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PRESENTATION ON
CARDIOVASCULAR DRUGS
BY
RAJEE RAVINDRAN
Drugs that have beneficial action on the heart
LUSITROPIC
Heart Rate
Strength of
contraction
Conduction speed
in AV node
Degree of
excitability
Effect on
relaxation
TYPES
CARDIAC
GLYCOSIDES
SYMPATHOMIMETICS
PHOSPHODIESTERASE
INHIBITORS
DIGOXIN
DOPAMINE,
DOBUTAMINE
MILRINONE
DIGOXIN
FOXGLOVE PLANT
(Digitalis purpurea)
Potent inhibitors of cellular Na+/K+ ATPase
Therapeutic Action
 Positive inotropic effect
 Negative dromotropic effect
 Negative chronotropic effect
Indications
CHF, Atrial Flutter, Atrial Fibrillation, Paroxysmal Atrial Tachycardia
Pharmacokinetics
Route Onset Peak Duration
Oral 30-120 min 2-6 h 6-8 d
IV 5-30 min 1-5 h 4-5 d
T1/2:30-40h
Metabolism: N/A
Excretion: urine (unchanged)
Contraindications and Cautions
 Allergy to any component of digitalis preparation
 Ventricular tachycardia or fibrillation
 Heart block (sick sinus syndrome)- Can be worsened by drug’s effect on slowing conduction
through AV node
 Acute myocardial infarction (MI)- Increasing the force of contraction can damage the heart
muscles more.
 Renal insufficiency. Drug is excreted through urine and the existing renal insufficiency can
contribute to development of drug toxicity.
 Pregnancy and lactation
Adverse Effects
CNS: headache, weakness, drowsiness, vision changes (Blurry vision with a yellow tint and halos)
CV: arrhythmias
GI: GI upset, anorexia
The classic Digoxin Effect appears as a down sloping ST segment
depression, also known as the "reverse tick" or "reverse check" sign.
TREATMENT FOR DIGOXIN TOXICITY
Digoxin immune Fab or DigiFab/ Digibind-
These antibodies bind molecules of digoxin,
making them unavailable at site of action. Used
when serum digoxin is >10 ng/mL and serum
potassium is >5 mEq/L.
Each vial (40 mg) will bind approximately
0.5 mg of digoxin
Dose (vials) = Total IV digoxin body load in
mg /0.5
Nursing Responsibilities
 Check drug dose and preparation carefully to avoid medication errors because drug has narrow
safety margin.
 Do not administer drug with food and antacids to prevent decreased in drug absorption.
 Drug is withheld if pulse is less than 60 beats per minute in adults and 90 beats per minute in
infants.
 Assess pulse rhythm to detect arrhythmias which are early signs of drug toxicity.
 Weigh the patient daily to monitor for fluid retention and HF. Assess dependent areas for
presence of edema and note its degree of pitting to assess severity of fluid retention.
 Monitor serum digoxin level as ordered (normal: 0.5-2 ng/mL) to evaluate therapeutic dosing
and development of adverse effects.
 Provide comfort measures (e.g. small frequent meals for GI upset, instituting safety measures
for drowsiness and weaknesses, and providing adequate room lighting for patients with visual
disturbances) to help patient tolerate drug effects.
 Promote rest periods and relaxation techniques to balance supply and demand of oxygen.
 Ensure maintenance of emergency drugs and equipment at bedside (e.g. potassium salts and
lidocaine for arrhythmias, phenytoin for seizures, atropine in case of clinically significant low
heart rate, and cardiac monitor) to promote prompt treatment in cases of severe toxicity.
 Educate patient on drug therapy including drug name, its indication, and adverse effects to
watch out for to enhance patient understanding on drug therapy and thereby promote
adherence to drug regimen.
Natural catecholamine Synthetic catecholamine
Effect
on renal
blood
flow
Improves at low dose
by direct action
May improve due to improved
cardiac function
Shock, renal failure Cardiac failure, Ischemic LVF
2-20 mcg/Kg/min
2-5mcg/Kg/min- inotropic range
5mcg/kg/min- renal perfusion range
5-20mcg/kg/min- vasopressor range
(vasoconstriction)
Inotropic
Peripheral vasodilator
Unresponsive CHF to
other treatment
50mcg/kg/min- loading dose
0.375- 0.75mcg/kg/min
Therapeutic Action
Blocks receptor sites on the platelet membrane, platelet adhesion and
aggregation is inhibited. Also, platelet-platelet interaction as well as interaction of
platelets to clotting chemicals are prevented.
Indications
 Cardiovascular diseases that have potential for development of vessel
occlusion
 Maintenance of arterial and venous grafts
 Preventing cerebrovascular occlusion
 Adjunct to thrombolytic therapy for treatment of myocardial infarction.
Pharmacokinetics
Route Onset Peak Duration
Oral 5-30 min 0.25-2 h 3-6 h
T1/2: 15 min – 12 h, Metabolism: liver, Excretion: bile
Contraindications and Cautions
 Allergy to antiplatelet agents. Prevent severe hypersensitivity reactions.
 Known bleeding disorder. Increased risk of excessive blood loss
 Recent surgery. Increased risk of bleeding in unhealed blood vessels
 Closed head injuries. Increased risk of bleeding in injured blood vessels of the brain
 History of thrombocytopenia. Anagrelide decreased bone marrow production of platelets.
 Pregnancy, lactation. Generally inadvisable because of potential adverse effects to fetus or
neonate
Adverse Effects
 CNS: headache, dizziness, weakness
 GI: GI distress, nausea
 Skin: skin rash
 Hema: bleeding (oftenly occurs while brushing the teeth)
Nursing Responsibilities
 Administer drug with meals to relieve GI upset.
 Provide comfort measures for headache because pain due to headache may decrease patient compliance
to treatment regimen.
 Educate patient on ways to promote safety like using electric razor, soft-bristled toothbrush, and cautious
movement because any injury at this point can precipitate bleeding.
 Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for
to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.
 Monitor patient response to therapy (e.g. increased bleeding time, prevention of occlusive events).
 Monitor for adverse effects (e.g. bleeding, headache, GI upset).
 Evaluate patient understanding on drug therapy by asking patient to name the drug, its indication, and
adverse effects to watch for.
 Monitor patient compliance to drug therapy.
Interferes with clotting cascade and thrombin formation
Indications
 Stroke and systemic emboli risk reduction
 Nonvalvular atrial fibrillation
 Deep vein thrombosis
Heparin is used for prevention of blood clots in blood samples, dialysis, and venous tubing. It
also does not enter breastmilk so it is the anticoagulant of choice for lactating women.
Pharmacokinetics
Route Onset Peak Duration
IV Immediate Minutes2-6 h
Subcutaneous 20-60 min 2-4 h 8-12 h
T1/2: 30-180 min
Metabolism: cells
Excretion: urine
Contraindications and Cautions
 Allergy to anticoagulants. Prevent severe hypersensitivity reactions.
 Known bleeding disorder, recent trauma/surgery, presence of indwelling catheters, threatened
abortion, GI ulcers. These conditions can be compromised by increased bleeding tendencies.
 Pregnancy, lactation. Warfarin is a contraindication.
Adverse Effects
 Warfarin is associated with alopecia, dermatitis, bone marrow depression, and less frequently
with prolonged and painful erections.
 Direct drug toxicity is characterized by nausea, GI upset, diarrhea, and hepatic dysfunction.
 Interactions
 Anticoagulants, salicylates, penicillin, cephalosporin: increased bleeding if combined with
heparin
 Nitroglycerin: decreased anticoagulation if combined with heparin
 Cimetidine, clofibrate, glucagon, erythromycin: increased bleeding if combined with warfarin
 Vitamin K, phenytoin, rifampin, barbiturates: decreased anticoagulation if combined with warfarin
 Antifungals, erythromycin, phenytoin, rifampin: alteration in metabolism of dabigatran and
rivaroxaban
Nursing Responsibilities
 Assess for signs signifying blood loss (e.g. petechiae, bruises, dark-colored stools, etc.) to determine
therapy effectiveness and promote prompt intervention for bleeding episodes.
 Establish safety precautions (e.g. raising side rails, ensuring adequate room lighting, padding sides of
bed, etc.) to protect patient from injury.
 Maintain antidotes on bedside (e.g. protamine sulfate for heparin, Vitamin K for warfarin) to promptly
treat drug overdose.
 Evaluate effectiveness by monitoring the following blood tests: prothrombin time (PT) and international
normalized ratio (INR) for warfarin; and whole blood clotting time (WBCT) and activated partial
thromboplastin time (APTT) for heparin.
 Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for
to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.
Lysis of thrombin/ clot by activating plasminogen, resulting in the formation of plasmin, which
cleaves the fibrin cross-links causing thrombus breakdown.
INDICATIONS
CONTRAINDICATIONS
ALTEPLASE Acute MI: (>67kg): 15 mg IV bolus over 1-2 minutes, then 50 mg
over 30 minutes, then 35 mg over next 60 minutes. (<67kg): 15 mg
IV bolus, followed by 0.75 mg/kg (maximum 50mg) over 30 minutes,
then 0.5 mg/kg (maximum 35mg) over the next 60 minutes. Infuse
remaining 35 mg of alteplase over the next hour.
Acute PE: 100mg IV over 2 hours, then restart heparin when PTT <
twice normal.
Acute ischemic stroke: Doses should be given within the first 3 hours of the onset of symptoms.
Recommended total dose: 0.9 mg/kg (maximum dose should not exceed 90 mg) infused over 60
minutes. Load with 0.09 mg/kg (10% of the 0.9 mg/kg dose) as an IV bolus over 1 minute, followed by
0.81 mg/kg (90% of the 0.9 mg/kg dose) as a continuous infusion over 60 minutes. Heparin should not
be started for 24 hours or more after starting alteplase for stroke.
TENECTEPLASE
30 mg for weight < 60 kg(6ml)
35 mg for 60–69 kg(7ml)
40 mg for 70–79 kg(8ml)
45 mg for 80–89 kg(9ml)
50 mg for >90 kg(10ml)
Acute MI
The recommended total dose should not exceed 50
mg and is based upon patient weight.
Tenecteplase is incompatible with dextrose solutions. Dextrose-containing lines
must be flushed with a saline solution before and after administration.
Administer as a single I.V. bolus over 5 seconds.
RETEPLASE
10-U IV boluses given 30 min apart
 Statins (3-Hydroxy-2-Methylglutaryl Coenzyme A reductase Inhibitors)- Interfere with HMG Co
A reductase, the critical enzyme in the biosynthesis of cholesterol. Eg-Atorvastatin, Fluvastatin,
Lovastatin, Pitavastatin, Pravastatin, Simvastatin, Rosuvastatin
 Niacin(Nicotinic Acid)- B-complex vitamin that decreases both VLDL and LDL levels.
HYPOLIPIDEMICS CLASSIFICATION
 Bile Acid Resins or Sequestrants- Binds bile acids, thus increasing the excretion of cholesterol in
the stool. Example- Cholestyramine, Colestipol, Colesevelam
 Ezetimibe( Cholestrol Absorption Inhibitors)- Blocks the absorption of cholesterol from the
intestinal lumen by cells in the jejunum of the small intestine.
 Fibric Acid agents- Drug of choice in severe hypertriglyceridemia and excessive VLDL levels.
Example – Gemfibrozil, fenofibrate, finofibric acid
HYPOLIPIDEMICS CLASSIFICATION
10 mg, 20 mg, 40 mg, 80 mg ONCE DAILY
5 mg, 10 mg, 20 mg, 40 mg ONCE DAILY
5 mg, 10 mg, 20 mg, 40 mg, 80 mg ONCE DAILY
If given with Fibrates or niacin: Dose should not exceed 20 mg/day
Pharmacokinetics
Route Onset Peak Duration
Oral Slow 1-2 h 20-30 h
T1/2: 14 h, Metabolism: liver, Excretion: bile
Contraindications and Cautions
 Allergy to HMG-CoA reductase inhibitors. Prevent severe hypersensitivity reactions.
 Active liver disease- Exacerbated by drug’s therapeutic effect and has potential to lead to severe
liver failure.
 Pregnancy, lactation- Potential for drug adverse effects to fetus or neonate.
 Impaired endocrine function- Problems can arise due to alteration in the formation of steroid
hormones.
 Renal impairment- Caution is given to patients taking other statins and close monitoring in
instituted. Atorvastatin is not affected by renal diseases.
Adverse Effects
 CNS: headache, dizziness, insomnia, fatigue, blurred vision, cataract development
 CV: increased risk for cardiovascular effects with simvastatin started at 80 mg for new patients
 GI: flatulence, nausea, vomiting, cramps, abdominal pain, constipation
 Hepatobiliary: increase liver enzymes, acute liver failure with use of atorvastatin and
Fluvastatin
Interactions
 Cyclosporine, erythromycin, gemfibrozil, niacin, antifungal drugs: increased risk for
rhabdomyolysis
 Digoxin, warfarin: increased serum levels and resultant toxicity of HMG-CoA reductase
inhibitors
 Oral contraceptives: increased serum estrogen
 Grapefruit juice: increased serum levels and resultant toxicity
Nursing Responsibilities
 Administer drug at bedtime to maximize effectiveness of the drug because peak of cholesterol synthesis
is from midnight to 5 AM. However, Atorvastatin can be given at any hour of the day.
 Monitor serum cholesterol and LDL levels to determine effectiveness of drug therapy.
 Monitor results of liver functions tests to determine possible liver damage.
 Ensure patient has initiated a 3-6 month diet and exercise program before initiating drug therapy to
ensure need for drug therapy.
 Emphasize the importance of lifestyle changes to the patient to decrease risk of CAD and promote drug
effectiveness.
 Provide comfort and safety measures to help patient tolerate drug side effects.
 Educate patient on drug therapy
Cardiovascular agents are medicines that are used to treat medical conditions associated with the
heart or the circulatory system (blood vessels). Some work directly on the blood vessels surrounding
the heart, reducing how much force the heart has to pump against. Others lower cholesterol levels
and help reduce the formation of atherosclerotic plaques which cause blood vessel narrowing. Some
work in the kidneys to increase fluid and salt loss or improve blood flow through the kidneys. The type
of cardiovascular disease the person has determines which class of cardiovascular agent to use.
 Greenstein B: Drugs acting on the heart : Trounce’s clinical pharmacology for nurses; 18 (ed);Elsevier 2009:
Page 59-72
 Adams P M, Holland N L, Bostwick M P, The cardiovascular and Urinary systems: Pharmacology for Nurses;
Pearson education 2009; page 285- 418
 Dr. P.K. Panwar, Essentials of pharmacology for nurses, AITBS pub.2017, India, page 118-134
 Dr. suresh K sharma, Textbook of pharmacology, pathology and genetics for nurses, jaypee pub.2016 Indai .
page 362-452
 Lehne, R. A., Moore, L. A., Crosby, L. J., & Hamilton, D. B. (2004). Pharmacology for nursing care.
 Smeltzer, S. C., & Bare, B. G. (1992). Brunner & Suddarth’s textbook of medical-surgical nursing.
Philadelphia: JB Lippincott.
 Heart.org/en/health-topics/heart-attack/treatment-of-a-heart-attack/cardiac-medications
 https://www.britannica.com/science/cardiovascular-drug
 https://www.americannursetoday.com/emergency-cardiac-drugs-essential-facts-for-med-surg-nurses
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Cardiovascular Drugs

  • 2. Drugs that have beneficial action on the heart
  • 3. LUSITROPIC Heart Rate Strength of contraction Conduction speed in AV node Degree of excitability Effect on relaxation
  • 5. DIGOXIN FOXGLOVE PLANT (Digitalis purpurea) Potent inhibitors of cellular Na+/K+ ATPase
  • 6.
  • 7.
  • 8.
  • 9. Therapeutic Action  Positive inotropic effect  Negative dromotropic effect  Negative chronotropic effect Indications CHF, Atrial Flutter, Atrial Fibrillation, Paroxysmal Atrial Tachycardia Pharmacokinetics Route Onset Peak Duration Oral 30-120 min 2-6 h 6-8 d IV 5-30 min 1-5 h 4-5 d T1/2:30-40h Metabolism: N/A Excretion: urine (unchanged)
  • 10. Contraindications and Cautions  Allergy to any component of digitalis preparation  Ventricular tachycardia or fibrillation  Heart block (sick sinus syndrome)- Can be worsened by drug’s effect on slowing conduction through AV node  Acute myocardial infarction (MI)- Increasing the force of contraction can damage the heart muscles more.  Renal insufficiency. Drug is excreted through urine and the existing renal insufficiency can contribute to development of drug toxicity.  Pregnancy and lactation Adverse Effects CNS: headache, weakness, drowsiness, vision changes (Blurry vision with a yellow tint and halos) CV: arrhythmias GI: GI upset, anorexia
  • 11.
  • 12. The classic Digoxin Effect appears as a down sloping ST segment depression, also known as the "reverse tick" or "reverse check" sign. TREATMENT FOR DIGOXIN TOXICITY Digoxin immune Fab or DigiFab/ Digibind- These antibodies bind molecules of digoxin, making them unavailable at site of action. Used when serum digoxin is >10 ng/mL and serum potassium is >5 mEq/L. Each vial (40 mg) will bind approximately 0.5 mg of digoxin Dose (vials) = Total IV digoxin body load in mg /0.5
  • 13.
  • 14. Nursing Responsibilities  Check drug dose and preparation carefully to avoid medication errors because drug has narrow safety margin.  Do not administer drug with food and antacids to prevent decreased in drug absorption.  Drug is withheld if pulse is less than 60 beats per minute in adults and 90 beats per minute in infants.  Assess pulse rhythm to detect arrhythmias which are early signs of drug toxicity.  Weigh the patient daily to monitor for fluid retention and HF. Assess dependent areas for presence of edema and note its degree of pitting to assess severity of fluid retention.  Monitor serum digoxin level as ordered (normal: 0.5-2 ng/mL) to evaluate therapeutic dosing and development of adverse effects.  Provide comfort measures (e.g. small frequent meals for GI upset, instituting safety measures for drowsiness and weaknesses, and providing adequate room lighting for patients with visual disturbances) to help patient tolerate drug effects.  Promote rest periods and relaxation techniques to balance supply and demand of oxygen.  Ensure maintenance of emergency drugs and equipment at bedside (e.g. potassium salts and lidocaine for arrhythmias, phenytoin for seizures, atropine in case of clinically significant low heart rate, and cardiac monitor) to promote prompt treatment in cases of severe toxicity.  Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.
  • 15. Natural catecholamine Synthetic catecholamine Effect on renal blood flow Improves at low dose by direct action May improve due to improved cardiac function Shock, renal failure Cardiac failure, Ischemic LVF 2-20 mcg/Kg/min 2-5mcg/Kg/min- inotropic range 5mcg/kg/min- renal perfusion range 5-20mcg/kg/min- vasopressor range (vasoconstriction) Inotropic Peripheral vasodilator Unresponsive CHF to other treatment 50mcg/kg/min- loading dose 0.375- 0.75mcg/kg/min
  • 16.
  • 17.
  • 18.
  • 19. Therapeutic Action Blocks receptor sites on the platelet membrane, platelet adhesion and aggregation is inhibited. Also, platelet-platelet interaction as well as interaction of platelets to clotting chemicals are prevented. Indications  Cardiovascular diseases that have potential for development of vessel occlusion  Maintenance of arterial and venous grafts  Preventing cerebrovascular occlusion  Adjunct to thrombolytic therapy for treatment of myocardial infarction. Pharmacokinetics Route Onset Peak Duration Oral 5-30 min 0.25-2 h 3-6 h T1/2: 15 min – 12 h, Metabolism: liver, Excretion: bile
  • 20. Contraindications and Cautions  Allergy to antiplatelet agents. Prevent severe hypersensitivity reactions.  Known bleeding disorder. Increased risk of excessive blood loss  Recent surgery. Increased risk of bleeding in unhealed blood vessels  Closed head injuries. Increased risk of bleeding in injured blood vessels of the brain  History of thrombocytopenia. Anagrelide decreased bone marrow production of platelets.  Pregnancy, lactation. Generally inadvisable because of potential adverse effects to fetus or neonate Adverse Effects  CNS: headache, dizziness, weakness  GI: GI distress, nausea  Skin: skin rash  Hema: bleeding (oftenly occurs while brushing the teeth)
  • 21. Nursing Responsibilities  Administer drug with meals to relieve GI upset.  Provide comfort measures for headache because pain due to headache may decrease patient compliance to treatment regimen.  Educate patient on ways to promote safety like using electric razor, soft-bristled toothbrush, and cautious movement because any injury at this point can precipitate bleeding.  Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.  Monitor patient response to therapy (e.g. increased bleeding time, prevention of occlusive events).  Monitor for adverse effects (e.g. bleeding, headache, GI upset).  Evaluate patient understanding on drug therapy by asking patient to name the drug, its indication, and adverse effects to watch for.  Monitor patient compliance to drug therapy.
  • 22.
  • 23. Interferes with clotting cascade and thrombin formation Indications  Stroke and systemic emboli risk reduction  Nonvalvular atrial fibrillation  Deep vein thrombosis Heparin is used for prevention of blood clots in blood samples, dialysis, and venous tubing. It also does not enter breastmilk so it is the anticoagulant of choice for lactating women. Pharmacokinetics Route Onset Peak Duration IV Immediate Minutes2-6 h Subcutaneous 20-60 min 2-4 h 8-12 h T1/2: 30-180 min Metabolism: cells Excretion: urine
  • 24. Contraindications and Cautions  Allergy to anticoagulants. Prevent severe hypersensitivity reactions.  Known bleeding disorder, recent trauma/surgery, presence of indwelling catheters, threatened abortion, GI ulcers. These conditions can be compromised by increased bleeding tendencies.  Pregnancy, lactation. Warfarin is a contraindication. Adverse Effects  Warfarin is associated with alopecia, dermatitis, bone marrow depression, and less frequently with prolonged and painful erections.  Direct drug toxicity is characterized by nausea, GI upset, diarrhea, and hepatic dysfunction.  Interactions  Anticoagulants, salicylates, penicillin, cephalosporin: increased bleeding if combined with heparin  Nitroglycerin: decreased anticoagulation if combined with heparin  Cimetidine, clofibrate, glucagon, erythromycin: increased bleeding if combined with warfarin  Vitamin K, phenytoin, rifampin, barbiturates: decreased anticoagulation if combined with warfarin  Antifungals, erythromycin, phenytoin, rifampin: alteration in metabolism of dabigatran and rivaroxaban
  • 25. Nursing Responsibilities  Assess for signs signifying blood loss (e.g. petechiae, bruises, dark-colored stools, etc.) to determine therapy effectiveness and promote prompt intervention for bleeding episodes.  Establish safety precautions (e.g. raising side rails, ensuring adequate room lighting, padding sides of bed, etc.) to protect patient from injury.  Maintain antidotes on bedside (e.g. protamine sulfate for heparin, Vitamin K for warfarin) to promptly treat drug overdose.  Evaluate effectiveness by monitoring the following blood tests: prothrombin time (PT) and international normalized ratio (INR) for warfarin; and whole blood clotting time (WBCT) and activated partial thromboplastin time (APTT) for heparin.  Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.
  • 26.
  • 27. Lysis of thrombin/ clot by activating plasminogen, resulting in the formation of plasmin, which cleaves the fibrin cross-links causing thrombus breakdown.
  • 28.
  • 29.
  • 32. ALTEPLASE Acute MI: (>67kg): 15 mg IV bolus over 1-2 minutes, then 50 mg over 30 minutes, then 35 mg over next 60 minutes. (<67kg): 15 mg IV bolus, followed by 0.75 mg/kg (maximum 50mg) over 30 minutes, then 0.5 mg/kg (maximum 35mg) over the next 60 minutes. Infuse remaining 35 mg of alteplase over the next hour. Acute PE: 100mg IV over 2 hours, then restart heparin when PTT < twice normal. Acute ischemic stroke: Doses should be given within the first 3 hours of the onset of symptoms. Recommended total dose: 0.9 mg/kg (maximum dose should not exceed 90 mg) infused over 60 minutes. Load with 0.09 mg/kg (10% of the 0.9 mg/kg dose) as an IV bolus over 1 minute, followed by 0.81 mg/kg (90% of the 0.9 mg/kg dose) as a continuous infusion over 60 minutes. Heparin should not be started for 24 hours or more after starting alteplase for stroke.
  • 33. TENECTEPLASE 30 mg for weight < 60 kg(6ml) 35 mg for 60–69 kg(7ml) 40 mg for 70–79 kg(8ml) 45 mg for 80–89 kg(9ml) 50 mg for >90 kg(10ml) Acute MI The recommended total dose should not exceed 50 mg and is based upon patient weight. Tenecteplase is incompatible with dextrose solutions. Dextrose-containing lines must be flushed with a saline solution before and after administration. Administer as a single I.V. bolus over 5 seconds.
  • 34. RETEPLASE 10-U IV boluses given 30 min apart
  • 35.
  • 36.  Statins (3-Hydroxy-2-Methylglutaryl Coenzyme A reductase Inhibitors)- Interfere with HMG Co A reductase, the critical enzyme in the biosynthesis of cholesterol. Eg-Atorvastatin, Fluvastatin, Lovastatin, Pitavastatin, Pravastatin, Simvastatin, Rosuvastatin  Niacin(Nicotinic Acid)- B-complex vitamin that decreases both VLDL and LDL levels. HYPOLIPIDEMICS CLASSIFICATION
  • 37.  Bile Acid Resins or Sequestrants- Binds bile acids, thus increasing the excretion of cholesterol in the stool. Example- Cholestyramine, Colestipol, Colesevelam  Ezetimibe( Cholestrol Absorption Inhibitors)- Blocks the absorption of cholesterol from the intestinal lumen by cells in the jejunum of the small intestine.  Fibric Acid agents- Drug of choice in severe hypertriglyceridemia and excessive VLDL levels. Example – Gemfibrozil, fenofibrate, finofibric acid HYPOLIPIDEMICS CLASSIFICATION
  • 38. 10 mg, 20 mg, 40 mg, 80 mg ONCE DAILY 5 mg, 10 mg, 20 mg, 40 mg ONCE DAILY 5 mg, 10 mg, 20 mg, 40 mg, 80 mg ONCE DAILY If given with Fibrates or niacin: Dose should not exceed 20 mg/day
  • 39. Pharmacokinetics Route Onset Peak Duration Oral Slow 1-2 h 20-30 h T1/2: 14 h, Metabolism: liver, Excretion: bile Contraindications and Cautions  Allergy to HMG-CoA reductase inhibitors. Prevent severe hypersensitivity reactions.  Active liver disease- Exacerbated by drug’s therapeutic effect and has potential to lead to severe liver failure.  Pregnancy, lactation- Potential for drug adverse effects to fetus or neonate.  Impaired endocrine function- Problems can arise due to alteration in the formation of steroid hormones.  Renal impairment- Caution is given to patients taking other statins and close monitoring in instituted. Atorvastatin is not affected by renal diseases.
  • 40. Adverse Effects  CNS: headache, dizziness, insomnia, fatigue, blurred vision, cataract development  CV: increased risk for cardiovascular effects with simvastatin started at 80 mg for new patients  GI: flatulence, nausea, vomiting, cramps, abdominal pain, constipation  Hepatobiliary: increase liver enzymes, acute liver failure with use of atorvastatin and Fluvastatin Interactions  Cyclosporine, erythromycin, gemfibrozil, niacin, antifungal drugs: increased risk for rhabdomyolysis  Digoxin, warfarin: increased serum levels and resultant toxicity of HMG-CoA reductase inhibitors  Oral contraceptives: increased serum estrogen  Grapefruit juice: increased serum levels and resultant toxicity
  • 41. Nursing Responsibilities  Administer drug at bedtime to maximize effectiveness of the drug because peak of cholesterol synthesis is from midnight to 5 AM. However, Atorvastatin can be given at any hour of the day.  Monitor serum cholesterol and LDL levels to determine effectiveness of drug therapy.  Monitor results of liver functions tests to determine possible liver damage.  Ensure patient has initiated a 3-6 month diet and exercise program before initiating drug therapy to ensure need for drug therapy.  Emphasize the importance of lifestyle changes to the patient to decrease risk of CAD and promote drug effectiveness.  Provide comfort and safety measures to help patient tolerate drug side effects.  Educate patient on drug therapy
  • 42.
  • 43. Cardiovascular agents are medicines that are used to treat medical conditions associated with the heart or the circulatory system (blood vessels). Some work directly on the blood vessels surrounding the heart, reducing how much force the heart has to pump against. Others lower cholesterol levels and help reduce the formation of atherosclerotic plaques which cause blood vessel narrowing. Some work in the kidneys to increase fluid and salt loss or improve blood flow through the kidneys. The type of cardiovascular disease the person has determines which class of cardiovascular agent to use.
  • 44.  Greenstein B: Drugs acting on the heart : Trounce’s clinical pharmacology for nurses; 18 (ed);Elsevier 2009: Page 59-72  Adams P M, Holland N L, Bostwick M P, The cardiovascular and Urinary systems: Pharmacology for Nurses; Pearson education 2009; page 285- 418  Dr. P.K. Panwar, Essentials of pharmacology for nurses, AITBS pub.2017, India, page 118-134  Dr. suresh K sharma, Textbook of pharmacology, pathology and genetics for nurses, jaypee pub.2016 Indai . page 362-452  Lehne, R. A., Moore, L. A., Crosby, L. J., & Hamilton, D. B. (2004). Pharmacology for nursing care.  Smeltzer, S. C., & Bare, B. G. (1992). Brunner & Suddarth’s textbook of medical-surgical nursing. Philadelphia: JB Lippincott.  Heart.org/en/health-topics/heart-attack/treatment-of-a-heart-attack/cardiac-medications  https://www.britannica.com/science/cardiovascular-drug  https://www.americannursetoday.com/emergency-cardiac-drugs-essential-facts-for-med-surg-nurses