exam 2 Flashcards by Callie Wanek

Increase the amount of urine produced
Increase sodium excretion
-prevent cells lining the renal tubule from reabsorbing sodium in the filtrate
-sodium, other ions, and water are lost in the urine
-those that block the most sodium work the best
Used for
heart failure, pulmonary edema, hypertension, renal disease, liver disease, hyperkalemia, glaucoma

Diuretics

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Types of Diuretics

Thiazide
Loop
Potassium sparing
Carbonic anhydrase inhibitors
osmotic

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ii. Hydrochlorothiazide (Hydrodiuril) (HCTZ) - can be used in children
iii. Chlorothiazide (Diuril) - IV route for pts with pulmonary edema
iv. Indapamide (Lozol) - edema with HF, liver/renal failure, often combo with antihypertensives (Lisinopril/HCTZ) Produces 10-20 mmHg drop in BP

Thiazide Diuretics

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Block the chloride pump in the early distal tubule
-sodium passively moves with chloride to maintain electrical neutrality
-keeps chloride and sodium in the filtrate
This segment of the tubule is impermeable to water and 90% of sodium is already reabsorbed
a. So there’s not a lot of sodium and water to get rid of at the end and that’s why it’s a mild diuretic
-little increase in the volume of urine produced
-mild diuretic when compared to others
Ability to produce diuresis diminishes with reduced blood flow through the kidney
-Diminished blood flow to the kidneys makes it not work as well
–Lasix or loop diuretic and every measures against it

MOA of thiazide diuretics

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I. Hypotension – because they’re losing sodium and water

ii. Hypokalemia - weakness, muscle cramps, arrhythmias
iii. Hypercalcemia - fatigue, confusion, weakness, N&V
iv. Increased uric acid levels - interferes with secretory mechanism
- Worried for patients with gout
v. Hyperglycemia - hypokalemia reduces insulin secretion
- If hyperkalemic and could have slightly elevated BS and worried about that in patients with diabetes

Adverse effects of thiazide diuretics

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i. Fluid and electrolyte imbalances
- Check potassium levels before administering a diuretic
ii. Severe renal disease
- Kick kidney and make them work a little better
- - Thiazidide less kick
iii. Systemic lupus erythematosus
- renal failure (degeneration), and adding something that adds a kick sends them to renal failure
iv. Diabetes mellitus
v. Gout
vi. Hyperparathyroidism
- Controls calcium levels in our body and hyperparathyroidism

cautions with thiazide diuretics

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I. Digoxin toxicity may occur due to hypokalemia

-Digoxin helps with heart failure and helps heat beat harder/faster to help with heart failure
digoxin binds at the same place as potassium within the NA/K ATPase pump
requires close potassium monitoring
ii. Decreased effectiveness of antidiabetic agents
dose adjustments may be needed due to increase in BS
iii. Lithium toxicity
lithium chemically is similar to sodium
body saves lithium from the filtrate

interactions for thiazide diuretics

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i. Work in the loop of Henle: which is where they get their name
ii. Also known as high-ceiling diuretics because they cause a greater degree of diuresis – so they pee a lot

loop diuretics

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Furosemide (Lasix) - ped dosing
- IV of this onset is 5 mins
Bumetanide (Bumex) - 40X more potent than Lasix, shorter 1/2 life
Toresmide (demadex) - 2X as strong as Lasix, longer 1/2 life, once/day dose, less ototoxicity

types of loop diuretics

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I. Block the chloride pump in the ascending loop of Henle where 30% of the filtered sodium is reabsorbed

results in copious amounts of sodium rich urine
-lots of urine coming out and all that fluid coming out makes blood slightly hypotonic. When blood travels to lungs, the hypotonic blood will help pull fluid out of the lungs and goes out of the kidneys and repeats
hypertonic intravascular fluid pulls fluid out of the interstitial space and delivers it back to the kidney
Only have an effect on blood that reaches the nephron
ii. Inhibits symporter membrane protein, to block reabsorption of sodium and chloride
this action also blocks potassium reabsorption

MOA of loops diuretics

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I. Dehydration - dry mouth, weight loss, headache

ii. Hypotension - dizziness, fainting
iii. Hypokalemia - weakness, muscle cramps, arrhythmias
iv. Hypocalcemia - weakness, muscle cramps, numbness and tingling of hands, feet, perioral, seizures
v. Hyperglycemia - hypokalemia reduces insulin secretion
vi. Increased uric acid levels -interferes with secretory mechanism
vii. Ototoxicity
- Effects nerves that come out of ear
- usually reversible
- occurs in high doses: infusion of 160 mg of Lasix and call you saying their ear is ringing

ADE of loop diuretics

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I. Fluid and electrolyte imbalances

ii. Severe renal disease
- Does a big kick to the kidneys
iii. Systemic lupus erythematosus
- renal failure
iv. Diabetes mellitus
v. Gout

cautions of loop diuretic

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I. Aminoglycosides (antibiotics) or cisplatin (anti-neoplastic)

Combined together and increased risk of ototoxicity
ii. Anticoagulants
increased effects
iii. NSAIDs
decreased loss of sodium & antihypertensive effects
iv. Digoxin
v. Lithium

interactions for loop diuretic

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I. Not as powerful as loop diuretics

ii. Benefit is they retain potassium instead of wasting
- used for those clients at high risk of hypokalemia
- -maybe on lasiks and can’t get potassium down so give this drug

potassium sparing diuretics

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iii. Spironolactone (Aldactone) prototype
- pediatric dosing with careful monitoring
iv. Amiloride (Midamor)
v. Triamterene (Dyrenium)
- Only available PO

types of potassium sparing diuretics

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I. Spironolactone is a aldosterone antagonist

Aldosterone, found in adrenal gland, and helps to save sodium & water and excrete hydrogen and potassium
drug of choice for hyperaldosteronism
ii. Others block sodium channels causing sodium to stay in the filtrate.
potassium is not excreted
iii. Work in the late distal tubule & collecting ducts
iv. Used as an adjunct with thiazide or loop diuretics
especially those at high risk of hypokalemia
digoxin, antiarrhythmics

MOA of potassium sparing

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I. Hyperkalemia - lethargy, muscle cramps, arrhythmias

Check potassium levels before giving **
ii. Binds to progesterone and androgen receptors
men - gynecomastia, impotence, diminished libido
women - menstrual irregularities, hirsutism, breast tenderness

AE of potassium sparing meds

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I. Hyperkalemia

ii. Severe renal disease and anuria
iii. Pregnancy
- cause teratogenic effects in animals
- category D

cautions in potassium sparing

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i. Diuretic effects is decreased if combined with salicylates (like asprin)
ii. Watch for hyperkalemia with ACE inhibitors

interactions with potassium sparing

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Block the effects of carbonic anhydrase enzyme in the proximal tubule
- - Catalyst for sodium bicarb
- - Sodium bicarb is a base in our body
- carbonic anhydrase is the catalyst for sodium bicarbonate formation
- prevents bicarbonate formation and reabsorption in the renal tubule
- without bicarbonate sodium reabsorption does not occur
Mild diuretic
- adjunct to other diuretics when a more intense diuresis is needed
Glaucoma, mountain sickness
- Because it reduces the amount of fluid in the eye
- Mountain sickness: reduce amount of sodium bicarb were making (base), body compensates by breathing harder to keep pH normal and helps us to breath better
They work early in the process

carbonic anhydrase inhibitors

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acetazolamide (Diamox)

Methazolamide (Zeptazane)

carbonic anhydrase inhibitors diuretics

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Metabolic acidosis
- loss of bicarbonate
Hypokalemia
- potassium is lost in an attempt to retain sodium
Monitor those on lithium
- increased excretion
Use with caution
- fluid & electrolyte imbalance
- renal or hepatic disease
- adrenocortical insufficiency
- respiratory acidosis

cautions with carbonic anhydrase inhibitors diuretics

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Pull water into the renal tubule without sodium loss
- osmotic pull
- large amounts of urine produced
- work outside of the kidney, works in the brain
- used to reduce intraocular pressure and increased ICP

osmotic diuretics

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mannitol (osmitrol) - IV only: used in glaucoma to increase ICP, works early in process

osmotic diuretics

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1. Monitor client for sudden drop in fluid levels - N&V, hypotension, confusion, headache, cardiac decompensation, shock - continual monitoring - - CPV line, constant BP monitoring, telemetry Contraindicated - rogressive renal disease, pulmonary congestion, intracranial bleeding, dehydration, HF - can exacerbate due to large fluid shifts - all this because it has a potential for a large fluid shift

cautions and contraindications

a. Monitor - edema - heart and lung sounds - blood pressure and pulse before we give - daily weight – same time, clothes and scale - electrolytes b. Administer early in the day c. Ensure access to bathroom after administration d. Provide potassium rich or low-potassium foods, potassium supplements may be needed e. Provide fluids to prevent fluid rebound f. Give with food if GI upset occurs I. Also helps with compliance g. Educate on importance of compliance

nursing considerations for diuretics

1. Vessel spasm and constriction - -- Collagen is exposed to air and makes the platelets become stick and adhere together and make plug. They make ADP and attracts other platelets and forms a weak plug that can be moved easily (not a blood clot) - -- The same collagen makes a cascade 2. Platelets become sticky and adhere together and to the damaged vessel - release adenosine diphosphate (ADP) which attracts other platelets - forms a weak plug 3. When collagen is exposed the coagulation cascade is started

clotting process

I. Coagulation occurs when fibrin threads create a meshwork that traps blood constituents ii. Two pathways - intrinsic pathway is activated in response to the vessel injury inside the vessel - extrinsic pathway is activated when blood enters tissue spaces - - blood leaks on outside of the vessel - inactive plasma proteins are converted to active forms - formation of fibrin clot iii. Intrinsic - Hageman (XII) factor is activated by exposure to collagen - - And starts extrinsic pathway iv. Extrinsic - release of tissue thromboplastin - - intrinsic and extrinsic start the pathway of cascade v. Start a number of reactions in the clotting cascade vi. Last step - prothrombin activator converts clotting factor prothrombin to an enzyme thrombin vii. Thrombin converts fibrinogen to long strands of fibrin - clotting occurs in approximately 6 minutes - - fibrin creates mesh work viii. Several clotting factors including fibrinogen are proteins made by the liver - vitamin K is required for production - clients with serious hepatic impairment usually have abnormal coagulation

coagulation cascade

I. Clot removal - initiated 24 to 48 hours of clot formation, continues until clot is dissolved ii. Vessels near a fibrin clot secrete tissue plasminogen activator (TPA) - TPA converts inactive plasminogen, present in the clot, to active plasmin - plasmin digests fibrin strands

fibrinolysis

I. Thromboembolic - formation of thrombi - decreased blood flow through a vessel - results in tissue hypoxia, anoxia, and necrosis - damage to endothelial lining - CAD ii. Hemorrhagic - excess bleeding - less common - lack of clotting factors or platelets - hemophilia, liver disease, bone marrow failure

disorders affecting coagulation - not that significant

I. Interfere with platelet aggregation - most work by blocking receptor sites on platelet membranes - Used to prevent clot formation in arteries - - Anticoag: vessels or veins - - Antiplatelet: arteries – like MI - MI, stroke, maintenance of AV grafts

antiplatelet agents

``` Aspirin Clopidogrel (Plavix) ticlopidine (ticlid) ticagrelor (brilinta) Abcixmab (ReoPro)/Eptifibatide (integrilin) = IV ```

types of antiplatelet agents

I. Bind irreversibly to the enzyme cyclooxygenase (COX) in platelets, this inhibits thromboxane A2 which is a powerful inducer of platelet aggregation ii. Anticoagulant effect after a single dose can last up to a week - discontinue 5-10 days before surgery iii. Should only be used with other coagulation modifiers with physician approval -Patient on coumadin: can’t take aspirin (NSAID) for headache Side effects: Gi upset, GI bleeding, tinnitus, dizziness

aspirin - blocks cox

I. ADP receptor blocker - irreversibly alters the plasma membrane of platelets, unable to receive chemical signals to aggregate - discontinue 5 days before surgery ii. Given orally for recent thromboembolic event such as stroke or MI - can also be used to prevent clots following PCI (percutaneous coronary intervention) iii. Similar efficiency as aspirin but more expensive iv. Mainly used for those that cannot tolerate aspirin because of GI bleeding is lessened Cautions I. Bleeding disorder and recent surgery ii. Closed head injuries iii. Anagrelide (Agrylin) blocks platelet production at the bone marrow - monitor for thrombocytopenia because it can cause them to not have enough platelets at all

Clopidogrel (Plavis)

Adverse Effects I. Bleeding: bruising, bleeding gums, black, tarry stools, change in LOC, abdominal pain ii. Headache iii. Dizziness iv. Weakness 1-All 3 of those are also signs of bleeding 2.-All signs of hypertension Nursing Considerations I. Small, frequent meals to relieve GI upset* ii. Bleeding precautions: soft toothbrush, electric razor, avoid contact sports, monitor for occult blood loss, avoid IM injections. care with fragile skin iii. Monitor blood pressure and CBC for signs of bleeding iv. Encourage a medical alert bracelet

Clopidogrel (Plavis) 2

i. Interfere with the normal coagulation process by interfering with the clotting cascade and thrombin formation ii. Heparin iii. Warfarin (Coumadin) iv. Enoxaparin (Lovenox) v. Rivaroxaban (Xarelto) vi. Dabigatran (Pradaxa) vii. Apixaban (Eliquis)

anticoagulants

I. Natural substance found in liver and lining of blood vessel ii. Enhances the action of antithrombin III, protein that inactivates thrombin - -Thrombin is the very last step – so if it is inactivated you can’t make fibrin - prevents enlargement of existing clots and formation of new clots - it does not dissolve existing clots iii. Poorly absorbed by the GI tract so has to be IV or subq - IV administration has immediate onset - subq takes an hour iv. IV is given by a weight-based nomogram - weight, aPTT value, clinical indication every day v. Normal activated partial thromboplastin time (aPTT) is 25-35 seconds - therapeutic is 1.5-2 times greater than pretreatment (60-75ish is where we want to be) - 90-100 is high and need to be worried about spontaneous bleeding vi. During IV therapy an aPTT is drawn 1 time per day and every 6-8 hours after dose changes vii. Stopping an infusion results in diminished action within hours - Keep on bedrest because if they fall and hit their head they will bleed a lot into the brain - discontinue 6-12 hours before surgery - dosed 2 times a day, in the morning and night

Heparin

I. Inhibits vitamin K and the hepatic synthesis of Factors II, VII, IX, X - - Fairly hard to control and that’s why they come in so often to get an INR test because it’s not super stable ii. Used to maintain anticoagulation - afib, heart valves, venous thrombosis iii. Those on heparin are often switched to oral warfarin when stabilized - during transition the two drugs can be given concurrently for several days - warfarin onset is 3 days and last 4-5 days - - because it takes 3 days to kick in, heparin can be given together. If you don’t, you will lose the therapeutic level - - hep and lovenox can’t overlap - -hep and coumadin can overlap 3. discontinue 4-5 days before surgery - Therapeutic INR levels are 2-3

Warfarin (Coumadin) | vitamin k is antidote

I. Low molecular weight heparin - shortened, modified heparin molecules - inhibit Factor X ii. Advantages - duration is 2 to 4 times longer - -so usually once a day dosing for 7 days - produces a more stable response - can be given at home - -drug of choice for DVT prophylaxis - less likely to cause thrombocytopenia iii. Drug of choice for DVT prophylaxis following surgery - usually 1 time per day for 7-10 days - Other Anticoagulants

Enoxaparin (lovenox)

I. Rivaroxaban (Xarelto), apixaban (Eliquis) super expensive - inhibit Factor Xa (a means it has been activated) - prophylaxis of DVT with knee or hip surgery, reduce risk of embolism due to afib ii. Dabigatran (Pradaxa) - inhibits thrombin (last step to create fibrin) - reduce risk of embolism due to afib iii .As effective as warfarin iv. No laboratory monitoring v. Less drug interactions vi. No food restrictions vii. Expensive

other anticoagulants

Cautions I. Conditions with increased bleeding potential: trauma, spinal tap, GI bleed, surgery ii. Warfarin is category X (will cause fetal demise) iii. Warfarin has lots of drug-drug interactions: salicylates, erythromycin, cefazolin, amiodarone 2. close client monitoring when adding or removing a drug iv. Combining with OTCs like NSAIDs v. HIT - Heparin Induced Thrombocytopenia -abnormal antibodies to heparin develop which activate platelets - high risk for clots so monitor carefully -usually appears 5-10 days after initiation of therapy Nursing Considerations I. Monitor for bleeding and bleeding precautions ii. Monitor lab: INR (coumadin), aPTT (for heparin) iii. know Antidote: heparin & lovenox are protamine sulfate; warfarin is vitamin K iv. Self-administration techniques - subq in abdomen because it is the most stable absorption -don't push out the air bubble from lovenox because it needs to be given deep in -don't rub the area because it will alter the way it is absorbed v. Heparin comes from animal sources (beef lung or pig intestine), allergic reactions are possible OR religious preference

nursing considerations and precautions for anticoagulants

iv. Urokinase (Abbokinase) v. Alteplase (Activase, Cathflo) – will see this the most (Cathflo) vi. Reteplase (Retavase) work best when administered no more than 4 hours after clot formation - monitor VS every 15 mins first hour, then ever 30 mins and for 1st 8 hours after hold pressure on site for 30 mins

Thrombolytics

Adverse Effects I. Allergic reaction due to foreign proteins - headache, flushing, fever, lethargy ii. Human donors - HIV, hepatitis Nursing Considerations I. Double check that the correct clotting factor is being used ii. Administered through the IV route only iii. Watch for signs of bleeding and thrombosis iv. Type and crossmatch v. Monitor for allergic reactions

Antihemophilic factor, VIII, (Bioclate)

``` Systemic 1. aminocaproic acid (Amicar) Topical – give these more 1. absorpbale gelatin (Gelfoam) 2. human fibrin sealant (Atriss, Evicel) 3. microfibrillar collagen (Avitene) 4. thrombin (Thrombinar) 5. thrombin, recombinant (Recothrom ```

Hemostatic Agents AKA antifibrinolytics used to stop bleeding

I. Used for surface injuries where clotting does not occur ii. Available in sponge, spray, and powder iii. Can be used in conjunction - gelfoam and thrombin iv. Thrombin is a bovine product - allergic reactions are possible v. Infection risk due to trapped bacteria

topical hemostatic agents

I. Inhibits plasminogen activator ii. Given oral or IV iii. IV reduces bleeding in 1-2 hours - aplastic anemia, hepatic cirrhosis, postoperative iv. IV can cause hypotension or bradycardia v. Excessive clotting Contraindications/Cautions 1. DIC - tissue necrosis 2. urinary tract bleeding - promotes clots in renal pelvis or ureters 3. dizziness, drowsiness, headache - changes in cerebral blood flow, will it make clot in brain 4. N&V, cramps, diarrhea - clotting in GI tract 5. muscle pain, increased CPK - clots in muscle tissue Nursing Considerations I. Monitor for clinical response ii. Monitor for signs of thrombosis - chest pain, leg pain, difficulty breathing, confusion - immediately discontinue the medication & notify provider iii. Monitor the IV site for extravasation iv. Monitor vitals and urine output

Aminocaproic Acid (Amicar) only systemic one of hemostatic agents

Phase 0: depolarization, sodium channels open, sodium rushes into cell Phase 1: sodium concentration equalizes Phase 2:calcium slowly enters cell, potassium begins to leaves cell to counteract all the Na and Ca that entered in - more calcium, harder/better heart will pump Phase 3 – getting everything back - repolarization, sodium channels close, potassium rushes out of cell Phase 4: cell rests, sodium-potassium pump resets cell

automaticity

Goal: prevent or terminate dysrhythmias Medications can cause serious side effects Reserved for those who can't control by other means: cardioversion, defibrillation, ICD, pacemaker treating asymptomatic dysrhythmias with med is little-no benefit (med is short term treatment and bridges until you get long term treatment)

treatment of dysrhythmias

Action potentials depend on the opening of sodium channels, blocking these channels will prevent depolarization - slows impulse conduction across the heart, ectopic pacemakers will be suppressed, depress phase 0 (so it slows things down) Use most are reserved for treatment of life threatening ventricular arrhythmias Quinidine/Procainamide - effective against a wider range of dysrhythmias Lidocaine - drug of choice when monitoring isn't available for exact arrhythmia lidocaine prototype drug procainamide, quinidine, propafenone (Rythmol) (see this most often in practice)

class 1 sodium channel blockers

Adverse Effects Potential to create new dysrhythmias or worsen existing ones - Can lead to cardiac arrest - Use this one if other things don’t work Bradycardia and hypotension -dizziness, syncope Bone marrow depression - Quinidine – older drug N&V, diarrhea, dry mouth, urinary retention - So give small meals, take with food Cautions Bradycardia or heart block without a pacemaker - Slow conduction down in some form, so could make them bradycardic or cause heart block - Assess BP and heart rate before administration Heart failure, hypotension, shock - If in heart failure be careful. Monitor closely when giving this Electrolyte disturbances Combined with other medications known to produce arrhythmias - Digoxin (is used for heart failure, so be very careful when combining this), beta blockers Quinidine - when combined with digoxin monitor digoxin levels -- reserve for people who can’t use other things - avoid grapefruit juice because it will enhance absorption - avoid foods that alkalinize the urine -- milk can alkalinize urine

sodium channel blockers - class 1

``` Block beta1 receptors in heart slow conduction through AV node - decreased HR depression of phase 4 Uses: Supraventricular tachycardia (Something above ventricle/atria based like afib, aflutter, SVT), PCVs, hypertension, Post MI pts propranolol (Inderal) - prototype acebutolol (Sectral): oral only esmolol (Brevibloc): IV only ```

class 2 beta adrenergic blockers

Adverse Effects 1. Hypotension, bradycardia, arrhythmias 2. Bronchospasm, dyspnea – important for patients with COPD/asthma - blocking of beta2 receptors 3. Alterations in blood glucose - mask effects of hypoglycemia - B2 receptors in the liver control hepatic glucose production - insulin resistance 4. Decreased libido, impotence – patients will stop taking Cautions 1. Withdraw slowly to prevent rebound hypertension, dysrhythmias, and MI 2. Bradycardia, heart failure, shock 3. COPD, asthma 4. Diabetes( insulin dose adjustments, frequent blood sugar monitoring)

class 2 beta adrenergic blockers

Block potassium channels and slow the outward movement of potassium (delays repolarization and lengthens the refractory period; phase 2-3) Uses: serious dysrhythmias r/t serious S/E (proarrhythmic, IV Amiodarone usually limited 2-4 days), used for variety atrial/ventricular dysrhythmias, Amiodarone isn't drug of choice amiodarone (Cordarone) - prototype sotalol (Betapace) (beta-blocker with class III effects) dronedarone (Multaq)

class 3 potassium channel blockers

Adverse Effects Bradycardia and hypotension in a significant number of patients Worsen dysrhythmias or create new ones Amiodarone can cause pulmonary and liver toxicity, is fairly common (has a significant half-life; mild liver injury is common; ALT is the best for liver specifically ) Dronedarone increases the risk of death in serious HF -Black box warning: for Multaq - those with heart failure have increased risk of death; for Dronedarone - liver toxicity and pulmonary toxicity; pregnancy category X N&V, weakness, dizziness Cautions Bradycardia, shock, AV block - Coumadin with a fib and throw dronedarone with it, check the INR more frequently Amiodarone can increase serum digoxin levels by 70% Enhances the effects of anticoagulants

class 3 potassium channel blockers

black movement of calcium across cell membrane (depresses generation of action potentials/delays repolarization in phase 1/2 - need Ca to have strong beat) reduced automaticity in SA node and slowed impulse conduction through AV node Uses: Supraventricular dysrhythmias (afib, aflutter, SVT), hypertension, angina (helps relax vessels and get more oxygenated blood to heart) diltiazem (Cardizem) verapamil (Calan)

class 4 calcium channel blockers

Treatment of choice for paroxysmal suprventricular tachycardia (Because acts fast) Slows conduction through the AV node and decreases automaticity of the SA node Given as a 1-2 second IV bolus and will reset everything in heart **Dyspnea is common but self-limiting because of 10-15-second half life - Let them know dyspnea will occur, but will go away fast

Adenosine (miscellaneous for cardiac dysrhythmias)

Used primarily for heart failure - positive inotropic effect – helps heart beat harder with each beat - can eliminate dysrhythmias caused by cardiac hypoxia Decreases automaticity of the SA node and slows conduction through the AV node - slows calcium leaving cell Can cause dysrhythmias, interacts with many meds - careful monitoring is required, especially when you change drug regime - serum levels (normal is 1.8) and electrolytes

Digoxin (miscellaneous for cardiac dysrhythmias)

Assess VS - monitor apical pulse for a full minute, blood pressure because if you give a hypotensive and they don’t have high BP it can cause BP to decrease - educate on monitoring at home Assess heart rhythm, may need continuous telemetry Monitor daily weight – same time/scale/clothes Assess for severe SOB, frothy sputum, profound fatigue, swelling extremities Because this could be signs of HF or pulmonary toxicity Monitor labs - electrolytes, digoxin level, bone marrow suppression, coagulation studies, LFTs - educate about routine lab work Encourage medical alert bracelet Titrate to smallest dose Safety - first dose at bedtime, get up slowly, good lighting, don't double doses, don't skip doses, 12 hours apart or 24 hours apart

Nursing consideration for cardiac dysrhythmias meds

Progressive narrowing of coronary arteries, leads to decreased delivery of oxygen to cardiac muscle cells - atheromatous plaques causes the narrowing Plaques begin as fatty streaks, injure endothelial lining, causes an inflammatory response - draw C reactive protein to tell basic informing on inflammation in body – tests CAD Platelets, fibrin, other fats, collect on the injured lining narrowing the blood vessel Scarring develops which causes the vessel to thicken Atheromas can rupture and block a vessel - Can travel down the vessel and get caught and that’s how an MI occurs

Coronary artery disease

``` Elevated cholesterol and lipids - high fat diets Unmodifiable -genetic predisposition – CAD in children -age -gender: men are more prone until women hit post-menopausal and then we are even Modifiable -Smoking – damages endothelial lining -sedentary lifestyle -hypertension -obesity Often asymptomatic until something drastic happens -At doctor and they test, or have heart attack and never go to doctor Treatment -Exercise -Low-fat diet -Smoking cessation -Weight loss -Stress management -Control of blood pressure -Control of blood sugar -Medications ```

Risk factors for CAD

Dietary fats are broken down to fatty acids (building block for triglycerides and phospholipids), lipids, and cholesterol by bile acids - small units called micelles are absorbed in the small intestine --triglycerides – float and get snagged on broken endothelial lining, stored in adipose tissue – use this for energy Used for 1. energy 2. stored for future use 3. processed into lipoproteins

Fat metabolism

Lipoproteins are produced mainly in the liver Consist of cholesterol, triglycerides, and lipids LDL – bad cholesterol and bad fats in body -broken down for energy -contain more cholesterol than HDLs --cholesterol is bad for our body -remnants are thought to initiate an inflammatory response -ideally <129 mg/dL but really want <100 HDL – good, want more of -used for energy -pick up remnants of LDL for transport to liver -like vacuum cleaner, suck up all the LDL bad stuff and recycles them -increase during exercise -ideally >60 mg/dL

LDL vs HDL

Required for -steroid hormone synthesis – like sex hormone (testosterone – need cholesterol in order to make that) -cell membrane formation --all cells have membranes, and to keep them intact we need cholesterol Every cell in the body has the ability to produce cholesterol -enzyme HMG-CoA – need this enzyme to make cholesterol If dietary cholesterol is limited, cellular synthesis will increase Total cholesterol <200

cholesterol

Bind with bile acids in the intestines to form an insoluble complex that is excreted in the feces -bile acids are high in cholesterol, so if we can bind up the bile acids we can get cholesterol down cholestyramine (Questran) colesevelam (WelChol) colestipol (Colestid) Use Were a mainstay of treatment until discovery of statins -produce 20% drop in LDL levels Often combined with statins for those not able to achieve control with statins alone Not used for monotherapy Not absorbed systemically -action is limited, only works when in intestines -most are taken multiple times per day, up to 6 times a day -compliance issue with this drug due to that

Bile acid sequestrants | not first line treatments

Adverse Effects Most are GI related: constipation, bloating, nausea, GI tract obstruction, malabsorption syndrome Rash Cautions -Can bind many drugs and reduce their absorption --warfarin, digoxin, penicillins, thiazide diuretics can bind anything you take orally, so monitor when they start new medications so you know how they will affect them Block absorption of iron and fat-soluble vitamins -vitamin K – fat soluble vitamin used for clotting factors and antidote to coumadin --so it patient takes coumadin and they don’t have vitamin K we need to watch for bleeding -can lead to malnutrition Caution with -complete biliary obstruction -abnormal intestinal function

Bile acid sequestrants

Nursing Considerations I. Monitor bowel sounds and function ii. Administer before meals because it has to be in intestinal tract when food is there to bind the bile acids iii. Powders should be mixed with at least 60 ml of any kind of liquid - to prevent esophageal irritation - the powder expands when it gets into GI tract if not mixed with enough water and can cause obstruction* iv. Administer other medications 1 hour before or 4 hours after

Bile acid sequestrants nursing considerations

HMG-CoA reductase is the primary regulatory enzyme for cholesterol biosynthesis -All cells can produce own cholesterol to maintain cell membrane integrity with is important for cell integrity As the liver makes less cholesterol, it responds by making more LDL receptors on the surface of liver cells -further reduces serum levels of LDL and cholesterol -more LDL on surface of liver cells and binds more serum to LDL and leaves lower levels of LDL and serum levels atorvastatin (Lipitor) – prototype pravastatin (Pravachol) rosuvastatin (Crestor) simvastatin (Zocor)

Statins

Use Reduce LDL 20 t0 40% - can be up to 60% Lower triglycerides and VLDLs -VLDLs are the primary carrier of triglycerides (fats that get stored in adipose tissue) Increase HDLs to get lower levels of bad fats and higher level of good fats Requires life-long treatment or until controlled through dietary/lifestyle changes – have to maintain the lifestyle change forever Nursing Considerations Best administered at night -liver is processing most lipids -best for those with a short half-life Administer with food if GI upset occurs – Nausea, dyspepsia Do not administer with grapefruit juice – increases absorption and can change levels Monitor LFTs Report increasing muscle pain* -Legs or any part hurt unusually, contact us

Statins

Adverse Effects Usually mild and most often affect the GI tract - dyspepsia, cramping, constipation, basic GI upsets Muscle or joint pain, headache, dizziness Rare rhabdomyolysis -Breakdown of muscle tissue, which released things that are dangerous to our body: potassium, and 2 other things (TEGRITY) --Can lead to cardiac issues, renal failure, muscle pain --Must be treated right away Cautions Hepatic impairment -all are metabolized/excreted through the liver except pravastatin (which is a renal excretion) -Dose adjustments may be needed for renal impairment -Pregnancy category X -Rhabdomyolysis risk increased with -erythromycin, cyclosporine (antibiotics), antifungals (systemic ones) Can increase digoxin, warfarin, oral contraceptive levels -So monitor patients closer: heart dysrhythmias, weakness

Statins

Decreases the absorption of dietary cholesterol from the small intestine Less cholesterol is delivered to the liver, the liver increases clearance of cholesterol from the serum to make up the difference ezetimibe (Zetia) Use Blocks absorption of cholesterol by as much as 50% -can cause the body to synthesize more cholesterol -may combine with a statin Not used as monotherapy – combined with Statin Reduces LDL by about 20% When combined with a statin LDL is reduced by an additional 15 to 20%

Cholesterol absorption inhibitors

Adverse Effects Usually well tolerated -abdominal pain -diarrhea – most common -upper respiratory tract infection – equally common --nasal stuffy, dripping nose, cough, sore throat -joint & muscle pain – careful when combined with Statin because of that pain Cautions Don't take with bile acid sequestrants -Will inhibit absorption Liver disease metabolized by liver -Cirrhosis, hepatitis – watch these patients very carefully Warfarin levels may increase Nursing Considerations Assess bowel sounds and function Access to bathroom Monitor for signs of upper respiratory tract infection

cholesterol absorption inhibits

Preferred drugs for severe hypertriglyceridemia Exact mechanism of action is unknown inhibit the breakdown of stored fat in adipose tissue reduce hepatic production of triglycerides fenofibrate (TriCor) gemfibrozil (Lopid) fenofibric acid (Trilipix) – most given ``` Cautions Most common side effects are GI related -cramping, diarrhea, dyspepsia Headache, dizziness, cholelithiasis (get gallbladder stones, which can increase production of stones in stone – so watch in people with gallbladder disease) Care with statins due to increased risk of rhabdomyolysis Care with warfarin -alters warfarin binding -report bleeding or unusual bruising May worsen gallbladder or liver disease -report right upper quadrant pain ```

Fibrates

Also called nicotinic acid or vitamin B3 and available OTC Inhibits the release of free fatty acids from adipose tissue, increases rate of triglyceride removal from plasma Reduces LDL by 20% More side effects that statins and not nearly as effective -most often used in lower doses as a supplement to statins or bile acid sequestrants Cautions Flushing and hot flashes occur in almost all patients -premedicate with an aspirin -take with cold water GI effects are common -nausea, gas, diarrhea Increases levels of uric acid (forms crystals in all our joints) -Watch for patients with gout Available OTC but self-medication should not be attempted because they do not know the right amount

Niacin - Misc CAD and HCL