Exam 2 Flashcards
Heart failure
The heart muscle (myocardium) weakens and enlarges causing decreased ability to pump the blood through the heart and into systemic circulation
CHF
Compensatory mechanisms fail and the peripheral tissues and lungs become congested (fluid overload)
Diastolic heart failure (EF, etc)
normal EF
heart doesn’t relax or fill enough
systolic heart failure (EF, etc)
low EF <55%
doesn’t pump strong enough
left sided HF S&S (5)
pulmonary congestion, dyspnea, cough, oliguria, weight gain
right sided HF S&S (3)
peripheral edema, JVD, weight gain
cardiac glycosides MOA
inhibits sodium-potassium pump
increased ICF sodium
cardiac fibers contract more efficiently
inotrope and chronotrope of cardiac glycosides
+ inotrope (increases CO)
- chronotrope (decreases HR by decreasing AV conduction)
What do cardiac glycosides do
Increases CO which increases renal perfusion and increased fluid excretion and less edema
Lanoxin (digoxin) use and 2 routes
2nd line treatment for HF
used for afib/aflutter
slows down HR not BP
PO/IV
therapeutic window of digoxin
0.5-2 ng/ml
SMALL
who can’t take digoxin (4) and half life
people with low protein (malnourished)
renal insufficiency (low dose)
thyroid issues (HYPO=low dose)
watch creatinine (excreted by kidneys)
long half life accumulation can occur from long HL
Digoxin toxicity
bradycardia, anorexia, N/V/D, visual changes, confusion, delirium, ventricular dysrhythmias, yellow halos
digoxin antidote
digibind, ovine
drug interactions of digoxin
K+ loss diuretics increase risk of toxicity
cortisone taken PO/IV increases hypokalemia increasing risk of toxicity
antacids decrease absorption, stagger doses
nursing considerations of digoxin
obtain apical pulse before administration
assess for toxicity and monitor levels of drug and potassium
primacor (milrinone) inocor (class, MOA, route)
Phosphodiesterase inhibitor
increases SV, CO, and vasodilation (+ inotrope)
increases HR
IV
what are we concerned about with Primacor (milrinone) inocor
cardiac dysrhythmia (check EKG)
drop in BP since we’re vasodilating and getting rid of fluid
vasodilators in terms of HF
decrease venous blood return to the heart, decrease preload
arterial dilators for HF
decrease afterload increasing cardiac output, increased renal perfusion by dilating arterioles, improve circulation to muscles
ACE inhibitors for HF
dilate venules, arterioles, improve renal blood flow, decrease blood volume, certain ARBS also (diovan, atacand)
aldactone (spironolactone) for HF
K+ sparing diuretic, blocks the secretion of aldosterone causing decreased fluid retention
natrector for HF
Inhibits ADH, promotes vasodilation, diuresis (acute CHF), BiDil (hydralazine and isosorbide dinitrate)
left arm pain
heart
right arm pain
gallbladder
classic (stable) angina
occurs with stress or exertion
unstable (preinfarct) angina
occurs frequently with progressive severity unrelated to activity
variant (prinzmetal, vasospasm) angina
occurs during rest
how to antianginals work
increases blood flow to the heart by increasing supply or decreasing demand
3 types of antiaginals
nitrates
beta-blockers
Ca+ channel blockers
what do nitrates do
cause generalized vascular and coronary vasodilation increasing blood flow to coronary arteries, reducing ischemia
important stuff about nitroglycerin
don’t touch the med (drops BP)
patches go everywhere except chest
SL 0.4mg or 1/150 gr
take 3 times q5 min, call 911
keep away from light and heat and children
DO NOT SWALLOW SL
pharmacodynamics of nitroglycerin
acts on smooth muscle of blood vessels causing relaxation and dilation
decreases preload and afterload and myocardial O2 demand
remove patch for 8-12 hours
side effects of nitroglycerin
HA, hypotension, dizziness, weakness, and faintness
adverse effects of nitroglycerin
reflex tachycardia if not tapered off
drug interactions of nitroglycerin
not taken with BB, Ca+ blockers, vasodilators, and ETOH may cause hypotension
not taken w viagra
beta blockers use
decrease HR and contractility, reducing O2 demands and angina
used for stable angina
things to avoid in BB and what happens if d/c abruptly
avoid in 2nd and 3rd degree AV block (lower HR)
taper dose to avoid reflex tachy, recurrent angina, and SOB
side effects of BB
Mild and transient bradycardia, AV block, hypotension, bronchoconstriction, mask symptoms of hypoglycemia, inhibit glycogenolysis
Ca+ channel blockers
used for variant and stable angina
Relax peripheral arterioles and coronary spasm decreasing myocardial O2 demand (dilates coronary arteries)
decreases contractility, afterload, PVR, workload
Ca+ channel blocker side effects
bradycardia, dizziness, hypotension, constipation
Lowers BP AND HR
P wave
atrial activation
QRS
ventricular depolarization
T
ventricular repolarization
P-R interval
AV conduction time
Q-T
ventricular action potential
what are dysrhythmias caused by
MI, hypoxia, hypercapnia, thyroid disease, CAD, electrolyte imbalance (K+, Mg++)
class 1 antidysrhythmics
3 types
decreases sodium influx into cardiac cells
decreased conduction velocity, automaticity, and ectopy
class IA antidysrhythmic
quinidine, procainamide, disopyramide
slows conduction and prolongs repolarization (PAT, SVT)
class IB antidysrhythmic
lidocaine (IV), mexiletine HCL (oral)
slows conduction and shortens repolarization (VT, vfib)
class IC antidysrhythmic
flecainide
class 2 antidysrhythmic
Decrease conduction velocity, automaticity and recovery time
Examples: Propranolol (Inderal), acebutolol (Sectral), esmolol (Brevibloc), Sotalol (betapace)
BETA BLOCKERS
acebutolol (sectral)
class II antidysrhythmic
beta1 blocker
for refractory VT, recurrent stable VT, angina, HTN
contraindications of acebutolol (sectral)
2nd-3rd degree HB, bradycardia, HF, cardiogenic shock
caution for acebutolol (sectral)
undergoing major surgery, renal or hepatic impairment, labile mellitus
interactions of acebutolol (sectral)
increased effects with diuretics, prolonged hypoglycemia
antagonist effect with albuterol, terbutaline, and metaproterenol
may increase ALT, AST, ALP, BUN, K+
side effects of acebutolol (Sectral)
dizziness, nausea, HA, hypotension, diaphoresis, fatigue, bradycardia
Class III antidysrhythmic
increase refractory period and prolong action potential
amiodarone (cordarone) for afib or vtach
Monitor thyroid and pulmonary function (may cause pulmonary fibrosis)
Class IV antidysrhythmics examples
Ca+ channel blockers (ONLY ONES THAT LOWER CONDUCTION)
verapamil (calan, isopitin), diltiazem (cardizem)
Class IV antidysrhythmics MOA
blocks Ca+ influx, decreasing excitability and contractility, increases refractory period of AV node, decreasing ventricular response
Class IV antidysrhythmics contraindications and side effects
contra: AV block and heart failure
side effects: hypotension, orthostatic hypotension, bradycardia, heart block
LDLs (tight or loose, what are they for, what increases them)
tight
carried by proteins that enter circulation, broken down for energy
diabetes and alcohol increase risk of LDLs
HDLs (tight or loose, what are they for, what increases them)
loose
used for energy, pick up remnants of fat left in periphery by LDL breakdown
Exercise!
LDL levels
risk for MI or CVA <70
Optimal: <100
normal: 100-129
borderline: 130-159
high: 160-189
very high: >=190
HDL levels
Good: >=60
low: <40
triglyceride levels
normal: <150
borderline: 150-199
high: 200-499
very high: >=500
drugs for hyperlipidemia (5)
Bile acid sequestrants
HMG-CoA inhibitors
Fibrates
Niacin
Cholesterol absorption inhibitors
Bile acid sequestrants MOA
Bind bile acids in the intestine, allow excretion in feces instead of reabsorption
cholesterol iodized in the liver and serum cholesterol levels begin to fall
bile acid sequestrants indications and 3 examples
For patients with primary hypercholesterolemia and pruritus associated with partial biliary obstruction
Examples: Welchol, Questran, Prevalite
bile acid sequestrants adverse effects
HA, fatigue, and drowsiness
Direct GI irritation: nausea and constipation
Increased bleeding times
Vitamin A and E deficiencies bc fat soluble and we’re preventing fat absorption
drug-to-drug interactions of bile acid sequestrants
malabsorption of fat soluble vitamins
HMG-CoA inhibitors actions
decreases serum cholesterol, LDLs, and triglycerides
increases HDL
indications of HMG-CoA inhibitors
hyperlipidemia, prevention of MI, CVA
examples of HMG-CoA inhibitors
-statins
HMG-CoA inhibitors contraindications and caution
allergy
metabolized by cytochrome P450 3A4
active liver disease or alcoholic liver disease
pregnancy and lactation
caution: impaired endocrine function
adverse effects of HMG-CoA inhibitors
myopathy
liver failure
rhabdomyolysis
drug to drug interactions of HMG-CoA inhibitors
grapefruit juice BAD
rosuvastatin (crestor)
prototype
indication: decreases lipids, especially LDL and triglycerides
inhibits HMG-CoA reductase
side effects of rosuvastatin (crestor)
HA, constipation, diarrhea, myalgia
adverse effects of rosuvastatin (crestor)
rhabdomyolysis, photosensitivity, hyperglycemia, elevated LFTs
contraindications of rosuvastatin (crestor)
pregnancy, lactation, liver disease
adverse effects of zetia
abdominal pain and diarrhea
HA, dizziness, fatigue, URI, back pain
muscle aches and pain
niacin
vitamin B3, inhibits release of fatty acids from adipose tissue
increases rate of triglyceride removal
chest and face swell up
fenofibrates
inhibit triglyceride synthesis in the liver, decreases LDL
increases uric acid secretion, stimulates triglyceride breakdown
gemfibrozil
inhibits peripheral breakdown of lipids
reduces production of triglycerides and LDL
increases HDL
2 PSK9 inhibitors
alirocumab (praluent)
evolocumab (repatha)
-CUMAB
2 times to use injectable lipid lowering therapy
intolerable to -statins
patients goal is not achievable with highest statin dose
patient education for injectable lipid lowering therapy (how long to leave it outside the fridge)
take out of the fridge 30 min prior
peripheral vasodilators and 2 examples
increase blood flow to extremities in PAD and PVD
effective in raynaud’s or buerger’s disease
cilostazol (pletal)
trental
pletal class and trade name
peripheral vasodilator
cilostazol
pletal contraindications and caution
contraindications: CHF class III-IV, arterial bleeding, severe hypotension, postpartum, tachy
caution: bleeding disorders, tachy
pletal interactions and route
hypotension with antihypertensives
PO
therapeutic effects of pletal
increased circulation caused by PVD, raynaud’s, cerebral vascular insufficiency
inhibits platelet aggregation, causes vasodilation
side and adverse effects of pletal
S/E: N/V, dizziness, syncope, blood in the eye, HA, abd pain, abnormal stools, peripheral edema
A/E: tachy, palpitations
nursing considerations of pletal
obtain baseline VS
assess for signs of inadequate blood flow to extremities, pallor, coldness, and pain
monitor for tachy and hypotension
arterial blood clot (what type of cells and caused by what)
WBC and RBC
platelet aggregation
blood coagulation
venous blood clot (what type of cells, caused by what, CAN cause what, and prophylaxis)
RBC and PLT
blood stasis or slow flow
occurs rapidly
can cause DVT and PE
give heparin or lovenox
what to consider for artificial valves
pts HAVE to be on anticoagulants bc the body will attack the foreign object causing clotting and a stroke
anticoagulants given for what type of stroke
ischemic
fragmin class
anticoagulants
indication of heparin
rapid anticoagulation for thrombosis such as DVT, PE, CVA
during surgery to prevent thrombosis
DIC
DVT/PE prophylaxis
afib when off coumadin
MOA of heparin
Combines with antithrombin III, prevents formation and doesn’t break the clot
Inhibits conversion of fibrinogen to fibrin which prevents fibrin clot formation
prolongs PTT (effectiveness of heparin, bleeding is a worry)
Nomogram
like insulin sliding scale but for heparin
pharmacodynamics of heparin
poorly absorbed GI
destroyed by heparinase in the liver
IV or SQ
fast half life
flow sheet so nurses know how much to administer
How is lovenox administered
2 inches away from the umbilicus, MAINTAIN AIR BUBBLE
side effects of heparin (3)
bruising
itching
burning
adverse effects of heparin
bleeding
ecchymosis
thrombocytopenia (low platelets during allergic reaction so they start clotting, biggest concern)
hemorrhage
contraindications of heparin
bleeding disorder
peptic ulcer
hepatic or renal disease
hemophilia (clotting takes long)
CVA (hemorrhagic)
drug and food interactions of heparin
increased effect with ASA, NSAIDS, thrombolytics, and probenecid
decreased effect with nitroglycerin and protamine sulfate
antidote for heparin
protamine sulfate
nursing considerations of heparin
obtain history of abnormal clotting, ETOH, or renal or liver disease
check PTT q4 hours when changed
check stool melena
check H&H if they’re losing blood
indications of warfarin (coumadin)
bleeding disorder
peptic ulcer
hepatic or renal disease
hemophilia (clotting takes long)
CVA (hemorrhagic)
same as heparin!
how to adjust the dose of warfarin
according to pt/INR
check INR within 3 days of antibiotics
ranges of INRs for warfarin (afib, DVT/PE/mechanical valves)
afib: 2-3
DVT/PE/mechanical valve: 2.5-3.5
antidote for warfarin
vitamin K
novel anticoagulants
no antidote
no INR to monitor
for afib, DVT/PE, NOT MECHANICAL VALVES (use warfarin)
examples of NOAC
xarelto, eliquis, pradaxa
high incidence of bleeding but less than warfarin
dabigatran etexilate (pradaxa) use
thromboembolism (DVT/PE) treatment and prophylaxis, stroke prophylaxis (non-valvular afib)
MOA of dabigatran etexilate (pradaxa)
inhibits thrombin
important info about dabigatran etexilate (pradaxa)
excreted by kidneys, decrease dose in CKD, avoid in hemodialysis
side effects of dabigatran etexilate (pradaxa)
bleeding, bruising, gastritis (leads to bleeding)
adverse effects of dabigatran etexilate (pradaxa)
hemorrhage, hematoma, thrombocytopenia
black box warning of dabigatran etexilate (pradaxa)
increase thrombotic event and stroke risk when d/c prematurely, epidural and spinal hematoma risk PARALYSIS!!
antidote for dabigatran etexilate (pradaxa)
praxbind
MOA of antiplatelets
used to prevent thrombosis in arteries by suppressing platelet aggregation
indications of antiplatelets
prevention of MI, CVA, or TIA
examples of antiplatelets
ASA
ticagrelor (brilinta) must use with 100 mg ASA, or less usually 81mg
(prasugrel) effient
clopidogrel (plavix)
pletal
agrylin
reopro
integrilin
pletal is an antiplatelet for WHERE
peripheral, NOT heart
use of agrylin
If we’re concerned about MI or clots
clopidogrel (plavix) class, dose
antiplatelet
loading dose 300-600mg then 75 mg daily, check P2Y12
indications of clopidogrel (plavix)
prevent recurrence of CVA, vascular death
MOA of clopidogrel (plavix)
inhibits platelet aggregation
contraindications and caution of clopidogrel (plavix)
contra: intracranial hemorrhage, peptic ulcer
caution: liver disease, GI bleeding, surgery (talk to cardiologist if not brain or spinal), bleeding from trauma
side effects and adverse of clopidogrel (plavix)
S/E: URI, flu-like symptoms, dizziness, HA, fatigue, CP, diarrhea, bruising, bleeding
A/E: HTN, bronchitis
interactions of clopidogrel (plavix)
May increase bleeding when used with NSAIDS
Interferes with the metabolism of phenytoin, warfarin, fluvastatin, tamoxifen, tolbutamide, NSAIDS, and torsemide
May increase bleeding when taken with ginger, garlic, gingko, feverfew
thrombolytics MOA
STRONGEST
promotes fibrinolytic mechanism
converts plasminogen to plasmin DESTROYING fibrin in the clot
disintegrates within 4 hours
use of thrombolytics
MI, PE, DVT, CVA
must be EMBOLIC stroke
ending of thrombolytics
-ase
remember -ase is enzymes which speed things up and thrombolytics are strong and fast
Alteplase (tPA) drug class and indications
thrombolytic
dissolves clot following AMI, PE, acute ischemic stroke
for emergency situations!
MOA of Alteplase (tPA)
promotes conversion of plasminogen to plasmin, digesting the fibrin matrix of clots, initiating fibrinolysis
side and adverse effects of Alteplase (tPA)
S/E: bleeding
A/E: intracerebral hemorrhage, stroke, atrial or ventricular dysrhythmias
contraindications of Alteplase (tPA)
internal bleeding, bleeding disorders, recent CVA, surgery or trauma, bacterial endocarditis, severe liver dysfunction, uncontrolled HTN
drug-food interactions of Alteplase (tPA)
increased bleeding with anticoags, NSAIDS, cefotetan, plicamycin
Sodium-glucose Co-transporter 2 (SGLT-2) inhibitors ending
-flozin
MOA of Sodium-glucose Co-transporter 2 (SGLT-2) inhibitors
induced glucosuria independent of insulin secretion
reduces ability of renal tubules to absorb glucose, allows increased insulin sensitivity, decreased gluconeogenesis
used for diabetes and HF (low EF) even without diabetes
contraindications of Sodium-glucose Co-transporter 2 (SGLT-2) inhibitors
type 1 DM, DKA, severe renal disease (GFR <30), on HD
adverse effects of Sodium-glucose Co-transporter 2 (SGLT-2) inhibitors
hyperkalemia, mycotic infections, UTI, renal insufficiency, hypotension, fungal infection
empagliflozin (jardiance) dosing
10mg PO in the morning, titrate up to 25 mg
D/C if GFR persistently below 45
dapagliflozin (farxiga) dosing
5 mg can increase to 10
D/C if GFR <60
canagliflozin (invokana) dosing
100 mg before 1st meal of the day
increase to 300 for pt with normal renal function (GFR >60)
sacubitril/valsartan (entresto) indication
heart failure with reduced EF, NYHA class II-IV
sacubitril/valsartan (entresto) side effects
hypotension, dizziness, cough, hyperkalemia, renal failure
sacubitril/valsartan (entresto) adverse effects
hypersensitivity, angioedema, severe hypotension, renal failure
sacubitril/valsartan (entresto) black box warning
fetal toxicity