- ae and interactions
ae- hypokalemia, hypotension, inc uric acid (gout), hyperglycemia, gi (n/v, constipation), hepatitis (liver inflamm), pancreatitis
interactions- inc hypotension w/ o/ anti htn
corticosteroids- hyperglycemia, inc excretion k (hypokalemia)
digoxin- toxicity and hypokalemia
*similar to loop diuretics
aldosterone antagonist- type, action, indication
K+ sparing (dec aldosterone = inc K)
“Spironolactone” (Aldactone)
action- inhib aldosterone dec h2o and na resorption, inc K
indication- excess fluid assoc w/ HF and hepatic cirrohsis
can inc survival in pt w/ mod-severe HF
aldosterone antagonist- ae and interactions/ contraindicated
ae- hyperkalemia, skin rash, gi disturb, dizziness, sex hormone abnormalities (menstrual and gynecomastia)
interactions- caution w/ acei (inc risk hyperkalemia)
anticoag inc risk bleeding
digoxin- med can inc dig accum= inc risk toxicity
general diuretic considerations and pt ed
admin in am and early evening- prevent falls admin iV slowly 20mg/mL po diur w/ food dec gi monitor bp, hold if <100 weigh daily, I&Os labs- cr, bun, gfr, K bg's fluid imbalance (excess or deficiet) pt ed- older women don't take cause can cause incontin K+ supplements and s/s hypokalemia low sodium diet (no salt sub w/aci bc risk hyperkalemia) postural hyptension
structural effects hf meds- all types
acei / ARBs- dec afterl and prel, dec vent remodeling ANRI (neprilisyn inhib)- dec afterl and prel, dec vent remodeling cardiac glycosides (digoxin)- inc contactility diuretics- dec prel, afterl, and edema (pulm and peripheral) beta blockers- dec afterl, dec SNS stim of heart, dec vent remodeling
Virchow’s triad- purpose
factors involved in increased clotting risk
Virchow’s triad- genetic/ aquired
genetic- prothrombin deficiency, alteration in clotting cascade
aquired- inflamm response (inc platelet or rbc) Chronic hypoxemia (COPD), stimulation of erythropoietin (Polycythemia) Can vary w/ geographic areas (elevation changes)
Virchow’s triad- 3 causes
Damage to endothelium
IVs, fractures, dislocations, CVD (atherosclerotic changes)
Blood stasis
Surgery, decreased mobility, atrial fibrillation
Venous (DVT/PE)
Hypercoagulability
Dehydration (inc viscosity), hematological disorders
Drugs- ex. Oral contraceptive
anticoag action
prevent clot formation and extension
Taken after surgery
antiplatlet action- venous v arterial
interfere with platelet activity Venous v arterial clots V- DVT d/t venostasis Composed of clumped RBC A- caused by platelet aggregation (atherosclerotic changes) CAD Dec ratio of RBC
thrombolytic agent action
dissolve existing thrombi
clot lysis
anticaog- types
heparin (UFH)
low molecular weight heparin
enoxaparin (lovenox)- parental
oral- zarelto and warfarin (coumadin)
intrinsic pathway
contact activation
monitors heparin
labs- PTT
thrombin
extrinsic pathway
act. w/ tissue damage
warfarin
monitor PT/INR
prothrombin
role thrombin
converts fibrinogen to fibrin (end stage clot dev)
heparin inhib thrombin
warfarin inhib prothrombin (step before)
PTT lab
intrinsic (heparin)
range- 1.5-2.5 times baseline
heparin assay
same as PTT but more expensive
range- 0.3-0.7
PT/INR
extrinsic (warfarin)
range- 2-3 sec commonly
2.5-3.5 for mitral mechanical valves
PT/INR, heparin assay/ PTT needed in?
anticoag
not applicable if admin anti-thrombotics!!
short-acting parenteral anticoag- types
heparin and LMWH (Lovenox/ enoxaparin)
heparin- action and indications
Actions Potentiates the action of antithrombin Inhibits factor Xa Prevents formation of thrombin Blocks thrombin activity (converting fibrinogen to fibrin) Inhib intrinsic or common pathway
Indications
Prevention and management of thromboembolic disorders
Ex: DVT, PE, Atrial fibrillation, MI, CVA
Maintain patency of IV catheters
heparin- route
IV drip- for therapeutic trtment (PE)
SubQ- prophylactic (given q8/ 12 depending on risk)
Not Po (cannot cross GI mem., lrg molecular size)
heparin- pharmacokin
metab- liver,
elim- some renal, most endothelial cells
* no predictable action after subq
subq peak- 2h, duration8-12h
IV peak- 5-10 min, duration 2-6h
heparin– IV admin
used as therapeutic trtmnt
dosed as bolus w/ continuous IV (weight based)
heparin IV considerations
Monitor PTT (partial thromboplastin time)
Therapeutic range 1.5-2.5 Xs baseline or level determined by specific lab (varies w/ facility)
Normal PTT 25-35
Ex. Normal therapeutic range- 1.525 and 2.535= (37.5- 87.5)
Alternative: Monitor heparin assay (Anti-Factor Xa Level)—goal 0.3-0.7
Benefit- less variable btw individ.
heparin subq admin and considerations
abdomen only, dec risk bleeding, less mvmnt):
SubQ route effective for prophylaxis only
Dosed 5000 units SubQ every 8-12 hours
Never given IM (inc risk bleeding bc high vascularity)
most severe bleeding site v most common
common- GI
severe-cranial
protamine- def, indication
heparin antagonist
indication- GI, cranial bleed or neuro compromise
protamine- route, goal, considerations
loading dose + infusion (drip)
(roughly 1mg of Protamine neutralizes 100 units of heparin activity)
goal- return clotting factor levels to baseline
keep in mind heparin activity w/in last hr
800u/hr- give 8mg/ hr of protamine
PTT should be used to monitor the effect of protamine in neutralizing heparin
protamine- ae
flushing, nausea, vomiting, dyspnea
lovenox (LMWH)- action, indication, and route
Action: inhibits factor Xa
Indications:
Prevention and treatment of VTE (DVT, PE)
MI
Unlabelled use: systemic anticoagulation for other diagnoses
Route: SubQ (abdomen only)
Lovenox- pharmacokin
metab- liver
elim- kidneys (clearance dec by 30% w/ renal impairment) ei- do not give w/ severe renal fun
no need for IV drip
duration 12h
lovenox- dosing- prophylaxis v therapeutic
prophylaxis- for VTE (30-40mg every 12h)
therapeutic- MI, Afib, VTE (1 mg/kg every 12h)
heparin v enoxaparin- contraindications
Hypersensitivity Active, major bleeding GI ulcerations Intracranial bleeding Dissecting aortic aneurysm Recent eye/brain/spinal cord surgery Severe thrombocytopenia (low platelet count) Hemorrhagic CVA
heparin v enoxaparin- caution in
Uncontrolled HTN (inc p cerebral arteries, risk hemorr)
Severe liver or kidney dysfunction (drug accum wl LMWH)
Last trimester of pregnancy or immediate post-partum period (inc risk bleeding)
Spinal/epidural anesthesia or lumbar puncture (have bleeding at site= blood accum in epidural space, inc p on spinal c= permeant paralysis)
Hold anticoag 24h after dc anticoag
heparin v enoxaparin- ae
BLEEDING
Hematoma, bruising
Differentiate by palpation
Hematoma= hard
Bruise= soft
Thrombocytopenia
Heparin induced (HIT) – allergic rxn
Heparin causes inapprop act platelets (too much clotting)
Inc clotting- dec platelets (use platelets faster than can produce)
Presents w/ drop 50% platelets after admin heparin
Mre common in heparin (UFH)
enoxaparin- nursing considerations
Double check doses
Assess for bleeding
Petechiae, excessive bruises, drop in bp, inc hr, pale, cool skin color, dec urine output (dec renal perfusion), weak pulses, I+O’s, LOC, severe headache (hemorr stroke)
Assess for hypersensitivity (fever, chills, urticaria, hives)
Monitor H/H, platelets
SubQ route: rotate sites, assess for hematomas
IV heparin- considerations
Monitor aPTT or heparin assay to regulate therapy, double check compatibility with other IV solutions
For significant bleeding:
Hold heparin—short half-life when given IV
Consider Protamine or FFP (fresh, frozen plasma- replacing clotting factors) administration, if necessary
heparin v enoxaparin- disadvantages
hep- Short duration of action
Need for continuous IV gtt for full anticoagulation
Frequent lab draws (PTT, HA)
Inc risk HIT
enox- Longer duration of action
More accumulation with renal dysfunction
heparin v enox- advantages
hep- Effective anti-coagulation with IV gtt
Short duration of action- better for pre-procedure
Stop 1-2h before
enox- Does not require monitoring of blood ***coagulation tests
SubQ route can be used for full-dose therapy
Can be used for outpatient anticoagulant therapy
Less thrombocytopenia
Longer duration of action (12h)
direct acting oral anticoagulants- pros v cons
pros- predictable response (not need regular lab testing)
low incidence brain bleeds
cons- more expensive, inc risk bleeding GI tract
DOAC’s- zarelto or eliquis-action and indication
oral version enoxaparin
inhib factor Xa
indication- preve/trtmnt VTE, prev. embolic CVA in afib
DOAC’s- Pradaxa- action and indication
action- inhib thrombin (converting factor for prothrom to fibrin)
use- Prevention of embolic CVA in nonvalvular afib
Prevention/treatment of DVT/PE
long acting anticoag
warfarin (coumadin)
warfarin- action and indication
Action: Acts in the liver to prevent synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X)
**Not inhib existing factors- instead inhibits synthesis of factors in the liver
Vitamin K antagonist
Indications
Prophylaxis and treatment of:
Oral meds for full anticoag therapeutic trtment (not a prophylaxis)
VTE (DVT/PE)
Afib with embolization
Management of MI
Prevention of thrombus formation and embolization after prosthetic valve
warfarin- route, pharmacokin
Route: Oral Pharmacokinetics: Well-absorbed from GI tract Metabolized by liver, excreted by kidneys Half-life 42 hrs DD and food interactions
warfarin- dosing
start w/ 5mg
*overlap w/ heparin (or LMWH) by 4-5 days till drug kicks in
monitor w/ INR (PT) daily
until therap goal achieved, then 1-4 weeks
warfarin- therap INR goal
VTE, afib, MI, aortic mech valve- 2.0-3.0
mitral mech valve- 2.5-3.5
INR therap window- low v high
low- thromboemoblic = progression of clot
high- INR of 4, hemorrh complications (brain bleed, GI, hemorr shock)
warfarin- ae and considerations
ae- bleeding
Monitor for/prevent bleeding Monitor INR Patient education Consistent dietary intake of vitamin K No alcohol Bleeding precautions Follow-up lab work Drug/food interactions Foods high K- leafy green veg, in moderation, consistent w/ intake certain foods Drugs- high risk interactions, notify provider if add new vitamin or OTC
relationship btw vitamin K and INR in warfarin
Inc vitamin K= dec INR= inc risk overclotting
Dec K= inc INR= inc risk bleeding
Warfarin drug/food interactions
Drugs- inhibit (dec effect) anti-infectives (nafcillin), cardiovasc (cholestyramine), CNS (barbiturates)
Drugs- potentiation (inc effect, cause excess anticoag)
Anti-infectives (ciprofloxacin, erythromyacin) cardiovasc (fenofibrate, propranolol), CNS (alcohol, sertraline)
*no indivi vitamin supplements
supplements- ginseng, ginko, garlic suppl
Liquids- cranberry juice, alcohol
Foods- green leafy vegetables
Kale, spinach, greens, collards, parsley, broccoli (all can be bad if cooked too)
warfarin- antagonist- vitamin K and FFP
Vitamin K Used in less severe bleeding Takes around 24 hours to reverse INR Subq or IM Clotting factors have v different half lifes- prolonged time to see change
Fresh frozen plasma (FFP)
Immediately replaces clotting factors (warfarin not inactive. Existing Clotting factors, only synthesis in liver)
platelet lifecycle
sub endoth. Exposure, act. Platelet adhesion and later aggregation- forms platelet plug
risk for endothelial damage- atherosclerosis and PCI
HTN, Diabetes, Hyperlipidemia, smoking
CAD-MI
Cerebrovascular dis, carotid artery plaque- cva (ischemic)
S/P PCI (percutaneous coronary intervention) cath goes into artery and balloon expands w/ metal splice
antiplatelet- aspirin patho
inhib cyclooxygenase, dec production A2- dec expression GP receptor
antiplatelet- plavix patho
Plavix- blocks ADP recep, prevent stimuli of GP receptor
role of GP receptor
causes platelet aggregation
inhib by aspirin and plavix
aspirin- action, indication and dosing
Action MI prophylaxis Prevents thrombus formation by preventing the production of thromboxane A (TXA2), a prostaglandin that causes platelets to aggregate. Aspirin irreversibly inhibits cyclooxygenase, which synthesizes TXA2, in the platelet. Indications MI prophylaxis Ischemia CVA/TIA prophylaxis Dosing 81-325 mg po daily
aspirin- ae and interactions
ae-Nausea, vomiting GI upset Heartburn (take with food) Bleeding (easy bruising, gum bleeding) Tinnitus Thrombocytopenia
interactions- Oral anticoagulants, heparins
Steroids, alcohol, NSAIDS
clopidogrel (plavix)- action and indication
Mechanism of Action:
Irreversibly inhibits platelet aggregation by blocking ADP receptors on platelets, preventing platelet aggregation
Indications:
Prophylaxis against thrombotic events in patients with recent MI, recent stroke
Prophylaxis against thrombotic events s/p stent
(super aspirin, stronger action)
Use w/ coronary stents (PCI)
clopidogrel- dosing, ae, interactions
Dosing
Recent MI or stroke: 75mg daily
Acute coronary syndrome/stent: 600mg po x 1 then 75mg daily with aspirin
Adverse effects
Minor bleeding, headache, dizziness
Rash, abdominal pain, hypertension, edema
Thrombocytopenia Dec platelets= exacerbate clotting factors
Interactions
Increased risk of bleeding with NSAID, warfarin
PPIs may decrease effectiveness
thrombolytics- first gen
streptokinase, urokinase
thrombolytics- second gen
tPA
thrombolytics- third gen
reteplase, TNKase
thrombolytics- action, dosing and indications
Action—breaks down fibrin clot lysis Dosing IV Based on patient’s weight or fixed dosing (depending on drug and indication); not to exceed maximum doses for particular agents Immediate onset Indications Myocardial infarction CVA (ischemic ONLY) Pulmonary embolism (not systemic, only at specific site) Deep vein thrombosis Arterial thrombosis Occluded intravenous catheter temporary treatment
thrombolytics- ae
Cardiac arrhythmias (good sign, indicates perfusion) with coronary reperfusion; hypotension
BLEEDING, especially watch for: INTRACRANIAL HEMORRHAGE, GI/GU BLEEDING. Most common sites of bleeding—venipunctures
Urticaria, nausea, vomiting, fever
Anaphylaxis, especially with Streptokinase (first gen)
thrombolytics- absolute contraindications
Intracranial hemorrhage (ICH) on CT or history of ICH
Suspected subarachnoid hemorrhage
Uncontrolled HTN (SBP> 185, DBP>110) (inc risk intracranial hemorrhage)
Neurologic surgery, serious head trauma or previous stroke in previous 3 months. (area brain damaged frm prev stoke has inc risk for bleeding)
Seizure at stroke onset
Arteriovenous malformation (AVM), neoplasm, or aneurysm
Suspected/confirmed endocarditis (risk bleeding brain)
Known bleeding risk (thrombocytopenia, receiving anticoagulants, prolonged bleeding times)
BG <50 or >400 (need to be able to determine what change in mentation is from)
thrombolytics- considerations (labs)
Only administered in critical care settings: ED, ICU, cath lab
Assess bleeding times prior to administration (PTT, INR, platelet count, fibrinogen). Fibrinogen is assessed 2-3 hrs after start of therapy to check for fibrinolysis.
thrombolytics- considerations (time constraints)
Begin therapy ASAP after onset of symptoms
Time windows (time after which the risk outweighs benefit):
STEMI—within 12 hours (MI w/ ST elevation)
Permanent damage heart occurs after 12 h
Ischemic CVA—within 4.5 hours (previously 3)
thrombolytics- considerations (assessment)
Assessment:
VS—continuously
Assess pt carefully for bleeding every 15 min during 1st hr of therapy
Neuro changes (H/A, decreased LOC)
GI bleeding- Abdominal pain with coffee-ground emesis or black, tarry stools
GU bleeding- Hematuria
Avoid invasive procedures (IM injections, arterial punctures). If punctures necessary, hold pressure for at least 30 min after.
Start 2 IVs prior to initiating infusion
