drugs for angina pectoris and myocardial infarction - PowerPoint PPT Presentation

slide1 n.
Skip this Video
Loading SlideShow in 5 Seconds..
drugs for angina pectoris and myocardial infarction PowerPoint Presentation
Download Presentation
drugs for angina pectoris and myocardial infarction

play fullscreen
1 / 24
drugs for angina pectoris and myocardial infarction
Download Presentation
Download Presentation

drugs for angina pectoris and myocardial infarction

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

    1. Drugs for Angina Pectoris and Myocardial infarction Chapter 25

    3. Angina Pectoris Acute chest pain that occurs when myocardial oxygen supply is less than the demand. Identify the classic presentation of Angina. What else would you expect the patient to experience? What assessment findings would you expect? Identify precipitating factors What would you expect to relieve the symptoms?

    4. Angina Pectoris Compare and Contrast the following types of Angina Pectoris: Stable Vasospastic (Prinzmetal’s) Silent Unstable

    5. Angina Pectoris What did you notice about the presentation of Angina Pectoris? What is the implication of this information? What pharmacologic therapy can help make the determination? What is differential diagnosis based upon? What are non-cardiac causes of chest pain?

    6. Non-Pharmacologic Management Limit alcohol No high saturated fat/high cholesterol foods Maintain normal blood lipid levels Maintain blood pressure within normal range Regular exercise Optimal weight Maintain blood glucose within normal range No tobacco

    7. Interventional Procedures Percutaneous Transluminal Coronary Angioplasty (PTCA) Stent Coronary Artery Bypass Graft (CABG) What is the goal of these interventions?

    8. Pharmacotherapy of Angina Pectoris Identify: Primary goal Additional goals Long-term goals Pharmacotherapy must be accompanied by behavior modifications. Basic Therapy Categories Drugs to stop episode Drugs to decrease frequency of episodes Mechanisms: Decrease O2 demand Decrease HR Decrease preload Decrease contractility Decrease afterload

    9. Pharmacotherapy of Angina Pectoris Three classes Beta-adrenergic antagonists Calcium channel blockers Organic nitrates Short acting Long acting What do each of these classes do? When will 2 or more classes be used?

    10. Organic Nitrates Prototype: nitroglycerin , p. 351 Routes of administration: Sublingual, Oral, Transdermal, Intravenous Tolerance Common and serious problem Magnitude is dose dependent Develops and disappears rapidly How could you delay the development of tolerance?

    11. NCs: Organic Nitrates Baseline BP prior to administration Contraindicated: Cardiac tamponade, pericarditis, head injury, shock, increased ICP Use cautiously: Severe liver or kidney disease, early MI No alcohol intake

    12. Organic Nitrate: Client Teaching Avoid alcohol Rotate transdermal patches Do not chew or swallow SL tabs Sit or lie down when taking SL tabs Call EMS if CP continues after 3 doses @ 5 min. intervals Immediately report symptoms of overdose Keep in original container Replace SL every 6 months

    13. Beta-Adrenergic Antagonists Prototype: atenolol (Tenormin) p. 353 As effective as nitrates in decreasing frequency and severity of angina caused by exertion Ideal for those with HTN and CAD Drug of choice for prophylaxis of chronic angina What is the major benefit of beta-blockers over organic nitrates?

    14. Calcium Channel Blockers Prototype: diltiazem (Cardizem), p. 354 Effects similar to beta blockers Drug of choice in vasospastic angina Monotherapy in stable angina if beta blockers not tolerated Will be given with organic nitrate or beta blocker for persistent angina

    15. Myocardial Infarction What do you know about Myocardial Infarctions? What is the primary cause of MI? Describe the pathophysiology of a Myocardial Infarction.

    16. Diagnostic Markers Cardiac markers are helpful in diagnosis of MI Table 25.2: Changes in Blood Test Values with Acute MI, p. 355 Troponin I and T and CPK-MB are key markers ECG changes: Abnormalities of: Q waves T waves S-T segment

    17. Myocardial Infarction: Goals What are the overall goals associated with treatment of myocardial infarction? What are the pharmacological goals of treatment of myocardial infarction? How will these goals be accomplished?

    18. Thrombolytics Aka: “clot busters” Prototype: reteplace, p. 357 Followed by anticoagulants “Time is muscle” Clinical practice guidelines Narrow margin of safety What is the primary risk associated with thrombolytics? What should be done if signs of bleeding are noted?

    19. NCs: Thrombolytics Assess for contraindicating conditions Recent trauma, biopsies, surgery, LP, GI bleed, within 10 days PP, cerebral hemorrhage, bleeding disorders, thrombocytopenia; septic thrombophlebitis) Use cautiously in any condition with a significant potential for bleeding (e.g., liver or kidney disease) Start all lines (intravenous, arterial) and insert Foley prior to initiating therapy

    20. NCs: Thrombolytics Monitor VS, I&O, lab values Assess for mental and neurological changes Continuous ECG CBC, PT and INR, aPTT At risk for bleeding for 2 – 4 days post therapy What are the immediate patient needs? What will be done to prevent re-infarction and reduce mortality from episode?

    21. Antiplatelet and Anticoagulant Theapy What drug should be given as soon as an MI is suspected? Why? What other antiplatelet classes will be used? What is the anticoagulant that will be initially used?

    22. Nitrates In client with suspected MI SL nitro with initial onset of CP Three doses, 5 minutes apart Pain persisting > 5-10 minutes: Seek medical attention IV nitro for 24 hours if: Persistent pain Heart failure Severe HTN

    23. Beta-Adrenergic Antagonists Decrease myocardial oxygen demand Research: Beta-blockers decrease MI associated mortality if administered within 8 hours of onset Initially IV then PO Calcium channel blockers can produce same effect but are reserved for those unable to tolerate beta-blockers.

    24. ACE-Inhibitors Research Captopril (Capoten) and lisinopril (Prinivil, Zestril) increase survival following acute MI Most effective when therapy is initiated within 24 hours of symptom onset Initially IV PO after thrombolytic therapy completed and condition stable