ATI Pharmacology Made Easy

ATI Pharmacology Made Easy--CV Overview of CV System  BLOOD FLOW – Hemodynamics s DEOX: Superior/Inferior Vena Cava  R Atrium  Tricuspid  R Ventricle  Pulmonary Valve  pulmonary artery  lungs s OX: pulmonary veins  L atrium  Mitral  L ventricle  aortic valve  aorta  body  Blood Vessels s Leaves heart and enters into blood vessels  Arteries (away from heart)  Capillaries  Veins (to heart) s Blood vessel that has a larger diameter has a decreased amount of resistance and lower pressure s Blood vessel with smaller diameter exerts more resistance and higher pressure s Contraction = systole s Relaxation = diastole  Cardiac Output s Contractility is the force of the hearts contractions  Increase in calcium increases contractility vice versa  Positive inotropic drug increases availability of calcium  Negative decreases s Preload – blood in heart before contraction  Affected by amount of blood entering heart via vena cava and ability of heart to stretch and accommodate amount of blood s Afterload – amount of pressure the heart must exert to move the blood in the heart out into the aorta/pulmonary artery  Affected by back-pressure exerted on the blood by the systemic arterial BP and pulmonary arterial pressure s CO = HR x SV  Electrical Impulses s Depolarization is the change that occurs in a cell membrane from negative to positive when calcium/sodium move into the cell, stimulating action potential, int turn stimulate heart to contract s Repolarization = change in cell membrane back to neg status after an action potential occurs s P wave = atrial depolarization s QRS complex = ventricular depolarization s T wave = ventricular repolarization s PR interval = time needed for depolarization and impulse to travel through the conduction nodes/purkinje fibers s QT interval = time it take for ventricular depolarization and repolarization to occur  Factors that affect ARTERIAL PRESSURE s Sympathetic nervous system stimulates constriction s Kidneys regulate water – decrease = decrease in blood s RAAS regulates release of chemicals that cause constriction of the arterioles and veins, and any increase in blood pressure (activated when kidneys detect decrease in blood flow) s Angiotensin 2 stimulates kidneys to decrease salt/water excretion, stimulates aldosterone release which increases sodium resorption  Cause body to retain fluid = BP increase s Atherosclerosis – fatty deposits in the intima of arteries which causes impaired blood flow/occlusion  When coronary blood flow = angina pectoris  If blocked = MI = no O2 getting to tissues (aka heart attack/stroke)  Also can break off and travel to occlude small vessels = heart attack, stroke, pulmonary embolism in the lungs  Thrombi/DVT DRUG THERAPY s GOAL = tx HTN, HF, coronary heart disease, dysrhythmias FOR HTN – goal = below 130/80  RAAS Suppressants s ACE  Also tx HF, nephropathy, L ventricular dysfunction follow MI  TYPES:  Captopril (Capoten, enalapril/Vasotec, fosinopril/monopril, lisinopril/prinivil)  Action:  Block production of angiotensin II causing arteriolar vasodilation and urinary excretion of sodium/water AND K+ retention  Adverse Effects:  Severe hypotension (common w/ pts w/ severe HTN, taking diuretics, sodium-restricted diet)  Rash, metallic taste, hyperkalemia, neutropenia (decrease in WBC)  SIDE EFFECTS  Dry nonproductive cough due to increase in bradykinin, angioedema  Notify MD of cough  Interventions  Start with low dose and gradually increase  Diuretics may be temp stopped  Admin  Oral use only  2-3x/day for HTN, 3x/day for HF  Captopril one hour before meals o Others may not be given with food  EDU  No K+ supplements, don’t take if preg/breastfeeding  Contraindications  Preg/breastfeeding, decreased renal, bone marrow depression, using durgs that cause immunosuppression, have autoimmune (Rheumatoid arthritis), caution in older adults/pts who have hx of CV disease, stroke, HF, hyperkalemia, hyponatremia  Less effectives in blacks, increased risk of angioedema s ARBS (angiotensin II receptor blockers) TX HTN  Losartan/cozaar (valsartan/diovan, irbesartan/Avapro, candesartan/atacand)  Effects  Block production of angiotensin II causing arteriolar vasodilation and urinary excretion of sodium/water AND K+ retention o Less able to protect pt from CV events = seond choice o Don’t cause cough/hyperkalemia tho  Side effects  Angioedema (less common than ACE), dizzy, hypotension, HA, insomnia  Admin  Oral, w/orw/out food  Contraindications  Not for preg, kids under 6 and over 6 with low Cr clearance  Caution w/ diuretics, hyperkalemia, liver/renal disorder, planning preg  NSAIDS decrease effectiveness s Aldosterone antagonists  Eplerenone (inspra), spironolactone (Aldactone)  Action  Block aldosterone receptors, results in urinary excretion of sodium/water, retention of K+  S/E  Hyperkalemia  Interventions  Hyperkalelmia (monitor for s/s of palpitation, twitching, weakness, paresthesia, slow irregular HR, muscle cramps, progressive weakness, hyperactive bowel sounds/runs)  Monitor BUN/CR  Admin  Oral, alone or with other HTN Rx, max effect takes up to 4 weeks s DRIs – direct renin inhibitors  Aliskiren (tekturna)  Binds with renin, inhibits activation of agntiotensin I, causing vasodilation and excretion of sodium/water  Adverse: stomach pain, runs, dyspepsia  Admin-oral, don’t give with high fat meal, pref hour before eating at same time, may take up to 2 weeks before works  No preg = fetal injury TERATOGEN  Decreases furosemide and intreases Lipitor and ketoconazole  Avapro/irbesartan decreases it Calcium Channel Blockers  2 types s Effect peripheral arterioles (dihydropyridines)-nifedipine/adalat, procardia s Effect both arterioles and arteries (used for dysrhtyhimias) – verapamil/calan  Block channels in vascular smooth muscle cells of peripheral arterioles and minimally in cardiac arteries = vasodilation  Dihdropyridines increase heart rate – reflex tachy (in fast acting tablets) – bcuz decrease in BP stimulates baroreceptor reflex  Headache, lightheadedness, dizzy, facial flushing, hot, peripheral edema, arrhythmias, gingival hyperplacia  May be given with beta-blocker to prevent tachy  Oral and ER (best for HTN) capsules  Bad for BP less than 90, AV block, sick sinus, grapefuirt, rifampin, rifabutin, pheno, st johns wort, carbamazepine ARDS CASE STUDY  Rapidly progressive disease occurring in critically ill pts  complications = fluid leaking into the lungs, no breathing pH – measures acidity/alkalinity PaCo2 measures ventilation HCO3 measures metabolic (fenal function) SaO2 measures % of hemoglobin sat with O2 In ARDS = O2 admin, ventilate, suction Repositiong pt every 1-2 hrs, communicate in calm manner, limit visitors so pt can reset, assess nutritional needs  If deteriorating, sedate/ventilate with PEEP  Restrict fluid to decrease the amt of fluid available that will leak into the alveolar interstitial spaces, causing alterations in the capillary bed (basically want to reduce hydrostatic pressure as much as possible)  PEEP = pressure is applied in the airways at the end of the expiration phase to help prevent alveolar collapse       COPD CASE STUDY debilitating and can become life-threatening. Characterized by recurring respiratory symptoms and limited airflow caused by airway and/or alveolar abnormalities brough on by prolonged exposure to toxic particles or gases, smoking = major risk factor. The obstructed airflow that results cannot be wholly reversed w/ medication  First reposition to 75-90 degrees  Bronchodilator: Decrease airway resistance, facilitate mucus drainage, increase vital capacity  Incentive spirometer to increase lung expansion  Increased urine output after Lasix-nurse concerned with dehydration and cardiac dysrhythmias  High concentration pay decrease pts hypoxic drive COPD & PERIPHERAL VASCULAR DISEASE CASE STUDY  COPD: long-term pulmonary disorders characterized by airflow resistance s Include asthma, chronic bronchitis, emphysema s Chronic bronchitis/emphysema are more closely related to cause, pathogenesis, and Tx and are more likely to occur together s Asthma is more acute and intermittent s Predisposing factors: smoking, recurrent/chronic respiratory infections, allergies, hereditary factors  SMOKING, impairs ciliary action/macrophage function  Peripheral Vascular Disease s Common complication of atherosclerosis and may create arterial occlusive disease s Risk factors = smoking, aging, HTN, hyperlipid, DM, family hx of vascular disorders, MI, stroke s In arterial occlusive – obstruction or narrowing of an arterial lumen causes an interruption of blood flow, usually in legs/feet  S/S depend on severity and site  paralysis, pain, paresthesia, pallor, diminished/absent pulses, intermittent claudication (pain w/ exertion/exercise, relieved by rest), severe burning pain, ulcers/gangrene, pallor on the elevation of an extremity, decreased cap refill, hair loss  Rest pain = persistent pain in foot/digits at rest = severe degree of arterial insufÏciency s Ankle/brachial index = provides degree of stenosis  Pt: s Ineffective peripheral tissue perfusion-arterial s s/s-claudication and rest pain, absent R pedal and post tibial pulses, R foot cool/cap refill less than 6, numbness/tingling R foot, inability to feel/moving toes as unit s ankle-brachial index is the ratio of ankle systolic pressure to arm systolic pressure. It is an objective measurement of arterial disease that provides quantification of the degree of stenosis. Normal PAD is 0.9 to 1.1, mild – mod PAD is 0.4-0.9, severe PAD is 0.00-0.4 s S/S of chronic venous insufÏcient = edema, altered skin pigmentation s Hold metformin before angiogram – ionized contrast can fuck with renal and lactic acidosis can occur, should be stopped 48 hours before and wait until 48 hours after to take again s After contrast dye, monitor urine output—it is nephrotoxic and decreasing urine output could be an indication of renal failure s CVP monitoring (central venous pressure) in vena cava or R atrium assess fluid status – normal is 0-8 s Artery bypass graft-arterial diversion around occlusion or stenosis Pneumonia Case Study  Inflammation of lung parenchyma  Frequently either CAP or HAP  In olds, may be primary dx or complication of chronic disease  Types s CAP – occurs in community or within first 48 hours of a hospitalization  Streptococcal, haemophilius, legionnaires, mycoplasma, viral, chlamydial pneumonia s HAP – nosocomial, occurs 48 hour sor more following admission  Ex: psudomonas, staphylococcal, klebsiella s Pneumonia in immunocompromised = pneumocystis, fungal, TB s Aspiration – results from endo or exogenous substance in the lower airway tract and is caused by aspiration of bacteria from the upper airway and gastric contents  Sudden onset of shakey chills = bacterial pneumonia – streptococcal  Temp of 38 C (100 F) = symptom of pneumonia  SOB when lying down (orthopnea) = decreased lung expansion  Productive cough w/ tinged blood sputum = indicates bacterial pneumonia  RR 30 = sign of respiratory distress  Chest x ray – could reeal lung infiltration  Blood cultures – ID causative agent  Sputum culture – ID causative agent and cellular changes for viral pneumonia  Throat culture – not needed  Pulmonary function test differentiate between restrictive/obstructive forms of pneumonia  Monitor lab findings – ID abnormalities  Monitor respiratory status and SaO2 – finds any increase in respiratory rate/effort and abnormal breath sounds  Monitor chest pain – indicator of complications/if worsening  Interventions s Encourage cough – to increasea lung capacity and allow for gas exchange s Turn 1-2 hr – move secretions/mucus so pt can cough them up s Admin O2 – helps tissue perfusion  Azythromycin side effects (macrolide) s HA, dizzy, N/V/D, ab pain, hepatotoxicity, liver function mild elevation  Gastro = Runs, V, hepatotoxicity Pulmonary Edema Case Study  Occurs when an abnormal amount of fluid accumulates in the interstitial spaces and alveoli of the lungs s Heart disease = most common cause s Any condition that triggers pulmonary fluid overload can cause it  Cardiogenic pulmonary edema is brough on by heart or lung disease  Noncardiogenic pulmonary edema occurs when the etiology results from trauma to the CNS, reactions to certain Rx, toxin, or high altitude exposure  S/S s Cough w/ frothy, pink sputum, dyspnea, wheezing, restlessness, confusion  Complications = edema in lower extremities, ascites, pleural effusion  Lasix – furosemide – too high/too quick = hypotension, dehydration, electrolyte disturbance (specifically K+), ototoxicity