Angiotensin-converting enzyme inhibitor (ACEI)

Transcription

1 Aldosterone Alpha1 blockers Alpha 2 blockers Angina pectoris Week Four Terms and Meds to Know In the renin-angiotensin-aldosterone system. Helps regulate sodium, wherever this goes sodium goes in turn so does water. Block alpha1-adrenergic receptors. Ex of medications: doxazosin, and prazosin. Causes vasodilation, works on heart rate. Alpha constricts when not blocked. Peripheral Alpha 1 Blockers block alpha 1 adrenergic receptors. (Doxazosin and pazosin). Block norepinephrine at alpha 1 receptor sites and increases vasodilation and decreases BP. Venous dilation causes decrease in peripheral vasculat dilation and BP and decrease enlarged prostate and bladder. Can be helpful w/ urination. An adrenergic agonist that works in the CNS by blocking the SNS, blocks heart and kidneys. Used in a patch, make sure patients take off old patch before putting on new one otherwise can cause OD. First dose can casuse syncope. Used for ADHD. suffocation of the chest Chest pain, when supply doesn t meet demand. Drugs: nitrates, beta-blockers, and calcium channel blockers mainly. Can use Angiotensin Converting Enzyme(ACE) medications after an MI for this problem. Angiotensin-converting enzyme inhibitor (ACEI) DRUGS END IN --pril Actions: blocks ACE from converting angiotensin I to II, leads to decreased BP and aldosterone production. Small increase in serum potassium levels, sodium and fluid loss. Indications: HTN, CHF (congestive heart failure), Slow progression of ventricular hypertrophy after an MI, Renal protective effects in pts w/diabetes. Kidney sparing due to vasodilation. Pharmacokinetics: metabolized in liver and excreted in urine/feces

2 Angiotensin II receptors Atheroma Baroreceptors Adverse Effects: Dizziness, dry non-productive cough, due to bradykinins (vasodilator) and ace inhibitor, that could potentially get pt off med, Angioedema (swollen throat) (rare but could be fatal), first-dose hypotensive effect can occur. These are related to the effets of vasodilation and alteration in blood flow. Drugs: Captopril, benazepril, enalapril, lisinopril. NOTES: look out for liver fxn, BUN, Cr, and urine output. Angiotensin II is a vasoconstrictor causing an increase in pressure. Elevate potassium levels, ask if pt is on K+ supplement, too much K+ or too little can kill somebody!! ARBS (Angiotensin II Receptor Blockers) Drugs: --sartan, losartan, eprosartan, valsartan, irbesartan, candesartan. Contraindications allergy, pregnancy & lactation Caution hepatic or renal dysfunction (pt may not metabolize/excrete drug completely causing overdose) and hypovolemia. Use: works in RAA system by blocking the biding of angiotensin II to specific receptors in vascular smooth muscle and adrenal gland. Tx: used to tx HTN and HF (heart failure) Drug-to-Drug interactions phenobarbitol. Adverse Effects: headaches, dizziness, syncope, weakness, GI complaints, symptoms of uppers resp. infection or cough BUT not as extensive as w/ ACE inhibitors. Skin rash, dry skin, and assoc. w/ cancer in preclinical trials. POTASSIUM SPARING Plaque in endothelial lining of arteries contains fats, blood cells, lipids inflammatory agents and platelets. Leads to narrowing of lumen of the artery stiffening of the artery and loss of dispensability and responsiveness. Pressure receptors, located in the arch of the aorta and in the arotid artery. Responds to changes in pressure and influences the medulla to stimulate the sympathetic NS to increase or decrease BP.

3 Beta Blockers Calcium Channel Blockers Cardiac output Cardiomegaly Cardiomyopathy Cardiovascular center Chronotropic (+/-) Beta usually dilates when not blocked. Indications Angina, HTN, cardiac dysrthythmias, cardioprotective effects, migraine headaches, essential tremors, stage fright and glaucoma. see notes Adverse Effects: bradycardia, heart block, HF, fatigue, impotence, wheezing, N/V/D, and constipation Action: blocks receptors in the heart causing decrease HR, force of contraction and rate of AV contraction. Side Effects:lethargy, GI disturbances, CHF, decrease BP, and depression. Indications angina, HTN and supraventricular tachycardia, coronary artery spasms (Prinzmetal s angina) A-fibrilation/Flutter *People w/ migraines can be put on this drug as well. Drugs: verapamil, nifedipine (both are dyhropyine, not used for arrhythmias) and Diltiazem and amiodipine (used for rhythm disturbances) Side Effects: decrease BP, Bradycardia, A-V Block, headache, abdominal discomfort (constipation/nausea) and peripheral edema. DO NOT give to pts w/ 2 nd or 3 rd degree heart block. Adverse Effects: dizziness, HA, edema, rash, hypotension, palpations, bradycardia, AV block, nausea, dyspnea, constipation (may be due to drugs MD gives pt). 4-8L/min. HR multiplied by stroke volume. The amount of blood pumped out of ventricles in one minute. Disease of the heart muscle that leads to an enlarged heart and death Chronic disease of the heart muscle that causes it to become stiff losing the ability to pump blood. Area of the medulla at which stimulation will activate the SNS to increase BP, HR etc. (vasomotor center) Drugs that effect the heart rate or impulse through the SA node. (+) increase HR

4 (-) decrease HR Regulated by the ANS from the medulla oblongata Coronary artery disease (CAD) Diuretics Dromotropic (+/-) Dyspnea Dysrhythmias Essential hypertension Heart failure Hemoptysis Hypotension Ischemia Characterized by progressive narrowing of coronary arteries leading to decreased delivery of oxygen to cardiac muscle cells. Leading killer of adult in US. Drugs that cause a person to urinate frequently Drugs that effect the speed of cardiac impulse through the heart conduction system. (+) speed up the conduction of impulses through the heart (-) slow down conduction of impulses through the heart. Shortness of breath. (SOB) r/t left sided HF Disturbance of rhythm can be heartbeat or brain waves. Sustained BP above normal limits with no discernible underlying cause. Low ejection fraction causes s/s of this. Condition in which the heart fails to effectively pump blood throughout the body. Five year survival rate is ~50%. Drugs: ACE inhibitors, ARBS, BBs, diruetics. Cardiac glycosides SEE NOTES ON CHF Blood-tinged sputum seen in left sided HF wehen blood backs up into lungs and fluid leaks out into lung tissue.d Decreased BP, use Midodrine to increase BP. (See notes) Poor oxygen supply

5 Inotropic (+/-) Myocardial infarction Nitrates Nocturia Orthopnea Prinzmetal angina Pulmonary edema Pulse pressure Renin-angiotensinaldosterone system Shock Stable angina Drugs that effect the strength/force of contraction of the heart muscle (myocardial contractility). (+) increase the strength of heart muscle contraction. (-) decrease strength of heart muscle contraction. Heart Attack. Vessel blockage in the heart, leads to ischemia and then necrosis of the area cut off from the blood supply. It can heal w/ the dead cells replaced by scar tissue. Drugs used to cause direct relaxation of smooth muscle, vasodilates, decrease oxygen demand and restore balance b/w blood delivered and blood need in the heart in pts w/ angina Increased renal perfusion when supine Causes one to urinate often during the night Difficulty breathing when lying down, often referred to by number of pillows required to allow a person to breathe comfortably. Drop in blood flow through coronary arteries caused by vasospasms in artery. Treated w/ Calcium channel blockers. Severe left sided HF w/ backup of blood into lungs leading to loss of fluid into lung tissue. Systolic BP minus diastolic BP. Refelcts filling pressure of coronary arteries. Compensatory process that leads to increase BP and blood volume to ensure perfusion of the kidneys, important in continual regulation of BP. Severe hypotension that can lead to accumulation of waster products and cell death. Pain due to imbalance of myocardial oxygen supply

6 and demand that s relieved by rest of activity. Stroke volume Systemic Peripheral resistance Tachypnea Unstable angina Amount of blood pumped out of the ventricle w/ each beat important in determining BP Forcec that resists the flow of blood through the vessels; mostly determined by the arterioles which contact to increase resistance; important in determining overall BP Fast respiratory rate or breathing. R/t left sided HF Episode of myocardial ischemia w/ pain due to myocardial oxygen supply and demand when person is at rest. Beta blockers ( olols ) atenolol esmolol metoprolol propranolol sotolol Vasodilators hydralazine sodium nitroprusside Calcium channel blockers amlodipine diltiazem nifedipine verapamil Nitrates isosorbide dinitrate isosorbide mononitrate Ace Inhibitors ( prils ) benazepril captopril enalapril lisinopril Centrally acting alpha 2 receptor agonist clonidine Alpha receptor agonist Midodrine Alpha blockers ( sins ) Phentolamine (except this one) tamsulosin doxazosin Angiotensin II receptor blockers ( sartans )

7 nitroglycerin Cardiac glycoside digoxin digoxin immune Fab (antidote) candesartan eprosartan irbesartan losartan valsartan Piperazineacetamide ranolazine Phosphodiesterase inhibitor milrinone NOTES: 1. Combined Adrenergic Antagonists/Blockers: a. Mechinism of action: i. Peripherally acting alpha 1, beta 1&2 receptor blocker ii. Reduces HR, (beta1 receptor blockade) iii. Causes vasodilation (alpha1 receptors blockade) iv. EX:carvedilol, and labetalol (in extreme HTN cases) b. Cardio-Selective Beta Blockers i. Decreased myocardial oxygen demand ii. End in olol 1. Atenolol 2. Metoprolol 3. Esmolol short-acting, used in active situation iii. Most of the time effects heart (beta1) iv. Chatelcholamines epinephrine & norepinephrine. c. Nonselective beta blockers (beta 1& beta 2) i. Cause same effects on heart as cardio-selective beta blockers ii. Also constrict bronchioles iii. Produce vasoconstriction of blood vessels 1. Propranolol 2. Sotolol iv. Asthmatics

8 1. Inhalers cause dilation (beta agonist) but the beta blocker causes constriction therefore if asthmatic is on an inhaler and a beta blocker use caution. 2. Vasodilators a. Used when symptoms are severe, onset is immediate, and is through an IV. b. Diazoxide IV for hospitalized pts w/severe HTN, increases blood glucose levels. c. Hydralazine maintains increased renal blood flow d. Minoxidil used only for severe and unresponsive HTN e. Nitroprusside used for HTN crisis, maintain HTN during surgery (IV) f. Actions: i. Act directly on vascular smooth muscle to cause muscle relaxation leading to vasodilation and drop in BP g. Indications: i. HTN emergencies 1. Sodium nitroprusside and IV diazoxide, hydralazine HCl h. Pharmacokinetics i. Rapidly absorbed and widely distributed, metabolized in liver, and primarily excreted in the urine. ii. DECREASES AFTERLOAD i. Contraindications i. Allergy, pregnancy lactation, cerebral insufficiency j. Adverse Effects: i. Dizziness, HA, dysrhythmias, hypotension, N/V, cyanide toxicity (rare, due to breakdown of nitroprusside) 3. Midodrine a. Actions: i. Activates alpha-receptors in arteries and veins to produce nad increase in vascular tone and an increase in BP. b. Indications: i. Symptomatic tx of orthostatic hypotension c. Pharmacokinetics:

9 i. Absorbed form the GI tract, metabolized in liver, excreted in the urine. d. Contraindications: i. Supine HTN, CAD (coronary artery disease) phenochromocytoma (tumor of adrenal gland) and w. urinary retention. e. Caution: i. Pregnancy, lactation, and visual problems f. Adverse Effects: i. R/t stimulation of alpha-receptors g. Drug-to-Drug Interactions: i. Cardiac glycosides, beta blockers, alpha-adrenergic agents and corticosteroids. 4. Congestive Heart Failure (CHF) a. Condition in which the heart fails to effectively pump blood throughout the body. Five year survival rate is ~50%. b. Primary Tx: i. Allows the heart muscle to contract more efficiently in an effort to bring the system back into balance. c. Underlying Problems: i. Muscle Damage 1. Atherosclerosis or cardiomyopathy ii. Increase in workload to maintain an efficient output 1. HTN or valvular disease iii. Structural Abnormality 1. Congenital cardiac defects d. Cause of CHF i. CAD ii. Cardiomyopathy iii. HTN iv. Valvular heart disease e. RT side HF S/S: i. Elevated jugular venous pressure ii. Splenomegaly (enlarged spleen) iii. Hepatomegaly (enlarged liver)

10 iv. Decreased renal perfusion when upright v. Increased renal perfusion when supine (nocturia) vi. Pitting edema vii. Weakness/ fatigue f. Left Sided HF S/S: i. Anxiety ii. Tachypnea iii. Orthopnea iv. Hemoptysis v. Rales (fluid in lung tissue) vi. Cardiomegaly (enlarged heart) (increases HR) vii. GI upset viii. Nausea ix. Abdominal Pain x. Decrease peripheral pulses xi. hypoxia