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78 Cards in this Set
- Front
- Back
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Nitrates: cellular mechanism
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-interact with nitrate receptors on endothelium
-end up dephosphorylating Myosin-LC which leads to relaxation |
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Nitrates: prototypes (2)
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-nitroglycerin (short-acting)
-isosorbide dinitrate (long-acting) |
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Nitrates: administration
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-most popular for anginal attacks is sublingual nitroglycerin
-can do oral extended release for chronic use |
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Nitroglycerin: Timeline and Metabolism
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-2-5 min onset
-significant first-pass metabolism- need to use sublingually |
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Isosorbide Dinitrate: Timeline and Metabolism
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-15 min onset
-longer acting than nitroglycerin |
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Nitrate: Primary Clinical Goal, Main Heart Effects and Mechanisms
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-systemic vasodilation (veins more than arterites)
-decreased preload- decreases wall tension which decreases myocardial oxygen demand all are looking to decrease myocardial oxygen demand -dilates collateral vessels in myocardium, allowing perfusion of ischemic area -can decrease afterload at higher doses |
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Nitrates: Side Effects
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all are due to systemic vasodilation
-orthostatic hypotension -reflex tachycardia and contractility -headache effects can be limited with combination therapy of beta blockers or ccb |
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Variant Angina: Treatment
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nitrates and calcium channel blockers
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Stable Angina: Treatment
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nitrates
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Beta blockers: Clinical Effects in Angina
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-decrease frequency of attacks
-increase exercise tolerance -decrease nitroglycerin consumption |
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Treatment for Frequent Anginal Attacks
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-beta-blocker with nitroglycerin
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Beta blockers: Prototypes for Angina
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-propranolol and nadolol
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Beta Blockers: Main Heart Effects
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-decreased heart rate
-decreased contractility |
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Calcium Channel Blockers: prototypes (3)
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Nifedipine (smooth muscle selective)
Verapamil (cardio selective) Diltiazem (intermediate) |
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Nifedipine: Main Physiological Effects
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-coronary dllation
-peripheral vasodilation -reflex increased HR and contractility |
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Verapamil: Main Physiological Effects
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-coronary dllation
-peripheral vasodilation -decreased HR and contractility |
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Diltiazem: Main Physiological Effects
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-marked coronary dilation
-no change in heart function |
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Verapamil: Contraindications
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-severe left ventricular dysfunction or heart failure
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Diltiazem: Contraindications
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-acute MI
-pulmonary congestion |
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Calcium Channel Blocker: main physiological effects
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-block of calcium influx leads to deceased heart contractility, reducing oxygen demand
-also systemic vasodilation, decreasing blood pressure and wall tension, reducing myocardial oxygen demand |
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When using anti-anginal drugs in combination, which side effects are being mitigated
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-reflex tachycardia and contractility from nitrates
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What are the four possible elecrophys actions of Antiarrhythmics?
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-decreased spontaneous depolarization (decreased phase 4 slope)
-increased depol threshold -more negative diastolic potential -increased action potential duration |
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Antiarrhythmics
Class 1b electrophys effects |
-mild Na+ channel block leads to decreased automaticity
--decreases pase 4 slope -shortened repolarization |
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Antiarrhythmics
Class 1a electrophys effects |
-moderate Na+ channel block leads to decreased automaticity
--decreased phase 4 slope --increased threshold -prolonged repolarization leads to increased refractoriness -usually local anesthetic properties too |
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Antiarrhythmics
Class 1c electrophys effects |
-marked Na+ channel block
-most dangerous? |
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Quinidine
Type and Effects and Use |
-class 1a antiarrhythmic
-decrease automaticity and increased refractoriness- increases PR, QRS, QT interval -probably won't use clinically |
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Quinidine
Side Effects |
-increased QT can lead to torsades de pointes
-many patients get diarrhea |
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Procainamide
Type and Effects and Use |
-class 1a antiarrythmic
-decrease automaticity and increased refractoriness- increases PR, QRS, QT interval -ventricular arrhythmias |
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Disopyramide
Type and Effects and Use |
-class 1a antiarrythmic
-decrease automaticity and increased refractoriness- increases PR, QRS, QT interval -ventricular arrhythmias |
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Disopyramide
Side Effects |
-anticholinergic
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Lidocaine
type and effects |
-class 1b antiarrhythmic
-decreased phase 4 slope -decreases refractory period |
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Lidocaine
clinical use |
-widely used antiarrhythmic
-ventricular arrhythmias -acute MI or digitalis intoxication |
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Lidocaine
administration |
-parenteral
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Phenytoin
type and effects |
-class 1b antiarrhythmic
-decreased phase 4 slope -decreased refractory period |
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Phenytoin
clinical use |
-digitalis induced arrhythmias
-otherwise a second-line drug |
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Phenytoin
administration and metabolism |
-oral
-extensive first-pass metabolism |
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Mexiletine
type and use |
-class 1b anti-arrhythmic
-actually the class 1b used in clinic |
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Flecainide
type and use |
-class 1c anti-arrhythmic
-used in life threatening supra-ventricular arrhythmias |
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Flecainide
contraindications |
-MI
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Propafenone
type and use |
-class 1c anti-arrhythmic
-used in life threatening supraventricuar arrhythmias- not first line |
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Anti-Arrhythmics
Class 2 electrophys effects |
-beta adrenergic blockade
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Beta blockers
-anti-arrhythmic type and effects |
-class 2 anti-arrhythmic
-reduce slope of action potential of pacemaker cells -increase PR duration |
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Beta blockers
-anti-arrhythmic use |
-main use when arrhythmia due to hyperadrenergic state (e.g. ansesthesia)
-supraventricular arrhythmia -torsades de pointes |
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Anti-Arrhythmic
Class 3 electrophys effects |
-prolong refractory period by blocking K+ repol channels
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Amiodarone
-class and effects and use |
-technically class 3, but has actions for all four anti-arrhythmic classes
-increases action potential duration and increases refractory period -increases QT interval, but does NOT cause torsades -has become widely used off-label |
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Amiodarone
metabolism/duration |
-3 week duration- very long acting
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Amiodarone
side effects |
75% of patients have some side effects
**-irreversible pulmonary fibrosis -hypotension -thyroid problems |
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Sotalol
type and effects |
-class 3 anti-arrhythmic
-increases action potential by blocking K+ channels -increases QT |
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Sotalol
side effects |
-increased QT, increased EAD leads to torsades
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Ibutilide
type and effects and use |
-class 3 anti-arrhythmic
-selective block of K+ channels -increased action potential duration and increased QT -used to convert atrial fibrillation to sinus rhythm |
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Ibutilide
side effects |
-prolonged QT leads to torsades de pointes
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Anti-Arrhythmic
Class 4 electrophys effects |
-block L-type Ca+ channels
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Verapamil
anti-arrhythmic type and effects |
-class 4
-blocks L-type Ca+ channels- leads to profound AV block -also acts on peripheral vessels- leads to decrease in blood pressure |
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Verapamil
clinical use |
-treatment of reentrant ventricular arrhythmias (i.e. reentrant supraventricular tachycardias)
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Verapamil
side effects |
-AV block
--possible heart block with other anti-arrhythmics --acute heart failure with CHF -hypotension -bradycardia (possible, may be masked by baroreflex) |
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Adenosine
clinical use |
-recently approved for acute reentrant ventricular tachycardia
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Digoxin
anti-arrhythmic clinical use |
-atrial fibrillation
-reentrant ventricular tachycardia (increased vagal tone inhibits AV node) |
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Statin
Type and Mechanism |
-anti-hyperlipidemic
-reversibly inhibits HMG-CoA, an enzyme involve in intracellular cholesterol synthesis -all have *statin name |
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Statin
physiological effects |
-main effect is increase in LDL receptors (through DNA regulation)
--this causes decreased serum LDL -only mildly decreases cholesterol synthesis |
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Statin
clinical effects |
-main- greatly reduce LDL, also decrease cholesterol and increase HDL
-also have beneficial cardiovascular side effects --decreased intimal thickening --inhibit monocyte infiltration in plaques |
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Statin
metabolism and half-life |
-extensive first pass metabolism- 80-95%
-cyp-3A4, sensitive to grapefruit -half-life of 1-4 hours (atorvastatin is longer) |
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Statin
adverse effects |
-rhabdomyolysis or increased CK-MM
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Bile Acid-Binding Resins
type and mechanism |
-anti-hyperlipidemic
-prevents enterohepatic resorption of bile acids by ion exchange -all have choles* name |
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Bile Acid-Binding Resins
physiological effects |
-decreased resorption leads to increased LDL receptor expression (same mechanism as statins)
--this causes decreased LDL levels |
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Bile Acid-Binding Resins
cllinical effects |
-decrease in LDL, and minor increase in HDL
-no effect on triglycerides |
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Bile Acid-Binding Resins
adverse effects |
-prepared as a liquid resin- may have objectionable taste and texture
-may interfere with absorption of fat-soluble vitamins and drugs -constipation- relieved by increased fiber |
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Ezetimibe
type and mechanism |
-anti-hyperlipidemic
-inhibits intestinal absorption of cholesterol |
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Ezetimibe
clinical effects |
-modest decrease in LDL and trigyceride
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Ezetimibe
clinical use |
-used in combination with statins
-however, in combo, does not have same beneficial cardiovascular effects as statins alone |
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Niacin
type and clinical effects |
-anti-hyperlipidemic
-greatly increase HDL -also modest decrease in LDL and triglyceride |
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Niacin
adverse effects |
-40-50% of patients discontinue use of drug due to side effects
-cutaneous flushing and itchiing (can be prevented by pretreatment with aspirin or ibuprofen) |
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Fibric Acid Derivatives
type and clinical effects |
-anti-hyperlipidemic
-standard decrease in LDL, TG and increase in HDL |
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Clofibrate
adverse effects |
-increased incidence of gall stone, malignant cancer and GI disease
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Fibric Acid Derivatives
clinical use |
-gemfibrozil used in combination with statin
-others (clofibrate) used only in severe hypertriglyceridemia unresponsive to niacin and gemfibrozil |
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What is the main combination treatment of Hypercholesterolemia?
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statin with:
-bile acid-binding resin or -ezetimibe or -niacin |
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What is the main combination treatment of hypercholesterolemia and triglyceridemia?
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statin with:
-niacin or -gemfibrozil note- both may increase incidence of statin induced myopathy |
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Fish Oil
physiological effects |
-decrease triglycerides
-no real effect on LDL or HDL |
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Do postmenopausal hormones help to protect against heart disease
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no, sorry ladies
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