Exam 2 Study Guide
Exam 2 Study Guide NSG 335
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This 23 page Study Guide was uploaded by Brieanna Phipps on Sunday March 6, 2016. The Study Guide belongs to NSG 335 at University of North Carolina - Wilmington taught by Dr. Sauer in Spring 2016. Since its upload, it has received 128 views. For similar materials see Pathology and Pharmacology in Nursing and Health Sciences at University of North Carolina - Wilmington.
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Date Created: 03/06/16
Systemic Circulation -Heart -Arteries -Arterioles -Capillaries -Venules -Veins Factors Affecting Blood Flow -Pressure -force exerted on a liquid unit per area -measured in mm of Hg -Resistance -opposition to force -diameter and length of the blood vessels contribute to resistance -inversely related to blood flow. Blood flow is measured in L/min (CO) -Velocity -Velocity is the distance blood travels in a unit of time (cm/sec) -Laminar vs. turbulent flow -Laminar straight ahead vs. turbulent flow obstructed flow causing whirls and eddys. Can hear murmur on auscultation -Vascular compliance -Vascular compliance is the ability of vessel to take on more value with increased pressure. -Stiffness is opposite of compliance. -Veins have more compliance than arteries Regulation of BP -Arterial Pressure -Mean Arterial Pressure (MAP) -Average pressure in the arteries throughout the cardiac cycle -MAP= [(2xDP) + SBP] divided by 3 -minimum is 60 to keep organs perfused -Effects of CO (HR x SV) -Effects of total peripheral resistance -vasoconstriction higher BP -vasodilation lower BP -Effect of hyperemia -Effects of hormones vasoconstriction -Epinephrine and Norepinephrine -ADH, RAAS, and natriuretic peptides -Adrenomedullin -secreted by adrenal medulla and smooth muscles of and mediates vasodilatation and sodium excretion -Insulin -increases vasodilation -Venous Pressure Diastole -heart is relaxed -ventricles filling -coronary perfusion occurs -2/3 of total cardiac cycle time -Early diastole -the ventricles fill passively -Late diastole -the atria contract and “top off” the ventricles with additional volume -AKA “atrial kick” (can equal 10-30% of blood in the ventricle) -HR increases, diastolic time decreases -filling time is shortened less blood in ventricles less blood pumped out -coronary perfusion time is decreased while myocardial O2 demand is increasing -valves are closed Systole -active contractile phase -blood is being pumped -right ventricle pulmonary artery lungs left ventricle aorta systemic circulation Cardiac Output (CO) -HR x SV (stroke volume) -normal CO is 4-6L -SV is how much blood is in the ventricle, affected by fluid in the body -dehydrated, lower SV Cardiac Performance -Preload -left ventricular end-diastolic volume -Afterload -load muscle must move after it starts to contract -determined by system vascular resistance in aorta, arteries, and arterioles Preload -degree of the stretch of the heart before contracting -volume in the ventricle increases preload -a stretch beyond their limits causes a decrease in contractility Afterload -arterial resistance during contraction -the force needed for the ventricle to push blood past the valves -Arterial BP -EF (Ejection Fraction): amount of fluid leaving the ventricle with contraction -55-75% is normal Contractility -measure of cardiac performance -degree to which muscle fibers can shorten to function and contract to push the blood around -decreased by diseases that impact myocyte activity -ischemia/MI -myocarditis -cardiomyopathies -drugs that increase contractility are called intropes Diseases of the Veins -Varicose Veins -a vein in which the blood has pooled; distorted, tortuous and palpable; valves don’t work as well -caused by trauma or gradual venous distention -risk factors -age -female -family hx -obesity -DVT -prior leg injury -Chronic Venous Insufficiency -inadequate venous return over a long period of time due to varicose veins or valvular incompetence -venous stasis ulcers -capillaries are enlarged -Deep Venous Thrombosis (DVT) -obstruction of venous flow which increases venous pressure -factors: -Virchow’s Triad -venous stasis -venous endothelial damage -hypercoagulable states -cancer, orthopedic surgery/trauma, HF, immobility -use Doppler to find DVT -Superior Vena Cava Syndrome (SVCS) -occlusion of the SVC that leads to venous distention of upper extremities and head -oncologic emergency Diseases of the Arteries and Veins -Hypertension (HTN) -isolated systolic HTN- becoming prevalent in all age groups -elevations of systolic are caused by inc CO, total peripheral resistance, or both -Primary HTN -essential or idiopathic -genetic and environmental factors -risk factors -high sodium -natriuretic peptide abnormalities -obesity -insulin resistance -Complicated HTN -chronic damage to the walls of the systemic blood vessels -smooth muscle cells undergo hypertrophy and hyperplasia -affects heart, kidneys, and retina -can result in transient ischemic attack/stroke, cerebral thrombosis, aneurysm, and dementia -Malignant HTN -rapidly progressive -diastolic pressure is usually >140 mm/Hg -life threatening organ damage -Orthostatic HTN -decrease in both systolic and diastolic BP upon standing -lack of normal blood pressure in response compensation in response to gravitational changes in the circulation -can be both acute or chronic -Thrombus formation -blood clot that remains attached to the vessel wall -Risk factors -intimal injury, inflammation, obstruction of flow, pooling (stasis) -thromboembolus: moving -thrombophlebitis: inflammation at vessel -arterial and venous thrombi -Embolism -bolus of matter that is circulating in bloodstream -dislodged thrombus, air bubble, amniotic fluid, aggregate of fat from a broken bone, bacteria, cancer cells, foreign substance -Peripheral Artery Disease -artherosclerotic disease of the arteries that perfuses the limbs Medications used to treat HTN -RAAS suppressants -Calcium Channel Blockers (CCBs) -Sympatholytic -Direct Vasodilators -Alpha/Beta Blockers Renin-Angiotensin Aldosterone System -ACE Inhibitors- block conversion of angiotensin I to angiotensin II -decreases BP by relaxing vessels and increasing venous compliance -ADR: cough, hyperkalemia, HA, dizziness, fatigue -CONTRAINDICATED IN PREGNANCY Pril’s -Enalapril- ACE used to treat HTN, HF -Captopril- ACE used to treat HF, post-MI left ventricular dysfunction, diabetic retinopathy -alter dose with decreased renal function RAAS -Losartan -Angiotensin II receptor blocker (ARB): prevents angiotensin II from binding to receptors -HTN, HF, post MI, CAD, CKD -has LESS side effects than ACE -ADR: hypotension, HA, dizziness Direct Renin Inhibitor (DRI) -Aliskiren- acts directly on renin, suppressing the RAAS -DO NOT take DRIs with ACE and ARB concurrently -ADR: hypotension, diarrhea, dizziness -CONTRAINDICATED IN PREGNANCY -very potent, used infrequently, strong SE Aldosterone Antagonists -Spironolactone -lowers BP by promoting excretion of Na and water -potassium sparing diuretic -ADR: hyperkalemia -used a lot in HF Calcium Channel Blockers (CCBs) -two categories 1. Dihydropyridines act only on arterioles- Nifidipine -lowers BP by vasodilation -angina, HTN -ADR: reflex tachycardia, flushing, HA, peripheral and gingival hyperplasia 2. Non-dihydropyridines act on arterioles and conduction- Verapamil and Diltiazem -lowers BP and decreases HR by vasodilation and blocks SA node -angina, HTN, dysrhythmias -ADR: constipation (only Verapamil), flushing, dizziness -prevents calcium ions from entering cells therefore affecting contractioin -relaxation of arterioles -used to treat HTN, angina, atrial cardiac dysrhythmias Sympatholytics (Anti-Adrenergic) Drugs 5 types: -Beta blockers -Alpha blockers -Alpha/Beta blockers -Centrally acting alpha agonist -Adrenergic neuron blockers Beta Blockers -Propanolol: non-selective BB -Metoprolol: cardio-selective BB, used after pts have MI -blocks the effects of epinephrine, decrease in HR and BP, suppress reflex tachycardia, reduce release of renin, reduces PVR (peripheral vascular resistance) over time -ADR: bradycardia, AV HB (heart block), HF, rebound excitation (with withdrawal), bronchoconstriction, altered glucose, fatigue, dizziness, loss of libido, SOB, depression -antidote for OD is epinephrine Alpha Agonist1 -Doxazosin- used to treat HTN and BPH (increases urine flow) -vasodilation from blocking alpha1 receptors on arterioles and veins -ADR: orthostatic hypotension, inhibit ejaculation, nasal congestion -DO NOT GIVE WITH VIAGRA Centrally-acting Alpha2 -Clonidine- act within brainstem to suppress sympathetic outflow to the heart and blood vessels -vasodilation, reduced CO -ADR: sedation, dry mouth, severe rebound HTN if treatment is stopped -usually people in renal failure Thiazide Diuretics -Hydrochlorothiazide (HCTZ)- first drug in line for HTN -reduces BP by decreasing blood volume and reducing arterial resistance -ADR: hypokalemia, dehydration, hyperglycemia, hyperuricemia (uric acid in urine) Loop Diuretics -Furosemide (Lasix)- not used routinely for HTN as it is more potent than needed. -reserved for pts who require greater diuresis and have a low GFR -ADR: hypokalemia, dehydration, hyperglycemia, hyperuricemia, hearing loss -IF POTASSIUM IS LESS THAM 3.5 HOLD IT Potassium Sparing Diuretics -Spironolactone -inhibits reabsorption of Na in kidneys -diuresis is small, can balance effects of other HTN therapies -ADR: hyperkalemia, dizziness HTN Emergency -Nitroprusside- Nipride (IV) -DBP >140 mm/Hg -severity is determined by end organ damage -relaxes smooth muscles of the heart -usual rate of infusion is 0.5-0.8 mcg/kg/min -continuous BO monitoring -prolonged infusion (72 hours) can result in toxic build up of thiocyanate Alpha/Beta Blockers -Carvedilol -decreases HR, BP, increases CO, decreased risk of death -HTN, HF, LVD after MI -ADR: bradycardia, pulmonary edema, dizziness, fatigue -Very potent, not given for HTN usually unless you have gone through a lot of drugs Arteriosclerosis -chronic disease of the arterial system -abnormal thickening and hardening of the vessel walls Artherosclerosis -type of arteriosclerosis that occurs from build up of fats, cholesterol to form plagues on arteries which restricts blood flow. -plaque development -begins with injury to the endothelial cells -risk factors for injury: -smoking, HTN, diabetes, increased LDL, decreased HDL, autoimmunity -non-traditional risk factors: -elevated C-reactive protein, increased fibrinogen, insulin resistance, oxidative stress, periodontal disease, infection -progression: -inflammation fat streak fibrous plaque complicated plaque -results in: -inadequate perfusion, ischemia, necrosis Myocardial Ischemia -local, temporary cut off blood supply to the heart via the coronary arteries -ST changes when you are having ischemia -STEMI: ST elevation, more severe -non-STEMI: don’t see changes on EKG, but there are enzymes that have spilled from damaged cells -increased stress levels and hormones can increase ischemia -Stable Angina: progressive pain that exacerbates during exercise and subsides with rest -treat with long acting nitrates -Printzmetal’s Angina: vasospasm of coronary artery that doesn’t allow enough blood to pass -can progress to an MI if the spasm does not cease -treat with CCBs -Silent Ischemia: brought on by mental stress -more common in women -no traditional signs of ischemia -fatigue, back pain Unstable Angina -stable angina that does NOT stop with rest -same process as AMI -treatment for ANGINA-MONA -Morphine -dec RR, lower BP and HR, decrease pain and stress -Oxygen -helps save cells, 2-4L NC -Nitrates -vasodilates causing BP to go down -Aspirin -makes platelets more SLIPPERY to continue blood flow -325 mg, CHEW IT so it is more effective Chest Pain -injury to the cells begins after 8-10 seconds of decreased blood flow. That is when pain/angina starts: -chest pain -arm pain -jaw pain -indigestion -glycogen is depleted, becomes acidotic, oxygen imbalance leads to electrolyte imbalance, stimulation of PNS and SNS, increased glucose levels form SNS -angiotensin II is released with lack of blood flow- which causes vasoconstriction, fluid restriction, and release of catecholamines which causes vasospasms Cellular Death -cells release enzymes as they die (non-STEMI) -the muscle is stunned which decreases contractility -left side stunned, fluid will go to lungs and cause crackles -remodeling is mediated by angiotensin II (blocked by ACE or ARB) -clinical manifestations: -increased HR and BP, S3 sounds, crackles, peripheral vasoconstriction (skin cool and clammy) Medications for Ischemia -Nitrates -vasodilate -Beta Blockers -slow HR, increase diastolic filling time -Calcium Channel Blockers -relaxes muscles -works for ischemia or angina -for ANY spasm, use a CCB Medications for Angina/AMI -goal is to decrease the demand for oxygen. -increase oxygen or blood supply. -Aspirin decreases platelet aggregation -used indefinitely at 81-325mg/day Anticoagulants -Heparin -used to prevent clot from getting better -ADR: bleeding, Heparin-induced thrombocytopenia (HIT) -antidote: protamine sulfate -Warfarin -inhibits activity of vitamin K, which activates certain clotting factors -DVT treatment, embolization from A-fib or heart valve replacement, pulmonary embolism -antidote: vitamin K Interventions for AMI -Percutaneous Coronary Intervention (PCI) -punctures through femoral or radial artery -catheter through aorta to heart -PTCA (angioplasty) -Stents -bare metal -drug eluding- cephalosporin to decrease chance of rejection -Tissue Plasminogen Activator (TPA) -medication for patients who had S/S less than 3 hours before administration and PCI will be delayed for more than 2 hours -greatest risk is intracranial bleeding -contraindicated if S/S started more than 24 hours ago, scheduled for CABG, recent surgery or trauma, PUD, severe HTN, brain cancer -often results in reocclusion of the artery and failure to restore blood flow -used more in places where cardiac catheterization is not available Sinus Rhythms Originate with SA node Regular Sinus Bradycardia o Rate <60 o Causes: high fluid volume, MI, BB o Med: atropine Sinus Tachycardia o Rate 100-150 o Causes: exercise, anxiety, fever, low O2 o Identify the causes and treat it Atrial Rhythms Start in atria, but not SA node Atrial Tachycardia o Rate: 150-250 o Absent P wave o Can cause decreased coronary perfusion and ventricular filling o Meds: amiodarone, adenosine o Tx: Vagal manuevers, synchronized cardioversion Atrial Flutter o Rate varies o “saw-tooth” waves o No PR interval; One cell is being a bully and no letting SA node be in control o Meds: remove cause, BB, CCB, amiodarone, digoxin o Tx: synchronized cardioversion Atrial Fibrillation o Rate varies o Atria are quivering- no atrial kick o Meds: anticoagulant for potential clotting, CCB, BB, amiodarone o Tx: synchronized cardioversion Ventricular Rhythms Originate in ventricles Ventricular tachycardia o Can be with/without a pulse o Rate: >100 o No P wave o If there is a pulse: amiodarone, synchronized cardioversion o No pulse: defibrillation and CPR Ventricular Fibrillation o Rate: not measurable o No pulse o Will lead to asystole- must defibrillate, CPR Difference between Cardioversion and Defibrillation -Cardioversion -done to correct ventricular tachycardia (pulse) and atrial dysrhythmias -done under sedation, unless there is a threat of cardiovascular collapse -may cause serious dysrhythmias -may cause a transient elevation of ST segment -may cause pulmonary edema (rare) -Defibrillation -emergency life-saving procedure for ventricular tachycardia (no pulse), ventricular fibrillation and cardiac arrest -restarts the heart -no anesthesia is needed -may cause myocardial necrosis Blood Flow Through the Heart -superior & inferior vena cava right atrium tricuspid valve right ventricle pulmonary artery lungs pulmonary arteries left atrium bicuspid (Mitral) valve left ventricle aortic valve aorta systemic body Left Heart Failure (Congestive Heart Failure) -Systolic Heart Failure -inability of the heart to generate adequate CO to perfuse tissues -ventricular remodeling -causes: myocardial infarction, myocarditis, cardiomyopathy -Diastolic Heart Failure -pulmonary congestion despite normal SV and CO -causes: myocardial hypertrophy, ischemia, diabetes, valvular and pericardial disease Systolic Diastolic -Inadequate CO -pulmonary congestion despite normal CO -Ventricular remodeling -preserved EF -Decreased LV compliance Manifestations of Left Sided HF -result of pulmonary vascular congestion & inadequate perfusion of the systemic circulation -dyspnea, orthopnea, frothy sputum (pulmonary edema), decreased urine output, edema, -physical exam: pulmonary edema (cyanosis, inspiratory crackles, pleural effusion), hypo or hypertension, S3 gallop, evidence of underlying CAD or HTN, tachycardia, diaphoresis, displaced point of maximal impact (PMI), altered BP Right Heart Failure -most commonly caused by a diffuse hypoxic pulmonary disease -can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation -caused by diseases/processes which cause hypoxia -may be caused by ischemia/RV infarct -increase in LV filling pressure -can also result from L heart failure -Symptoms: weakness, anorexia, indigestion, weight gain, mental changes -Physical Findings: peripheral edema, hepatomegaly, splenomegaly, ascites, JVD, increased central venous pressure (CVP), pulmonary HTN, abdominal distention -High-output failure -inability of the heart to supply the body with blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility (heart is doing what it is supposed to do, but something is going wrong) -causes: anemia, hyperthyroidism, septicemia NYHA Functional Classifications of HF -Class I (mild): No limitation of physical activity; ordinary physical activity doesn’t cause tiredness, heart palpitations, or shortness of breath. -Class II (mild): Slight limitation of physical activity; the patient is comfortable at rest, but ordinary activity causes tiredness, heart palpitations, and/or shortness of breath. -Class III (moderate): Marked limitations of physical activity; the patient is comfortable at rest, but less than ordinary physical activity causes tiredness, heart palpitations, or shortness of breath. -Class IV (severe): Severe limitation of physical activity; the patient is unable to carry out any physical activity without discomfort. Symptoms are present at rest, and any physical activity increases that discomfort. Treating Regimen for HF -lifestyle changes -medications -inotropic agents, beta-blockers, ACE, ARBs, diuretics, Heart Valves -determine direction of blood flow -Tricuspid and Mitral (Bicuspid) in b/t atria and ventricles -Pulmonary and Aortic from ventricle to artery -causes of dysfunctional valves: congenital defect, trauma, ischemic changes, degenerative changes, and inflammation -Atrioventricular valves are closed during systole -Semilunar valves are open during systole Stenosis -narrowing of the valve opening -requires extra pressure to force the blood through the valve -symptoms are first noticed in situation that causes increased flow i.e. exercise -valves affected are usually mitral and aortic -Mitral Valve Stenosis: enlargement and overfilling of left atrium -most common cause of Right Heart Failure -continuous progressive process -long stable course early on, and progressive acceleration in later years -S/S: pulmonary congestion, nocturnal paroxysmal dyspnea, CHF, weakness, fatigue, Premature Atrial Complex [early sign for Afib] (PAC’s)Afib, murmur during systole -Aortic Valve Stenosis: enlargement and overfilling of left ventricle -increase resistance of ejection of blood from LV to aorta -causes congenital valve malformation, acquired calcification -progresses slowly so LV has time to adapt -loud systolic murmur leads to diagnosis or symptoms become evident -S/S: angina, syncope, HF, decreased exercise tolerance or exertional dyspnea Incompetent Valve (Regurgitation) -backwards flow of blood when the valve should be closed -Mitral Valve Regurge: blood flows back into left atrium during systole -causes Rheumatic Heart Disease (RHD), rupture of chordae tendonaie or papillary muscle, or Mitral Valve Prolapse (MVP). -can be tolerated for years -enlarged LV, systolic murmur, can be treated with ACE and biV pacer to decrease preload -Aortic Valve Regurge: blood flows back into left ventricle during diastole -backwards backflow to LV, causing increase to SV to maintain CO -causes: RF, dilation of aorta, congenital, HTN, trauma and failure of prosthetic valve -symptoms appear in progressed disease, similar to LV failure Cardiogenic Shock -decreased CO with tissue hypoxia with adequate fluid status -cardiac muscle dysfunction (AMI, LHF, valve problems, ventricular or septal rupture) -manifestations: impaired mentation, dyspnea, tachypnea, systemic and pulmonary edema, hypotension, cool clammy skin, grey looking -Tx: Inner Aortic Balloon Pump (IABP), Ventricular Assist Device (VAD), pressors Hypovolemic Shock -caused by decrease volume -blood loss, burns, diaphoresis, diabetes -symptoms start when 15% of volume is missing -compensatory mechanisms: inc HR, SVR, liver and spleen empty into vasculature, kidneys secrete ADH, -compensatory mechanisms fail leading to Multi-Organ Dysfunction Syndrome (MODS) -Tx: replace fluid or blood Neurogenic Shock -widespread vasodilation caused from parasympathetic overstimulation or sympathetic understimulation -trauma to spinal cord -depressive drugs, anesthetic agents, severe emotional stress -loss of vascular tone relative hypovolemia -Tx: fluid and vasopressors Anaphylactic Shock -widespread hypersensitivity to substance -causes vasodilation relative hypovolemia decrease tissue perfusion and impaired cellular metabolism -clinical manifestations: anxiety, dizziness, swollen lips and tongue, abd cramps, dec BP, impaired mentation, decrease Systemic Vascular Resistance (SVR) -Tx: remove allergen, epinephrine IM Septic Shock -caused by bacteria -clinical manifestations: fever, tachycardia, tachypnea, leukocytosis, vasodilation, hypotension, tissue inflammation, myocardial depression, MODS Multi-Organ Dysfunction Syndrome -dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury -causes: sepsis, septic shock, severe injury (trauma, burns, surgery) -manifestations: respiratory, hepatic, GI, renal, myocardial failure Medications o HTN Emergency- Nitroprusside - (Nipride IV) The severity of emergency is determined by likelihood of end organ damage Pressure decreased in 1 hour vs. 18 hours Direct acting vasodilator relaxes smooth muscles of A & V Administered via IV infusion the usual rate is 0.5-8 mcg/kg/min Continuous blood pressure monitoring required. Prolonged infusion (72 hours) can result in toxic build up of thiocyanate. (Precursor for cyanide) Organs at risk for damage during a hypertensive crisis: eyes (swelling and bleeding), brain (IICP, CVA), kidneys, heart Prob a calculation question!!!**** Lisinopril (ACE)- Onest 1 hour Peak 6 hours Duration 24 hours o RAAS- Angiotensin II receptor blocker (ARB): prevents angiotensin II from binding to receptors: Losartan Decreases blood pressure. Indication: HTN, HF, post MI, CAD, CKD Has less side effects than ACE. ADR: hypotension, headache, dizziness http://www.mayoclinic.org/diseases-conditions/high-blood- pressure/in-depth/angiotensin-ii-receptor-blockers/art- 20045009?pg=1 o Calcium Channel Blockers- Two categories of CCB: Dihydropyridines act only on arterioles-nifidipine Nondihydropyridines act on arterioles and conduction- verapamil, diltiazem Prevents calcium ions from entering cells therefore effects contraction Relaxation of arterioles Used to treat HTN, angina, cardiac dysrhythmias (atrial). http://www.mayoclinic.org/diseases-conditions/high-blood- pressure/in-depth/calcium-channel-blockers/art-20047605 Decreases contraction leading to dec BP Verapamil and Diltiazem slows down conduction, dec rate Nifedipine-causes vasodilation Indications: angina, HTN ADR: reflex tachycardia, flushing, headache, peripheral, gingival hyperplasia Verapamil-causes vasodilatation, and block SA node Indications: angina, HTN, and dysrhythmia ADR: constipation, flushing, dizziness Diltiazem-Same as verapamil: except ADR doesn’t include constipation o Beta Blocker- Block the effects of epinephrine, decrease in HR and BP, suppress reflex tachycardia, reduce release of renin, reduces PVR over time Propranolol- non selective BB Metoprolol-cardio selective BB Often used after pt MI ADR: bradycardia, AV HB, HF, rebound excitation (with withdrawal), bronchoconstriction, altered glucose, fatigue, dizziness, loss of libido, SOB, depression http://www.mayoclinic.org/diseases-conditions/high-blood- pressure/in-depth/beta-blockers/art-20044522?pg=2 If you stop taking abruptly you will get rebound excitation = tachycardia and hypertension b/c of epinephrine (will see w/in 24 hours) Fatigue will resolve in 4-6 weeks but loss of libido will not See Chart for Beta Blockers** o Beta Blockers- Block chronic adrenergic stimulation especially of nodal tissue and the conducting system Decrease contractile force (promote relaxation) Inhibits Renin Decrease HR, contractility and atrial pressure Reduces cardiac remodeling Decreased HR (by decreasing sinus rate), contractility, pressure = decreased work of heart and decreased oxygen demand Beta-blockers have an additional benefit as a treatment for hypertension in that they inhibit the release of renin by the kidneys (the release of which is partly regulated by β -1 adrenoceptors in the kidney). Decreasing circulating plasma renin leads to a decrease in angiotensin II and aldosterone, which enhances renal loss of sodium and water and further diminishes arterial pressure. Decreases cardiac remodeling Do not give with CCB’s http://cvpharmacology.com/cardioinhibitory/beta- blockers.htm o Loop Diuretic- Furosemide (lasix)-aren’t used routinely for HTN as it is more potent than needed. Reserved for patients who require greater diuresis, have a low GFR. ADR: Hypokalemia, dehydration, hyperglycemia, hyper- uricemia, hearing loss http://www.nlm.nih.gov/medlineplus/druginfo/meds/a68285 8.html If you give it too fast it can cause hearing loss Potassium < 3.5 don’t give o Drug Class- HMG-CoA Reductase Inhibitors (Statins) Artorvostatin Actions o Inhibit enzyme responsible for converting HMG- CoA to mevalonate, ultimately reduce liver cholesterol Uses o In conjunction with dietary therapy to reduce LDL and total cholesterol levels Common adverse effects o Headaches; nausea, abdominal bloating, gas Serious adverse effects o Liver dysfunction; myopathy, rhabdomyolysis**; myoglobinuria For specific drugs, see Table 22-3. (Lehne) Best administered at night because of peak cholesterol production at this time. Statins do not differ in effectiveness, but they do differ in potential drug interactions. Grapefruit juice inhibits the metabolism of several statins and should be avoided. Reduces amount of cholesterol in LIVER Alters enzymatic activity in liver so you will see GI symptoms ADR – Muscles aches that lead to Rhabdo*** Myopathy: early signs are muscle aches, soreness, and weakness Rhabdomyolysis: kidney damage resulting from progressing myopathy (may have pinkish- or red- tinged urine) Liver function should be monitored. If AST, ALT rise to 3X normal, medication should be discontinued Nitrates o Nitroglycerin-can be given SL, IV, or patch Promotes vasodilation of vascular smooth muscles. Primarily on veins, small affect on arterioles Rapid metabolism by liver ½ life 5-7 minutes ADR-headache, orthostatic hypotension, reflex tachycardia. Severe hypotension if given with PDE5 inhibitors (Viagra) SL given every 5 minutes X3 for CP. Onset 1-3 minutes Transdermal: need patch free period of 10-12 hours. Put on in AM and remove at HS. IV titrate to effect-pain free or drop in B/P Supposed to be replaced every 6 months If it is tingling it is working Almost guaranteed that will get a headache from it Reflex tachycardia Drug Class Platelet Inhibitors o Drug: Clopidogral (Plavix) Oral antiplatelet- effects are irreversible Effect begins in 2 hours, plateau 3-7 days, platelets return to baseline 7-10 days Drug interactions: PPI (reduce effect of plavix) ADR: bleeding, TTP AE: bleeding, abdominal pain, dyspepsia, diarrhea, rash. TTP low incidence in first 2 weeks of taking. Interaction with PPI’s Some people can’t metabolize Expensive brand name $200/month Generic $15/month Right after PCI give a loading dose of Plavix If you take a PPI, it can dec level of available drug Can give with PPI but just accept you will not be getting highest dose of meds This only works on platelets, safer than warfarin o Drug: aspirin Actions: NSAID, platelet aggregation inhibition Uses: In men, reduces risk of MI, in females reduces risk of stroke; used in males and females with acute MI Lowest level anti platelet Drug Class: Thrombin inhibitor- o Drug: dabigatran (Pradaxa) Action: direct thrombin inhibitor, prevents conversion of fibrinogen to fibrin Uses: reduce risk of stroke with non-valvular atrial fibrillation Premedication assessment: assess for bleeding, monitor labs, assess for pregnancy Safety alert-capsules must be swallowed whole ADR: bleeding Marketed heavily right now b/c do not need monitoring (blood levels drawn) Problem it is $$$$$ Hard to stop them from bleeding , do not have anything to reduce effects Drug Class Glycoprotein IIb/IIIa inhibitors o Drugs: abciximab (ReoPro), eptifibatide (Integrilin)***, tirofiban (Aggrastat) Actions Block receptors on platelets, preventing aggregation and clot formation Uses Prevent clots forming from the debris often released during percutaneous coronary intervention (PCI) procedures Serious adverse effects Bleeding, thrombocytopenia Laboratory values to monitor: hematocrit, platelet counts, ACT. Lab values return to normal after 4 hours. Used specifically after a stent is put in Strongest antiplatelet Given for 18 hours after stent w/ Plavix Drug Class Fibrinolytic Agents- o Drugs: streptokinase, alteplase (tPA)(Activase), reteplase (Retavase), tenecteplase (TNKase) Actions Stimulate the body’s own clot-dissolving mechanism, converting plasminogen to plasmin, which digests fibrin Uses Dissolve fibrin clots secondary to coronary artery occlusion (MI), pulmonary emboli, cerebral emboli, deep venous thrombosis Streptokinase is still available but rarely used. Act during early phase of clot formation, limiting damage to surrounding tissues. Serious adverse effects: increased risk of bleeding, allergic reactions. o Thrombolytic (fibrinolytic) Clot busters-break up thrombi that are formed tPA-Activase used for AMI, CVA, PE Within 2-4 hours onset of symptoms is ideal time frame. For an MI can extend time frame out to 6 hours ADR: Bleeding Absolute contraindications for administrations: ICH (internal cerebral hemorrhage), Ischemic stroke in past 3 mo, internal bleeding, suspected aortic dissection o Digoxin Cardiac glycoside-increase force and velocity of contraction, a decrease in SNS activation, decrease in renin, slowing of the HR and decreased conduction Contraindications: Slow HR, decrease dose with decrease GFR, hypokalemia, hypomagnesia increases risk of toxicity. K sparing diuretics increase risk of toxicity ADR: AV block, anorexia, nausea vomiting and diarrhea, visual disturbances, (blurred or yellow vision) Need to maintain steady dose level of drug. Check serum level normal theapeutic dose is 0.8 ng/mL-2 ng/mL Antidote for digoxin toxicity is digibind. Heart Failure: Lanoxin is indicated for the treatment of mild to moderate heart failure. Lanoxin increases left ventricular ejection fraction and improves heart failure symptoms as evidenced by exercise capacity and heart failure-related hospitalizations and emergency care, while having no effect on mortality. Where possible, Lanoxin should be used with a diuretic and an angiotensin converting enzyme inhibitor, but an optimal order for starting these 3 drugs cannot be specified. Atrial Fibrillation: Lanoxin is indicated for the control ofventricular response rate in patients with chronic atrial fibrillation.
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