Presentation on theme: " Angina pectoris is clinical syndrome with primary s/s of chest pain/pressure/discomfort Results from deficit of supply and demand Most often 2ndary."— Presentation transcript:
Angina pectoris is clinical syndrome with primary s/s of chest pain/pressure/discomfort Results from deficit of supply and demand Most often 2ndary to atherosclerotic plaque formation Can also be secondary to vasospasm
Caused by development and progression of atherosclerotic plaque Plaque narrows the vessel lumen, decreases elasticity and impairs dilation of coronary arteries Result is impaired blood flow to the myocardium
From obstruction of coronary arteries secondary to athersclerotic plaque deposition Chest discomfort is usually precipitated by factors that increase workload of the heart like physical activity, exposure to cold and emotional upset Pain is usually relieved by rest, nitroglycerine or both
Described as substernal chest pain of a constricting, squeezing or suffocating nature May radiate to jaw, neck, shoulder, back or down left arm Sometimes mistaken for arthritis or indigestion especially because discomfort is accompanied by nausea & vomiting; dizziness, diaphoresis, shortness of breath and feeling of impending doom may also be present
Also called Prinzmetal’s Caused by spasms of the coronary artery that decreases blood flow to myocardium Spasms occur in vessels already partially obstructed by plaque Usu. occurs at rest and at night, often occurs same time each day Relieved by nitroglycerine Tx is by avoiding precipitants, taking anti- anginals
Rest, preinfarction and crescendo angina On continuum falls between classic angina and MI Occurs in advanced CAD Often leads to MI
Women have atypical s/s such as epigastric or back discomfort Older adults may have atypical s/s and may experience “silent” ischemia Individuals with diabetes mellitus may present w/o typical s/s
Begins with accumulation of lipid filled macrophages=foam cells on inner lining of coronary arteries Foam cells develop secondary to elevated cholesterol levels White blood cells attach to endothelium and move into subendothelial spaces, ingest lipids and become foam cells Early lesions progress to plaques containing foam cells and covered by smooth muscle cells and connective tissue Advanced lesions also contain hemorrhages, ulcerations and scar tissue
Commonly develops in coronary arteries Plaque lesions develop over time and enlarge, extend deeper into lumen of artery Eventually plaques rupture, thrombus formation occurs that largely occludes vessel lumen with resultant compromised blood flow Stenosis >80% blood flow cannot increase with increased demands If gradual, can develop collateral circulation
Occurs when coronary arteries are unable to provide sufficient blood and oxygen for normal cardiac functions May occur as acute coronary syndrome w/three consequences 1. Unstable angina 2. Silent MI diagnosed by markers only 3. MI w/or w/o ST segment elevation
Endothelium of normal coronary arteries synthesizes various substances that protect against vasoconstriction and vasospasm, bleeding, clotting, inflammation and excessive cell growth Impaired endothelium or hypertension leads to vasoconstriction, vasospasm, clot formation, plaque formation and growth of smooth muscle in blood vessels
Endothelium derived relaxing factor (NO) is produced by the endothelium of coronary arteries Released by shear stress on endothelium, sympathetic stimulation of exercise and interactions with various chemical mediators NO relaxes vascular smooth muscle and inhibits adhesion and aggregation of platelets With endothelial damage, vasodilatory and antithrombotic effects are lost
Also, production of strong vasoconstrictors (endothelin1, thromboxane A2 and angiotensin II) are increased Inflammatory cells enter injured area, growth factors stimulate growth of smooth cells Result—blockage of coronary arteries
Age, race, gender and family history Smoking, hypertension, hyperlipidemia, obesity, sedentary lifestyle, stress and use of drugs that increase workload of heart Diabetes mellitus
Lifestyle modification Weight loss Smoking cessation PTCA with intracoronary stents Laser therapy CABG
Relax smooth muscle in blood vessel walls==vasodilation Reduce venous pressure and venous return to heart, thus, preload this decreases cardiac workload and oxygen demand Increase blood flow to ischemic areas Decrease afterload
Prototype is nitroglycerine Nitrates are converted to nitric oxide in vascular smooth muscle. Activates guanylate cyclase affecting cAMP. Decreases calcium levels in smooth muscle thus decreased contraction of smooth muscle. End result: vasodilation. Contraindications are: Increased ICP, males taking phosphodiesterase enzyme type 5 inhibitors
Nitroglycerine—IV, SL, topical. For acute angina, prevent exercise induced angina Isordil (Isorsorbide dinitrate )acts in 2’, lasts 2-3 hours. Imdur (mononitrate). Imdur is metabolite of Isordil. Onset one hour, peaks between 1-4 hours, prophylaxis of angina
Block beta 1 receptors which increase heart rate and force of myocardial contraction, so increase MVO2 consumption. Reduce heart rate and contractility. Enhance blood flow. Block response to sympathetic neurotransmitters Caution in asthmatics and those with COPD
Inderal (propranolol) is prototype. Metabolized by liver.Need greater doses po due to liver metabolism. Tenormin (Atenolol), Lopressor (metoprolol )and Corgard (nadolol)— long half lives so given once daily. Usually end in -ol
Act on contractile and conductive tissues of heart and on vascular smooth muscle Accomplished by blocking calcium channels, preventing movement of extracellular calcium into the cell. Thus, coronary and peripheral arteries are dilated, myocardial contractility is decreased and conduction system is depressed
Improve blood supply to myocardium by dilating coronary arteries Decrease workload of heart by dilating peripheral arteries Reduce coronary vasospasm Slow rate of ventricular response in atrial fibrillation, flutter and supraventricular tachydysrhythmias Lower blood pressure by dilating peripheral arteries
Most have short half-lives so need frequent dosing 90% protein bound Peak within 1-2 hours Two types—dihydropyridines and nondihydropyridines Procardia (Nifedipine) is prototype of dihydropyridines-vascular smooth muscle to produce vasodilation
Nondihydropyridines—Cardizem (diltiazem) and Calan (verapamil)—better for heart rate management in SVTs, work on conduction system Nimodipine-use in subarachnoid hemorrhage to decrease cerebral vasospasm Contraindications—3 rd degree heart blocks, cardiogenic shock, severe bradycardia, hypotension, heart failure or renal impairment.
Many end in –ipine Plendil (Felodipine), DynaCirc (isradipine), Cardene (nicardipine), Procardia (nifedipine), Nimotopp (nimodipine), Sular (nisoldipine), Norvasc (amlodipine)
Use shorter acting ones to decrease tolerance or Use long acting ones but omit during night
Caution with nitrates in elderly due to potential hypotension For relief of acute angina, nitroglycerine is usually drug of choice Nitrates, beta blockers and calcium channel blockers are metabolized in liver, use with caution in patients with hepatic impairment
Obtain BP and heart rate before each dose on antianginal medication. Hold if BP<90 systolic Give antianginals on regular schedule If oral nitrates and topical agents being used also, stagger administration times Nitro SL—keep in cool, dry place; observe expiration date
IV nitro must be hung with special tubing and in delivered in glass bottle, medication otherwise is adsorbed onto tubing
Characterized by decreased blood supply to body tissues Common signs and symptoms include: hypotension, oliguria, heart failure, mental confusion, cool extremities, coma In a previously hypertensive individual, a drop in BP of 50mm Hg or greater can result in shock, even if BP is considered “normal”
Hypovolemic—caused by trauma, GI bleed, ruptured aneurysms, third spacing, dehydration Manifestations— hypotension,tachycardia, cool, clammy skin, diaphoresis, oliguria
Cardiogenic—acute MI, cardiac surgery, cardiomyopathy, dysrhythmias S/S—those of heart failure such as pulmonary edema, tachycardia, hypotension, cool, moist skin, confusion, restlessness
Management may vary according to type of shock Generally will use alpha adrenergics to increase peripheral vascular resistance (norepinephrine and phenylephrine) Beta adrenergic drugs are used to increase myocardial contractility and heart rate (isoproterenol and dobutamine) Some drugs have both alpha and beta activity (dopamine, epinephrine)
Dobutrex (dobutamine)—synthetic catecholamine. Provides less vascular activity than dopamine. Acts mainly on beta1 receptors to increase force of contraction w/o increasing heart rate. Most useful when need increased cardiac output. Short half life of 10 minutes.
Dopamine—stimulates alpha, beta and dopaminergic receptors. Action is dose dependent. Low dose stimulate dopaminergic receptors located in renal and splanchnic vascular beds. Low doses will increase renal blood flow and GFR (so long as cardiac function is improved). 0.5- 10mcg/kg/min provide this effect. At 3- 20mcg/kg/min have effect of increased heart rate, BP and contractility. 20- 50mcg/kg/min predominant alpha effect.
Epinephrine—catecholamine. Low doses stimulates beta receptors (so increases CO), causes bronchodilation as well. Larger doses act on alpha receptors. Drug of choice in anaphylaxis. Prevents release of histamine, so reverses vasodilation and bronchoconstriction. Can be given IV,subQ or even via ETT.
Isuprel (isoproterenol)—synthetic catecholamine. Works exclusively on beta receptors. Increases heart rate, myocardial contractility and variable BP effects. Limited usefulness as vasopressor. Increases myocardial oxygen consumption and decreases coronary flow. Causes cardiac dysrhythmias.
Primacor (milrinone)—used in combination with other agents in cardiogenic shock. Increases cardiac output and decreases SVR w/o increasing heart rate or myocardial oxygen consumption. Improved CO then increases renal perfusion, thus urinary output with decrease in circulating volume and decreased cardiac workload.
Levophed (norepinephrine)— catecholamine. Primarily alpha 1 stimulation but also beta1 receptors. Useful in cardiogenic and septic shock. Does cause reduced renal blood flow so limits its long term use.
Neosynephrine (phenyleprine)— adrenergic that stimulates alpha receptors. Longer duration of action than epinephrine. Reduction of renal and mesenteric blood flow limits prolonged use.
Use large vein for IV access site Infusion pump Start adrenergic slowly Stop drug gradually Manage patient, not the monitor. Observe for dysrhythmias, tachycardia, angina, tissue necrosis if extravasation
Hypovolemic shock best managed by fluids Cardiogenic shock may be complicated by pulmonary edema, may need to give diuretics, limit fluid intake Anaphylactic shock often managed with epinephrine. May also use histamine receptor blockers like Benadryl and Tagamet (H1 and H2 receptor blockers). May also use corticosteroids to increase tissue responsiveness and for anti- inflammatory effects.
Vasopressor agents used in critical care settings Require cardiac and BP monitoring May often have hemodynamic monitoring as well Vigilant monitoring is essential