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32 Cards in this Set
- Front
- Back
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Aspects that Decrease Oxygen Demand
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Arterial pressure
Heart Rate Wall Tension Contractility |
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Aspects that Increase Oxygen Supply
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Coronary Arterial relaxation
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Major drug Categories of Classic Angina
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Nitrate/Nitrites, Calcium Channel blockers, Beta Adrenergic Receptor Blockers (B-blockers)
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Nitrates and Nitrites Effects:
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On Oxygen Demand: Clinically improve angina by decreasing Oxygen Demand
On Coronary Bloodflow: No increase in total coronary blood flow Redistribution of blood flow across heart wall. Restore Endocardial Blood Flow in Atherosclerotic Coronary arteries of Importance in the treatment of Coronary Vasospasm |
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Benefeicial effects of Nitroglycerin
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Decreased Left Ventricular End Diastolic Pressure → Decreased Myocardial Oxygen Demand
Increased Subendocardial Bloodflow → Increased Oxygen Supply Epicardial coronary Vasodilation → relief of Coronary Vasospasm (Prinzmetal) |
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Harmful Effects of Nitroglycerin
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Reflex Tachycardia → Increased Oxygen Demand
Decreased diastolic Perfusion due to tachycardia → Decreased Myocardial Perfusion |
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Nitrates and Nitrites Pharmacokinetics
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Extensively metabolized by a hepatic nitrate reductase, (if given orally ≤ 10% of the drug is available).
Sublingual administration: onset of action within 2 minutes, (declines within 1 hour). Ointment application: effects within 60 minutes (persist for up to 6 hours). |
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Nitrates and Nitrites Toxicity and Tachyphylaxis
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Most common problem with NTS is facial flushing.
Orthostatic hypotension. Baroreflex-mediated tachycardia. Throbbing headache from cerebral arterial vasodilation. Combination of nitrates with sildenafil causes synergistic relaxation of vascular smooth muscle that can result in hypotension and hypoperfusion. Tolerance may develop |
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Calcium Channel blockers Mechanism of Action
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Clinically, block preferentially voltage-dependent calcium
channels. Act on both vascular smooth muscle and cardiac cells, (to a lesser extent on bronchial, gastrointestinal and uterine smooth muscle). |
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Calcium Channel Blocker Prototypes
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Nifedipine, Verepamil, Diltiazem
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Nifedipine
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Is a more potent vasodilator and its benefit in angina derives from its ability to decrease oxygen demand by decreasing afterload.
However, by decreasing systemic arterial pressure, it can Cause a reflex tachycardia Use of this drug in high Dose Short acting form may have detrimental effect on mortality in patients with coronary artery disease |
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Calcium Channel Blockers Pharmacokinetics
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Absorbed after oral administration, in initial treatment verapamil is extensively metabolized by first pass metabolism in the liver.
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Toxicities
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Excessive vasodilation
Negative inotropy Depression of sinus pacemaker rate Depression of AV nodal conduction. |
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Calcium Chanel Blockers Drug Interactions
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Caution with beta-adrenergic receptor antagonists because of
The possibility of severe depression of ventricular function and AV block. |
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Beta-Adrenergic Receptor Antagonists Mechanism of Action
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Competitively inhibit the effects of neuronally released or
circulating catecholamines on the beta adrenergic receptors. Decrease myocardial metabolic demand, primarily during activity or excitement. |
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Acebutolol & Alprenolol Selectivity And Classification
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B1 Selective Partial Agonist
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Atenolol Selectivity And Classification
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B1 selective Antagonist
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Metoprolol Selectivity And Classification
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B1 (Low Doses) Antagonist
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Oxprenolol & Pindolol Selectivity And Classification
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B1, B2 Non Selective Partial Agonist
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Propanolol, Sotalol, Timolol Selectivity And Classification
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B1, B2 Non Selective Antagonist
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Characteristics of Different Betablockers
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1. selectivity
2. Intrinsic Sympathomimetic Activity 3. Lipid solubility 4. Alpha Adrenergic Receptor Blocking Ability |
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Side effects and Problems
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a. Sinus bradycardia.
b. Bronchospasm in asthmatic patients. c. Mental depression (lipid soluble, particularly propranolol). d. Augmentation of hypoglycemic effect of insulin (blockade of beta 2 receptors may inhibit the catecholamine-induced glycogenolysis and thereby augment insulin induced hypoglycemic effects). e. Fatigue or lethargy (either from CNS effects or exaggerated decrease in cardiac output). |
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Angina General treatment Protocol
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1. Lifestyle Modification
2. Antiplatelet therapy for all patients 3. Stepwise addition of beta-blockers, Calcium Channel antagonists, and/or long acting nitrates if chronic 4.Persistent Angina → revascularization 5. Additionally, patients with high-risk coronary disease, as determined by Noninvasive testing, may benefit from revascularization concurrent with initiation of lifestyle modification and medical therapy |
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Stable Ischemic Heart Disease Treatment Approach
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Sublingual nitroglycerin is the therapy of choice to terminate acute episodes of
angina or for prophylaxis before activities known to induce anginal symptoms. Onset of action is within minutes. Failure to resolve anginal symptoms with a reduction in physical activity and a trial of sublingual nitroglycerin should prompt emergency evaluation for an acute coronary syndrome (unstable angina or myocardial infarction). Antiplatelet therapy: All patients should be given antiplatelet therapy in the form of aspirin, unless there is a contraindication, in which case clopidogrel is a suitable alternative. Management of lipids: All patients should have baseline lipids evaluated. •Blood pressure control: Lifestyle modification including physical activity, weight reduction, reduction of sodium intake, and moderation of alcohol consumption will help many patients adequately control blood pressure. Antihypertensive medications are warranted for patients with blood pressure greater than 140/90 mmHg or, for patients with diabetes or chronic kidney disease, greater than 130/80 mmHg. Management of diabetes: Patients with ischemic heart disease and diabetes are at high risk of morbidity and mortality from cardiovascular events. Intensive blood Non-dihydropyridine sugar control decreases incidence of microvascular complications, including retinopathy, nephropathy. |
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Ongoing Antianginal Pharmacotherapy
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1st Line Beta Blockers (Especially if has history of prior MIs)
Calcium Channel blockers May be added or substituted if Betablockers don’t work If those don’t work use long acting Nitrates (Not with PDE Inhibitors → Unsafe Hypotension) Combination of Beta-blockers with Verapamil and diltiazem or with patients with Systolic dysfunction should not be done → Effects on heart rate and Contractility |
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Contraindications for Beta Blockers as Antianginal
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Can cause worsening pulmonary symptoms in patients with asthma and they should be closely monitored.
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Patient with Prinzmetal Angina Treatment
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Calcium Channel Blockers or nitrates due to their effects on coronary vasospasm
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Acute Management of Unstable Angina
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Antiplatelet and antithrombotic therapy to reduce Myocardial Damage
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Cardiac Etiology Unstable Angina treatment
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Oxygen
Aspirin (Or Clopidogrel if Aspiring allergic) Morphine Nitroglycerin |
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Non-ST-Elevation Acute coronary Syndrome treatment
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IV unfractionated Heparin or subcutaneous Low molecular weight Heparin Preparations
Statins irrespective of blood cholesterol Levels |
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Patients with persistent Ischemic Pain or High risk patients Treatment
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Glycoprotein IIb/IIIa Inhibitors
Plus Considerations for Early coronary Catheterization and intervention |
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Non-Q Wave MI without Pulmonary Congestion Treatment
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Diltiazem and Verapamil
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