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Review. What element is essential to tissue and organ function?Describe Coronary Artery Disease (CAD)Identify the most common cause and consequence of CAD.Discuss physiologic changes associated with the gradual development of ischemia.Discuss the physiologic implication of persistent ischemia..
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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