Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Heart failure wikipedia , lookup
Cardiothoracic surgery wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Electrocardiography wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Jatene procedure wikipedia , lookup
Coronary artery disease wikipedia , lookup
Cardiac surgery wikipedia , lookup
Heart arrhythmia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Towards a Greater Understanding of Cardiac Medications But first a little cardiac patho… Foundational Cardiac Concepts: Cardiac Output (CO) …CO=SVxHR Stroke volume-amount of blood that returns to right atrium from venous circulation and left atrium from pulmonary veins o Larger SV increases workload of the heart o Faster HR increases cardiac O2 demands and workload o Goal of medication therapy with any cardiac client is to DECREASE cardiac workload through influencing SV, HR, Preload, Afterload and Contractility I. Preload • • • • • • Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also true Pressure/Stretch in ventricles end diastole just before contraction In a healthy heart, as you INCR Preload…You will increase stroke volume which will increase force of contraction Only up to a certain point-then further stretching may actually decrease contractility Drugs that cause venous dilation (nitrates)-DECREASE preload Diuretics that eliminate excess fluid volume DECREASE preload Starling’s Law of the Heart: • • • The greater the preload- greater quantity of blood that can be ejected during systole due ti INCR stretch of myocardium But only up to a maximal point. Greatest force of contraction is when the muscle fibers are stretched 2 ½ times their normal length Overstretch of cardiac muscle is like an overstretched rubber band-will DECREASE cardiac contractility and efficiency over time 2). Afterload • • • • Force of resistance that the LV must generate to open aortic valve Correlates w/SBP…How much pressure is needed to push blood out of the heart into the aorta and into entire systemic circulation Influenced by resistance of blood vessels in the body-are the arteries dilated or constricted Arterial vasodilators (Ca++ channel blockers (CCB), ACE inhibitors) DECREASE afterload ©2011 Keith Rischer/www.KeithRN.com 3) Contractility: Inotropic-influencing contractility independent of Starling mechanism • • • • • Ability of heart to change force of inherent contraction strength Influenced by Ca++ in action potential…therefore CCB will do what to contractility? Decrease contractility (inotropic) DECREASE cardiac workload and O2 demands Negative inotropic meds: CCB, beta blockers Positive inotropic: Digoxin, Dopamine & Epinephrine gtts. Ejection Fraction (EF) on echocardiogram – – – – – 65-70% normal reflects that with each contraction 65-70% of the blood in the LV is ejected into circulation As this % goes down it is reflecting the loss of cardiac contractility and degree of CHF 35% EF is half the normal cardiac output with each contraction 10-15% EF end-stage heart failure-near death I.Angiotensin Converting Enzyme (ACE) Inhibitors…(end in “pril”) Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Prinivil) Mechanism of Action: A normal plasma protein-renin is secreted by the kidneys when BP falls which converts inactive liver protein angiotensinogen to angiotensin I. The conversion to angiotensin II is enhanced by angiotensin-converting-enzymes (ACE) from the lungs to one of the most potent vasoconstrictors known. The effects of angiotensin II are: Vasoconstriction of arterioles and veins (incr. afterload) Stimulation of the sympathetic nervous system (incr. workload of heart) Retention of water by the kidneys due to aldosterone a hormone secreted by the adrenal glands (incr. preload) ACE inhibitors block the conversion of angiotensin I to angiotensin II. This inhibition decreases angiotensin II concentrations and causes: Vasodilation which decreases BP (decr. Afterload) and decrease sodium and water retention (decr. Preload). Uses: HTN, CHF, CAD Side Effects-most common: hypotension, dry cough, dizziness Angioedema (life threatening) Laryngeal swelling that can cause asphyxia. Facial swelling also concerning precursor. ©2011 Keith Rischer/www.KeithRN.com Nursing Considerations: Obtain BP before administering-hold typically if SBP <90 Change position slowly-especially with elderly to prevent orthostatic changes Monitor for decreased WBC count, hyperkalemia as well as liver function, and GFR, creatinine (metabolized by liver-excreted by kidneys) II.Beta Blockers…(end in “lol”) Metoprolol (Lopressor) Atenolol (Tenormin) Propranolol (Inderal) Mechanism of Action: Selectively inhibit beta (sympathetic/fight or flight) receptors primarily of the heart (Beta 1). Sympathetic nervous system (SNS) stimulation normally causes: Increased heart rate Increased BP Increase myocardium contractility and oxygen demand ALL THESE EFFECTS INCREASE WORKLOAD OF THE HEART By blocking the normal effects of SNS it effectively causes the opposite effects and DECREASES workload of the heart…decreased heart rate, decreased BP, and decreased contractility. This is why it must be used with caution in those with history of congestive heart failure (CHF). CHF clients have excessive activation of SNS which will worsen CHF over time. B-Blockers very effective to manage this complication of CHF. Uses: HTN, CHF, acute MI, CAD, ventricular dysrhythmias Side Effects-most common: bradycardia, hypotension, fatigue, weakness Nursing Considerations: Obtain BP and HR before administering-hold typically if SBP <90. HR <60 Change position slowly-especially with elderly to prevent orthostatic changes Contraindicated in worsening CHF, bradycardia of heart block…use with caution in diabetes, liver disease III.Calcium Channel Blockers Diltiazem (Cardizem)-arterial dilator and cardiac Verapamil (Calan)- arterial dilator and cardiac Nifedipine (Procardia)-primary arterial dilator ©2011 Keith Rischer/www.KeithRN.com Amlodipine (Norvasc)- primary arterial dilator Mechanism of Action: Inhibits or “blocks” the influx of extracellular calcium into the membranes of the heart and vascular smooth muscle cells of heart and body. This blocking of calcium ions is responsible for causing the following: Dilation of coronary and systemic arteries w/resultant decrease in BP (improves cardiac 02 supply & decr, afterload) Decrease of myocardium contractility (decr. Workload) Slows AV node conduction (decr. in heart rate) Uses: HTN, angina, controlling rapid heart rate in SVT or atrial fibrillation Side Effects-most common: peripheral edema, hypotension, constipation Nursing Considerations: Change position slowly-especially with elderly to prevent orthostatic changes Measure I&O closely and fluid status due to potential for edema Monitor liver and kidney function (metabolized in liver-excreted by kidneys) Obtain BP and HR before administering-hold typically if SBP <90. HR <60 IV. Nitrates Nitroglycerine subl. (Nitrostat)-SHORT acting Isosorbide Mononitrate (Imdur)-LONG acting Isosorbide Dinitrate (Isordil)-LONG acting Nitrodur topical patches-LONG acting Mechanism of Action: Able to relax and dilate both coronary arterial vessels and systemic venous smooth muscle. Dilation of veins reduces amount of blood that returns to heart (preload) so chambers contain smaller volume. With less blood to pump, cardiac output is reduced and workload of the heart decreased lowering myocardial oxygen demand Dilation of coronary arteries can help improve blood flow to heart as well as well as relieve angina caused by coronary artery vasospasm Uses: Angina Side Effects-most common: hypotension, tachycardia, dizziness, headache (dilates cerebral vessels causing mini migraine) Nursing Considerations: ©2011 Keith Rischer/www.KeithRN.com Tolerance common and serious problem with long acting nitrates. Nitrates lose their effectiveness if transdermal patches remain on continually. Patches must be taken off at night and then reapplied in the morning Contraindicated if client taking any erectile dysfunction meds as these are a similar nitrate that improves blood circulation to the penis-synergistic effect can cause dramatic hypotension V. Diuretics Lasix (furosemide)-most potent-Loop of Henle-K+ waster Bumex (bumetanide) Hydrochlorathiazide (HCTZ)-mod. Potency-mod. K+ waster Spirinolactone (Aldactone)-mild potency-K+ sparing Mechanism of Action: Loop diuretics-most potent diuretics that prevent sodium reabsorption in the loop of henle causing rapid/large diuresis with resultant loss of K+. Because of their potency are not used for maintenance but when large diuresis is desired such as in acute CHF exacerbation (decr. Preload). Thiazide diuretics-increases excretion of sodium and water by inhibiting sodium reabsorption in distal tubule. Most common maintenance diuretic Potassium sparing diuretics-weakest of all diuretics due to not blocking reabsorption of sodium. Used when client is at risk for developing hypokalemia Uses: HTN, CHF, renal insufficiency/acute renal failure Side Effects-most common: dehydration, orthostatic hypotension, hypokalemia, hyponatremia, hypomagnesemia with loop and thiazide diuretics, potential for hyperkalemia w/Aldactone Nursing Considerations: Change position slowly-especially with elderly to prevent orthostatic changes Obtain BP before administering-hold typically if SBP <90 Monitor sodium and K+ levels closely as well as GFR and creatinine Aldactone and ACE inhibitors can cause resultant hyperkalemia If on Aldactone-make sure does not use potassium based salt substitutes or foods rich in K+ ©2011 Keith Rischer/www.KeithRN.com ©2011 Keith Rischer/www.KeithRN.com