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Pharm 1057 Test 2 - Coagulation Modifiers, Nitrates,
Anti-lipemics, Cardiac Glycosides
PHARMACOLOGY FOR PRACTICAL NURSES I (George Brown College)
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Coagula'on Modifiers •
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6 General Classes of Coagula/on Modifiers: Drug Class
Purpose
Anti-Coagulants
PREVENT clot formation
Inhibit certain clotting factors
PREVENT platelets from working
Anti-Platelets
Anti-Fibrinolytics
PROMOTE clot formation
PREVENT lysis of fibrin
Thrombolytics
LYSE a formed clot
Directly break down the clot
Heparin and Warfarin
Na Antagonists
REVERSAL agents
An/-­‐Coagula/on: Clot Resolu+on a. Blood plasma has 2 main factors that inhibit blood clo+ng i. An/-­‐thrombin II: prevents forma+on of thrombin ii. Plasminogen: is converted to plasmin b. The conversion to plasmin is facilitated by: i. ADH ii. Norepinephrine iii. Urokinase iv. Streptokinase BLOOD CLOT
induces
secretion of
TPA
Blood Coagula+on Mechanism •
Complex process that involves: a. Vasoconstric+on b. Aggrega+on (platelet clumping) c. Coagula+on (series of clo@ng factors) •
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Model includes several pre-­‐cursor molecules (like vitamin K) and is a cascade of factors Disease that cause dele+ons of these factors = bleeding disorders (increase bleeding +me) Medica+ons that impose changes to these factors = increase/
decreased of clo@ng effects PROTHROMBIN
PLASMINOGEN
PLASMIN
Therapeu+c Drug Monitoring •
THROMBIN
FIBRINOGEN
plasmin
dissolves
blood clot
TISSUE
PLASMINOGEN
ACTIVATOR (TPA)
FIBRIN
BLOOD CLOT
Use blood tests to monitor effects of drug therapy and indicate if therapeu+c effect of medica+on has been achieved' a. PT (Prothrombin Time) i. Prolonged PT = deficiency of one of the factors ii. Normal = 11-­‐12.5 seconds b. PTT (Par+al Thromboplas+n Time) i. To detect haemophilia ii. Monitoring effect of heparin iii. Normal = 60-­‐85 seconds Downloaded by Chris Sequioa (arieskid123@gmail.com)
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c. INR (Interna+onal Normalized Ra+o) i. PT +mes will vary according to technique used in lab ii. INR is a way to standardize PT +me based on these varia+ons iii. Normal value = 1; therapeu+c range = 2-­‐3 iv. Ideal range for Warfarin therapy = 2.5-­‐3.5 d. Platelets •
Heparin is superior to Warfarin to prevent pulmonary complica+ons in cases of thrombophlebi+s a. Is also preferred for thrombophlebi+s in pregnancy b. Does not cross placenta barrier/enter breast milk •
Prophylac/c Uses (preven+on of) a. DVT/Thrombophlebi+s b. Pulmonary Edema c. MI d. Heart Failure e. Stroke f. Pre-­‐Op for major thoracic/abdominal surgery Therapeu/c Uses (treatment of exis+ng) a. DVT/Thrombophlebi+s b. Pulmonary Edema c. Hemodialysis d. Cardiovascular Surgery e. Blood Transfusion An+-­‐Coagulants •
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To prevent forma/on of clots by inhibi+ng certain clo@ng factors Only given prophylac/cally, a. Used to prevent b. Have no effect on a clot that has already formed Used to treat: a. MI b. Unstable angina c. Atrial fibrilla+on d. Indwelling devices (pacemaker/mechanical valves) All agents will reduce ac0vity of certain clo4ng factors Two Groups: a. Parenteral: i. Heparin ii. LMW Heparin iii. Heparin-­‐like compounds iv. Thrombin inhibitors b. Oral: Warfarin •
Mechanism of Ac+on •
Pharmacokine+cs •
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Standard Heparin •
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Endogenous Heparin: a. Mucopolysaccharide found in various body +ssues b. Most abundant in liver and lung Exogenous Heparin: a. Obtained from animal +ssue b. Lipophobic (hates lipids and does not cross cell membrane easily) so it should not be administered orally Inhibits conversion of prothrombin to thrombin a. This prevents thrombus forma+on b. Inac+vates clo@ng factors by binding with an+-­‐
thrombin II •
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Highly protein Onset: immediately aeer IV; 20-­‐30 minutes aeer SUCUT Absorp/on: only given parenterally because it is not important from the GI tract Metabolized: liver Excreted: kidney Adverse Effects •
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Heparin induced thrombocytopenia Thrombocytopenia: blood has lower than normal number of platelets Bleeding (spontaneous/generalized) Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Nursing Considera+ons •
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Administra/on: a. IV (not absorbed by IM or PO) b. SC for LMW c. Dose expressed in USP units for standardiza+on d. Apply pressure to minimize bruising but do not massage e. Administered based on PTT and APTT i. Therapeu+c range = 1.5-­‐2 +mes the normal (30-­‐40 seconds) ii. If PTT = 1.5-­‐2.5 +mes the normal discon0nue iii. If PTT = outside therapeu+c range hold medica0on and contact MD Interac/ons: a. Herbal remedies (cinchona bark/gingko biloba/
goldenseal) b. An+-­‐histamines c. Nitroglycerin d. Tetracycline e. An/dote/Reversal Agent i. Whole blood/plasma ii. Protamin suphate (dissociates the heparin-­‐
an0thrombin complex) Assessments: a. Before Treatment (allergic reac+ons) b. During Treatment (monitor for haemorrhage/bleeding gums/blood in stool) c. Stop Treatment (on MD order if complaints of chills/
spontaneous bleeding/back pain) •
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Warfarin More potent than standard Heparin Longer half-­‐life Less blood tests required Safer/effec+ve for managing thromboembolism Slightly less haemorrhaging that standard •
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Long-­‐term an+coagulant therapy Contraindica+ons/adverse effects similar to Heparin •
Treatment Uses: a. DVT b. Pulmonary Edema c. Preven+on of clo@ng with presence of indwelling devices d. Post Stroke e. Post MI f. Post Venous Thromboembolism Low Molecular Weight Heparin •
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Examples: a. Ardeparin (Normiflo) b. Dalteparin (Fragmin) c. Enoxaparin (Levonox) Mechanism of Ac/on: inhibits conversion of prothrombin to thrombin a. Prevents thrombus forma+on b. Inac+vate the factor Xa Administra/on: a. SC or IV only i. Not effec+ve PO (inac+vated by stomach) ii. Not IM (muscle +ssue bleeds easily) b. Con+nuous IV (for standard Heparin) c. Dose in USP or IN units d. Dose affected by i. Herbal remedies (cinchona bark/gingko biloba/
goldenseal) ii. An+-­‐histamines iii. Nitroglycerin iv. Tetracycline Adverse Effects: a. Uncontrolled bleeding b. Hypersensi+vity c. Large doses lead to renal suppression/osteoporosis Downloaded by Chris Sequioa (arieskid123@gmail.com)
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b. Diet rich in vitamin K or supplements c. Cime+dine (inhibits metabolism) d. Homeopathic medica+ons (can alter effect) Mechanism of Ac+on •
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Acts on liver to prevent the synthesis of vitamin K dependant clo@ng factors Has no effect on circula+ng clo@ng factors and platelets •
Overdose: a. Omit one or more un+l bleeding stops or PTT normal b. Treat with vitamin K (1-­‐10mg use) •
Implica/ons: a. Possible allergic reac+on b. Monitor for haemorrhage (bleeding gums/blood in stool) c. Normal INR = 1.0 i. Do not give dose if INR . 3.0 ii. Monitor and ensure regular blood tests d. Therapeu+c range = 2.0 -­‐ 3.0 e. Report bleeding and bruising Pharmacokine+cs •
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Onset: effect does not occur un+l 3-­‐5 days aeer it is started Metabolized: liver and inac+ve metabolites Excreted: kidney Adverse & Side Effects •
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Side Effects: a. Abdominal cramps b. Nausea c. Diarrhea d. Vomi+ng Adverse Effects: a. Leucopenia b. Fetal abnormality when given during early pregnancy An+-­‐Platelets •
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Nursing Considera+ons Act in several ways to prevent platelet aggrega+on Arterial thrombi = platelet aggregates (therefore, an/-­‐
platelets used) Venous thrombi = fibrin/RBC (therefore, an/-­‐coagulants used) •
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Drug Displacement: a. Highly protein bound (some drugs will displace warfarin form the proteins) b. Results in more free an+coagulants in blood = increase in an+coagulant ac+vity c. Example: i. ASA ii. Ibuprofen iii. Naproxen Drug Interac/ons: a. Penicillin type drugs i. Increase an+coagula+on effect by affec+ng platelet func+on ii. Causes GI upset •
Examples: a. Ibuprofen/ASA-­‐related drugs (effect is gone once excreted from body) b. Dipyridamole c. Clopidogrel (Plavix) •
Mechanism of Ac/on: a. Depends on agent b. Prevent platelets from clumping to begin forming a clot c. Some block a receptor on the platelet and prevent from binding with fibrinogen •
Drug Interac/ons: a. Carbonic anhydrase inhibitors (glaucoma medica+on) b. Cor+costeroids Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Adverse Effects: a. Hypersensi+vity b. Serious bleeding c. GI problems •
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Nursing Considera/ons: a. Cau+on for history of bleeding/liver disease b. Contraindicated for hematopoie+c diseases (neutropenia/thrombocytopenia) c. Monitor/Educate i. Stop if platelet < 80 000 cells/mm3 ii. Watch for bleeding iii. Repor+ng chest pain/palpita+ons d. Some administered with food to avoid GI upset •
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Mechanism of Ac/on: a. S+mulate conversion of plasminogen to plasmin (fibrinolysis) b. Plasmin breaks down fibrin (fibrin is what makes up the thrombus) Administra/on: usually IV HIGH RISK for hemorrhages Only used when the clot in the confirmed cause of an ischemic event ASA •
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Reducing incidence of thrombosis with 75-­‐100 mg/day Used to prevent thrombus in pa+ents with a. Indwelling devices b. TIA's c. Acute MI Mechanism of Ac/on: a. Causes acetyla0on of cyclooxygenase enzyme b. Inhibits synthesis of thromboxane A2(vasoconstric+on/
platelet aggrega+on inducer) c. Also alters hepa+c synthesis of coagula+on factors VII, IX, X (like warfarin does) Nitrates •
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Organic agent that is first choice for angina treatment End effect is to dilate the coronary arteries by ac+ng on smooth muscle in both arteries/veins of blood vessel walls •
Clinical Effects: a. Dila+on of veins decreases blood return to the heart i. Less volume of blood to pump = less workload b. Dila+on of coronary arteries at high doses i. Increased BF to ischemic areas of heart c. Dila+on of arterioles i. Lower PVR = lower systolic BP •
Type of Nitrates: a. Short-­‐Ac/ng: i. Taken sublingually will stop acute angina amack that is happening ii. Example: Nitro-­‐glycerine b. Long Ac/ng: i. PO or transdermal to decreased frequency/
severity of angina episodes ii. Decreases symptoms of heart failure iii. Example: Diltrate SR Thromboly+c Agents •
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Directly or indirectly convert plasminogen to plasmin Used to dissolve thrombi Goal is to re-­‐establish blood flow ASAP and to limit +ssue damage Follows an+-­‐coagulant/an+-­‐platelet therapy to prevent reforma+on of clot Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Mechanism of Ac+on Clinical Agents of Nitrates •
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Nitrate (NO2) is converted into nitric oxide (NO) NO is the ac+ve form in smooth muscle It causes a cascade of enzymes that results in decreased intracellular Ca levels Decreased Ca levels = vasodila/on •
Nitro-­‐Glycerine (NTG) a. Most important for angina b. 1 spray sublingual every 5 minutes maximum 3 +mes i. Sublingual goes directly to blood ii. PO affected by first pass iii. Transdermal is slow so not used for acute amacks c. Adverse Effects of NTG: i. Hypotension ii. Headache/dizziness iii. Tachycardia iv. Rash v. Flush vi. Swea+ng vii. Chest pain •
Isosorbide Dinitrate: a. To reduce frequency/severity of acute angina episodes b. 2.5-­‐30 mg QID maximum 480 mg/day i. Sublingual onsets in 2 minutes and lasts 2-­‐3 hours ii. PO onsets in 30 minutes and lasts 4 hours iii. Sustained release onset in 4 hours •
Isosorbide Mononitrate: a. Metabolite/ac+ve component of isosorbide nitrate b. Regular/extended-­‐releases tab 1 (30-­‐60mg) /day Uses of Nitrates •
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MI (Central Ac/on): a. Dila+on of veins/arteries b. Reduces myocardial O2 demand c. More efficient distribu+on of blood in myocardium Hypertension (Peripheral): a. Reduces peripheral resistance b. Peripheral vasodila+on and lowers BP Stable Angina: a. Dilates veins b. Dilates collaterals c. To decreased O2 consump+on Heart Failure: a. Dilates veins to reduce aeerload b. Dilates veins to reduce perload c. Reduces wall stress/mitral regurgita+on Acute Coronary Syndrome: a. Dilates conduit arteries b. Dialtes collaterals c. An+aggregant effects to increased O2 supply Adverse Effects, Contraindica+ons and Cau+ons •
Pharmacokine+cs •
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Onset: 15-­‐60 minutes Dura/on: 0.5-­‐12 hours (depends on form) Metabolized: liver Excreted: kidney Affects directly on muscles (do not influence nerves) Tolerance with long ac+ng nitrates over extending +me a. Magnitude of tolerance is dependant on dose and frequency Adverse Effects: a. Dizziness/headache b. Nausea/vomi+ng c. Increased pulse d. Blurred vision e. Orthosta+c hypotension f. Erythema (from topical applica+on) Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Contraindica/ons: a. Hypersensi+vity b. Severe anemia c. Hypotension/hypovolemia d. Cerebral haemorrhage/head injury (elevates CSF) e. Cardiac tamponade f. Constric+ve pericardi+s Cau/ons: a. Glaucoma (increases intraocular pressure) b. Hyperthyroidism c. Hypotension f. PO i. On empty stomach ii. 1 hour before meal or 2 hours aeer •
Assessments: a. Chest pain (pre/post administra+on) i. Scale ii. 5 minutes before and 5 minutes aeer each dose b. BP (pre/post administra+on) c. Orthosta+c Vitals (BP/HR) i. For long-­‐ac+ng nitrates d. Vitals aeer 1 hour of administra+on e. Signs of overdose i. Dry mouth ii. Blurred vision iii. Severe headache •
Pa/ent Teaching: a. Signs of possible overdose and when to report b. Avoid alcohol c. How to store/replace tablets d. Advise to carry fast-­‐ac+ng with them e. Avoid stress that precipitates angina or take 5 minutes before stressful events f. An+cipate light headedness and slight headaches g. Proper use and administra+on Nursing Considera+ons •
Drug Contraindica/ons: a. Not to be taken 24hr before or aeer erec+le dysfunc+on medica+ons i. Addi+ve effect when used with a nitrate because they are vasodilators b. Hypotension is high risk when taken with i. Sildenafil (Viagra) ii. Vardenafil (Levitra) iii. Tadenafil (Cialis) •
Administra/on: a. Maximum 3 +mes every 5 minutes (even if pain is unresolved) b. Supine before administering ini+al dose c. Transdermal patch i. Remove every 6-­‐12 hours or withhold night doses to avoid tolerance ii. Rotate areas/wash sites when removing patch iii. Apply for 12 hours when pain is greatest (day or night) d. Ointments i. Avoid using finger to apply e. Extended-­‐release tablet i. Not used at bed+me ii. May cause aspira+ons An'lipemics •
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Used in treatment of hyperlipidemia Drug Agents: a. Bile Acid-­‐Binding Resin b. HMG-­‐CoA Reductase Inhibitor (Sta+ns) c. Niacin (Nico+nic Acid) d. Fibric Acids Bile Acid-­‐Binding Resin •
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Inhibit absorp+on of bile acid/cholesterol in intes+ne Lack of absorp+on from intes+ne = removal of circula+ng cholesterol Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Agents: a. Cholestyramine (Questran) b. Colesevelam c. Coles+pol •
Mechanism of Ac/on: a. Binds bile acid in intes+ne to form a non-­‐absorbable complex b. Prevents enteric-­‐hepa+c redistribu+on of bile acids c. Due to removal of bile, liver cells increase cholesterol metabolism to produce bile acids d. This reduces LDL and cholesterol levels •
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Adverse Effects: a. Bloa+ng/cons+pa+on b. Decreased vitamin K, A and D absorp+on c. Rash d. Muscle ache/pain •
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Pa/ent Teaching: a. 1 hour before or 4 hours aeer meals b. Follow bulk diet/lots of fluids c. May need supplements d. Report change of colour in skin/eyes Mechanism of Ac/on: a. HMG-­‐CoA reductase is enzyme that acts during a step of cholesterol produc+on b. Reduceing cholesterol in liver increases reduc+on of LDL from blood c. Overall effect is reduc+on of LDL/cholesterol levels Adverse Effects: mainly GI a. Flatulence b. Cramps c. Abdominal pain d. cons+pa+on Adverse Events: (rhabdomyolysis = breakdown of muscle has been reported) Pa/ent Teaching: a. Monitoring of liver func+on b. Avoid alcohol use c. Report numbness/+ngling/pain in feet and hands Niacin (Nico+nic Acid) •
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For hyperlipemic treatment = 2-­‐3g/day For vitamin supplement = 25 mg/day •
Mechanism of Ac/on: a. Inhibits VLDL synthesis by liver cells b. Causes decrease in LDL and triglyceride produc+on c. Reduces LDL/cholesterol/triglyceride d. Increases HDL levels •
Adverse Effects: more than sta+ns a. Hot flashes b. Flushing c. Nausea d. Flatulence e. diarrhea HMG-­‐CoA Reductase Inhibitor (Sta+ns) •
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Inhibit synthesis of cholesterol by liver Liver develops for LDL receptors and remove more LDL from blood Result is lower serum levels of cholesterol and LDL To slow progression of coronary disease and reduces CVD mortality Agents: a. Atorvasta+n (Lipitor) b. Lovasta+n (Mevacor) c. Fluvasta+n d. Simvasta+n Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Cardiac Glycosides Pa/ent Teaching: a. No megadoses b. Take with cold water not hot c. With or aeer meals •
Fibric Acids •
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Used to lower lipid levels and VLDL Replaced by sta+ns usually, or used in combina+on with them For trea+ng hypertriglyceridema Agents: a. Gemfibrozil (Lopid) b. Fenofibrate •
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Mechanism of Ac/on: unknown •
Adverse Effects: a. GI i. Nausea ii. Vomi+ng iii. Diarrhea iv. Gallstones b. GU i. Erec+le dysfunc+on ii. Hematuria iii. Decreased urine iv. UTI c. Drowsiness/dizziness d. Rash e. Alopecia f. Headaches Pa/ent Teaching: a. Keep all medical follow ups and lab appointments b. Report bruising/bleeding/muscle cramps/stool colour •
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Inotropic: contrac+lity a. Posi0ve = increases force of contrac+on i. Dopamine ii. Epinephrine iii. Isoproterenol b. Nega0ve = decreases force of contrac+on i. Lidocaine ii. Quinidine iii. Propranolol Chronotropic: heart rate a. Posi0ve = increases HR i. Norepinephrine b. Nega0ve = slows HR i. Acetylcholine Dromotropic: cardiac nerves impulses a. Posi0ve = increases rate of electrical conduc+on i. Phenytoin b. Nega0ve = slows rate of electrical conduc+on i. Verapamil Cardiac Glycosides •
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Organic compounds with a glycoside (sugar) Potent in changing heart func+on a. Can be extremely toxic Naturally occur in nature a. Digitalis purpura plant has a glycoside used for heart disease treatment Agents: a. Digoxin (Lanoxin, Lanoxicaps) b. Phosphodiesterase Inhibitors ( just know they exist) Downloaded by Chris Sequioa (arieskid123@gmail.com)
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Digoxin •
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The only commonly used digitalis glycoside In regards to the 3 types of effects: a. Inotropic = posi+ve b. Chronotropic = nega+ve c. Dromotropic = nega+ve (not as important to note) •
Clinical and Adverse Effects •
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Clinical Effects: a. Improved CO = improved +ssue perfusion without supplementary O2 therapy b. Improved perfusion promotes diuresis = alleviates edema (along with diure+c therapy) •
Adverse Effects: a. Cardiac changes i. Ventricular fibrilla+on ii. Dysrhythmia iii. AV block b. Gastric irrita+on i. Vomi+ng (s+mula+on of chemoreceptor trigger zone) ii. Anorexia iii. Diarrhea c. CNS changes i. Disorienta+on ii. Hallucina+ons iii. Visual disturbance (par/cularly with colour percep/on; toxic when report of yellow-­‐blue halo) iv. Headache v. Weakness vi. Drowsiness Uses: a. Primarily in moderate to severe heart failure b. Arterial fibrilla+on c. Arterial flumer/parozysmal tachycardia Excreted: unchanged in urine a. Risk of accumula+on/toxicity if impaired renal func+on Does not enter breast milk but shown to affect neonate a. Effect on fetus unknown •
Reversal Agent: DIGIBIND (Digifab, Digoxin Immune Fab) a. An+body (Igb) fragments that bind to molecules of digoxin b. Lowers levels of free digoxin in blood c. Cleared by the kidney d. Used for life-­‐threatening digoxin toxicity or overdose Mechanism of Ac+on •
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Posi/ve Inotropic Ac/on: a. Inhibits Na/K pump i. Causes Ca to shie to outside of cell b. Large amounts of free Ca = increases cardiac muscle contrac+on c. Myocardium of failing heart will beat more forcefully = increased CO and decreased O2 demand Nega/ve Chronotropic Ac/on: a. Inhibits Na/K pump i. Causes membrane not to return to res+ng poten+al b. Results in slowing SA node = slowing HR Nursing Considera+ons •
Pharmacokine+cs •
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Absorp/on: rapid Distribu/on: widely throughout the body Administra/on: a. Route i. PO or IV ii. Elixir bemer than tablet for children iii. Bioavailability will change if route changes Downloaded by Chris Sequioa (arieskid123@gmail.com)
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b. Loading dose (to bring serum level to therapeu+c value) remember to check i. HR (apical and radial for 1 full minute) ii. Rhythm iii. BP iv. Renal func+on v. Electrolytes c. Maintenance doses = excreted amount d. Therapeu+c Drug Monitoring (narrow therapeu+c index) e. Presence of food = decreased absorp+on f. Risk of drug interac+on is high g. Withhold if pulse < 60 or > 100 b/min h. No+fy if irregular rhythm d. Renal i. Body weight ii. Electrolytes e. History of allergies •
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Drug Interac/ons: a. An+-­‐dysrhythmic drugs b. Magnesium sulphate (may alter conduc+on or cause heart block) c. Potassium salts d. Quinidine e. Spironolactone f. Sucralfate Ini/al Assessments: before therapy starts a. CVS i. BP ii. Apical pulse iii. Perfusion iv. ECG b. CNS i. Orienta+on ii. Affect iii. Reflexes iv. Vision c. Inetgumentary i. Skin colour ii. Lesions iii. Texture iv. Perfusion Phosphodiesterase Inhibitors •
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Group of inotropic agents Inhibit the enzyme phosphodiesterase Results in posi/ve inotropy and vasodila/on Agents: a. Inamrinone (Inocor) b. Milrinone lactate (Primacor) •
Indica/on for use: a. End stage heart failure (to improve quality of life) b. Primarily for those who do not respond to other treatments like digoxin c. Closely monitored d. Increase dose = increased adverse effects •
Recurring Assessments: during therapy a. CVS (dysrhythmias) b. Renal dysfunc+on i. Electrolyte imbalances ii. Increased weight (risk for reduces elimina+on = toxicity) c. CNS impairment i. Electrolyte imbalance from renal failure may present as cogni+ve impairment in older adults d. GI changes (vomi+ng/anorexia) Downloaded by Chris Sequioa (arieskid123@gmail.com)