Drugs for Angina Pectoris and Myocardial infarction

1
Drugs for Angina Pectoris and Myocardial
infarction

• Chapter 25

2
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.

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 (Prinzmetals)
• 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 _at_ 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, IO, 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 gt 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