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Step 1 Cardio2Testwe

What are the 5 T's causing R to L shunt in CHD "blue babaies"? Tetrology of Fallot, transposisition of great vessels, truncus arteriosus, Tricuspid atresia, TAPVR (totoal
What is a persistent truncus arteriosus? failure of truncus to divide into pulmonary trunk and aorta
What is tricuspid atresia? What does it require for viability? absence of tricuspid valacve and hypoplasia of RV. nneds ASD and VSD for viabilitity
What is total anomalous pulmonary venous return? pulmonary veins drain into RH circulation
What are 3 causes of a L to R shunt in CHD? VSD, ASD, PDA
What heart sounds are observed in an ASD? loud S1, fixed split of S2
What is used to close a patent ductus arteriosus? indomethacin
What is Eisenmenger's syndrome? uncorrected VSD or ASD or PDA causes compensatory pulmonary vasculature hypertrophy= progressive PHTN
How does Eisenmenger's cause a shunt reversal? What Sx will it cause? due to incr Pulmonary reistance, shunt reverse from L to R to R to L= late cyanosis and clubbing.
What is the tetrology of Fallot? 1. pulmonary Stenosis 2. RVH 3. overriding aorta 4. VSD
How does a patient typically compensate for Tetrology of Fallot and what is the mech? Patient learns to squat, which compresses the femoral arteries and incr TPR which will decrease the R to L shunt directing more blood to lungs
What is the mechanism of cyanosis and shunt in tetrology of Fallot? early cyanosis by R to L shunt across VSD because of stenotic pulmonic valve
What does a Tetrology of Fallot heart look like on CXR? boot shaped heart due to RVH
What causes Tetralogy of Fallot? anterosuperior displacement of infundibular septum
What is is D transposition of the great vessels and what is the only way it is compatible with life? Aorta leaves RV, pulmonary trunk leaves LV (separation of systemic and pulmonic circulations). Not compatible with life unless a VSD, PDA, patent foramen ovale exists
What causes a transpositon of the great vessels? failure of aorticopulmonary septum to spiral. infants die without surgical correction
What is infantile type of coarctation of the aorta? aortic stenosis proximal to insertion of ductus arteriosus (preductal).
What CHD is Turner Syndrome associated with? infantile (preductile) coarctation of the aorta
What is the adult type of coarctation of the aorta? stenosis distal to ligamentum arteriosum (post ductal).
What are the major associated Sx of adult coarctation of the aorta? associated with notching of ribs due to notching of ribs, HTN in uppe extermiteis with diminshed pulses in lower extremities. can get aortic regurgiation
What is a key physical exam toll to use in evaluation for aortic coarctation? checking femoral pulses
What other CHD is a coarctation of the aorta associated with? congenital bicuspid aortic valve
What is the mech and shunt of a patent ductus arteriosus? shunt is R to L in fetal period, but when lung R decr with birth it becomes L to R = RVH and failure
What murmur is hear in PDA and how is its patency maintained? machine like continuous murmur. patency maintained by PGE2 and low O2 tension
What type of cyanosis might be seen in an uncorrected PDA? late cyanosis of lower extremitites (differential cyanosis)
When might maintainig a PDA be neccessary for life? in transposistion of the great vessels
What CHD are 22q11 syndromes associated with? Truncus arteriosus, tetralogy of Fallot
What CHD is Down syndrome associated with? ASD,VSD, AV septal defect (endocardial cushion)
What CHD is congenital rubella associated with? septal defects, PDA, pulmonary artery stenosis
What CHd is Turner syndrome associated with? coarctation of aorta (preductal)
What CHD is Marfan's syndrome associated with? aortic insufficiency
What CHD is an infant of a mother with DM at risk for? transposition of great vessels
How is HTN defined? BP >140/90
What are the major RF for high BP? incr age, obesity, DM, smpoking, black>white>asian
What is the mech of primary HTN? either incr CO or incr TPR
What does chronic HTN expose you to ? atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection
What are atheromas and what are they a sign of? plaques in BV walls. sign of hyperlipidemia
What are xanthomas and what are they a sign of? plaques or nodules composed of lipid laden histiocytes in skin esp in eyelids. sign of hyperlipidemia
What is a tendinous xanthoma and what is it a sign of? lipid deposit in tendon, especially achilles. hyperlipidemia
What is corneal arcus and what is it a sign of? lipid deposit in cornea, nonspecific (arcus senilis).
What is Monckeberg atherosclerosis? Does it obstruct blood flow? calcification in media of arteries esp radial or ulnar. Usually benign; "pipestem arteries. doesnt obstruct blood flow because intima isnt involved.
What is arteriolosclerosis, where is it seen and how might it appear in malignant HTN? hyaline thickening of small a in HTN or DM. see hyperplastic onion skinning in malignant HTN
What is atherosclerosis? fibrous plaques and atheromas forming in intima of arteries
What are the major RF for atherosclerosis? smoking, HTN, DM, hyperlipidemia, FHx
What is the usually progression of atherosclerotic plaque? Endothelail cell DysFx-->macrophage and LDL accumulation-->foam cell formation-->fatty streaks-->SMM migration (PDGF and TGF beta)--->fibrous plaque--->complex atheroma
What are some major complications of atherosclerosis? aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
What are the major locations of atherosclerosis? abdominal aorta>coronary a>popliteal a>carotid a
What are some Sx of atherosclerosis? angina, claudication, but can be Asx
What is an abdominal aortic aneurysm and who gets them? associated with atherosclerosis. occurs more frequently in male than female. also smokers, >50 y/o
What are 2 things associated with a thoracic aortic aneurysm? associated with HTN, cystic medial necrosis(Marfan's)
What is the tear in an aortic dissection and how does it present? longitunial intraluminal tear forming a false lumen associated with HTN and cystic medial necrosis (MArfans). Get tearing chest pain radiating to the back
What does the CXr show in an aortic dissection? mediastinal widening
How much must a CAD be occluded to cause angina? 75%
What is stable angina, how does it present? mostly secondary to atherosclerosis; ST depression on ECG. retrosternal CP with exertion
What is Prinzmetal's variant angina and how does it present ? occurs at rest secondary to coronary artery spasm. ST elevation on ECG
What is unstable/crescendo angina and how does it present? thrombosis but no necrosis. ST depression on ECG. worsening CP at rest or with minimal exertion
What is coronary steal syndrome? vasodilator may aggrivate ischemia by shunting blood from area of critical stenosis to area of higher perfusion
What is the usualy cause of an MI? most often acute thrombosis due to coronary artery atherosclerosis, resulting in myocyte necrosis
What is sudden cardiac death and the most common cause? death from cardiac causes within 1 hr of Sx onset. commonly due to lethal arrythmia like V fib
What is the presentation of chronic ischemic HD? progressive onset of CHF over years doe to chronic ischemia of myocardium
What is the order of likelihood for coronary artery occlusion? LAD>RCA>Circumflex
What are some acute Sx of MI? diaphoresis, n/v, severe retrosternal pain, pain in left arm or jaw, SOB, fatigue, adrenergic Sx
What is the major complication risk risk in an MI 0-4 days? arrythmia
What are the gross changes observed in an MI 4-24hrs old? dark mottling pale with tetrazolium stain
What are the microscopy findings in an MI 4-12 hrs old? early coagulative necrosis, edema, hemorrhage, wavy fibers
What are the microscopy findings 12-24 hrs post MI? contraction bands, release of necrotic cell content into blood. see beggining of neutrophil emigration
What gross changes are seen in the heart 2-4 days post MI? hyperemia
What microscopy changes are seen 2-4 days post MI? extenisve coagulative necrosis, tissue around infarct with acute inflammation, n eutrophil emigration
What gross changes are seen in the heart 5-10 days post MI? hyperemic border with central yellow softening
What microscopy changes are seen 5-10 days post MI? appearance of granulation tissue
What are the major complication risks for an MI 5-10 days post MI? WHy? free wall rupture, tamponade, papillary muscle rupture, IV septal rupture sue to macrophage degrading of structural components
What gros changes are seen in the heart 7 weeks post MI? recanalized artery and a gray white area
What microscopy changes are seen 7 weeks post MI? completeion of contracted scar
What is the major complication risk 7 weeks post MI? ventricular aneurysm
What is the gold standard for MI Dx in the 1st 6 hrs? ECG
What protein markers is the most specific for an MI confirmation and when does it appear? cardiac troponin I, rises after 4 hrs and elevated for 7-10 days
What is CK-MB and what is its usefulness for MI Dx? found in myocardium but can also be released by skeletal muscles. useful to Dx an reinfarction on top of acute MI
What is the use of ASt for MI Dx? nonspecific can also be found in liver and SM
What ECG changes are seen in a transmural infarct? ST elevation, pathological Q waves
What ECG changfes are seen in an subendocardial infarct? ST depression
What are some general properties of transmural infarcts? incr necrosis, affects whole wall, ST elevation and Q waves on ECG
What are some general characterisitcs of a subendocardial infarct? due to ischemic necrosis of <50% of ventricular wall.. subendocardium is especiually vulnerable to ischemia, ST depression on ECG
What leads have Q waves or other abnormaility in an anterior wall infarct? Which CA? LAD. V1-V4
What leads have Q waves or other abnormality in an anterospetal infarct and what CA? LAD. V1-V2
What leads have Q waves or other abnormalities in anterolateral infarct and what CA? LCX. V4-V6
What leads have Q waves or other abnormalities in lateral wall infarct and what CA? LCX. I, aVL
What leads have Q waves or other abnormalities in inferior wall infarct and what CA? RCA. II, III, aVF
What complication of MI might cause death before reaching the hospital? when is it most common? cardiac arrythmias, seen most in first few days
What is the major complication of a ventricular free wall rupture? cardiac tamponade
What are the major Sx of an papillary muscle rupture post MI? severe mitral regurgiation, pulmonary edema
What are the complications that could happen in an aneurysm formas post MI? decr CO, risk of arrythmias, embolus from mural thrombus
What might be seen and when in a post infarction fibrinous pericarditis? friction rub (3-5 d post MI)
What is Dressler's Syndrome? autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI
What are some major presenting Sx of bacterial endocarditis? fever, Roth spots on retina, Osler's nodes (raised lesion on finge or toe pads) new murmur, Janeway lesion (palm or sole), splinter hemorrhages on nail bed
What is a common pathogen for accute endocarditis and what is seen? S. aureus, large vegetations on a previously normal valve
What are some common pathogens for subacute endocarditis and what is seen? viridans strep. smaller vegetations on congentially abnormal or disease valves. sequela of dental procedures
When might endocaridits be secondary? malignancy, hypercoagulable state, lupus. S bovis in colon cancer, S epidermidis in prosthetic valves
What valve is most frequently invovled in bacterial endocarditis? mitral valve
When is the tricuspid valve invovled in endocarditis? What pathogens? IVDA. S. aureus, Pseudomonas, Candida.
What are some major complications of bacterial endocarditis? chordae rupture, glomerular nephritis, suppurative pericarditis, emboli
What is a mnemonic for the Sx of bacterial endocarditis? FROM JANE: fever, Roth spots, Oslers nodus, murmur, Janeway lesions, Anemia, Nail bed hemmorrhage, emboli
What cuases rheumatic HD? pharyngeal infection with beta hemolytic strep
What are the early and late problems caused by rheumatic fever? early death due to myocarditis. late valve disease (mitral>aortic>>tricuspid) which goes from mitral valve prolaspe to mitral stenosis
What is seen pathoglogyically in rheumatic HD, and what titers might be elevated? Aschoff bodies (granuloma with giant cells), Anitschkow's cells ( histiocytes), elevated ASO titers
What mediates Rheumatic fever? immune mediate, type II hypersensitivty, not direct effect of bacteria. Anitbodies to M protein of beta hemolytic strep
What is the mnemonic for the presentation of rheumatic fever? FEVERSS: fever, erythema marginatum, valvular damage (vegetation and fibrosis, incr ESR, Red-hot joint(migratory polyartritis), subcutaneous nodules, St. Vitus's dance (chorea)
How does acute pericarditis present? sharp pain. aggrevated by inspiration and relieved by sitting up and leaning forward
What is fibrinous pericarditis? How does it present and what might cause it? most frequent type. caused by dressler's syndrome, uremia, radiation. loud friction rub
What is serous pericarditis, and what causes it? noninfectious inflammatory disease (rheumatic fever, SLE)
What cuases suppurative/purulent pericarditis? infectious agents
What is the mech of cardiac tamponade? compression of heart by fluid in pericardium, leading to decr CO
What happens to pressures in all 4 heart chambers in cardiac tamponade? all 4 chambers diastolic P is eequal
What are the major findings seen in cardiac tamponade? hypotension, incr venous P (JVD), distant heart sounds, incr HR, pulsus paradoxus
What is pulsus paradoxus? decr in amplitude of systolic BP by 10mmHg during inspiration. Seen in tamponade, astma, sleep apnea, pericarditis, croup
What is the mechanism and complication risk of syphilitc HD?> tertiary syphilisdisrupts the vasa vasorum with dialtion of aorta and valve ring. can lead to aneurysm of ascending aorta and aortic valve incompetence
What happens pathologically to the arota in syphilitic Hd? calcification of aortic root, tree bark appearance of the aorta
What is the most common primary tumor in adults of the heart and where does it occur? myxomas, ball valve obstruction in LA (associated with multiple syncopal episodes)
What is the most frequent primary cardiac tumor in children? rhabdomyomas associted iwht tuberous sclerosis
What is Kussmaul's sign? incr in JVP on inspiration
What are varicose veins? dilated, tortuous superficial veins due to chronically elevated venous P.
What are 2 things that a varicose vein could predispose one to? poor wound healing and varicose ulcers. thromboembolism is rare.
What is Raynaud's disease? decr blood flow to skin due to arteriolar vasospasm in response to cold temp or stess. most often in fingers
What is Raynaud's phenomenon? when Raynaud's disease is secondary to mixed CT disease like SLE or CREST syndrome
What is the epidemiology of Temporal arteritis? elderly females. unilateral HA, jaw cladication. may cause irreversible blindness sue to occlusion of opthalmic a.
What disease is temporoal (giant cell) arteritis associated with? polymyalgia rheumatica
What is the pathology labs, and Tx for Temporal (giant cell arteritis)? affects branches of carotid a. focal granulatomous inflammtion, incr ESR. tx: high dose steroids
What is the epidemiology and presentation of takayasu's arteritis? Asian females <40. Pulseless disease (weak upper extermity pulses), fever, night sweats, artritis, myalgia, skin nodules, ocular disturbances
What are the pathology and labs of takayasu's arteritis? granulatomous thickening of aortic arch and proximal great vessels. incr ESR
What is the epidemiology and presentation of polyarteritis nodosa? young adults. HepB positive in 30%. get fever, wt loss, malaise, HA, GI: abd pain, melena. HTN neuro dysfx, cutaneous disruptions
What vessels are most commonly invovled in polyarteritis nodosa? renal and visceral vessles. NOT pulmonary a.
What mediates polyarteritis nodosa and what pathology is seen? immune complex mediated. get transmural fibrinoid necrosis with lesions of different ages
What might you see on an arteriogram of polyarteritis nodosa? multiple aneurysms and constrictions
How do you Tx polyarteritis nodosa? corticosteroids, cyclophosphamide
What is the epidemiology/presentation of Kawasaki disease? Asian children<4 y/o. fever, lymphadenitis, conjunctivits, changes in lips/oral mucosa (strawberry tongue). hand foot erythema, desquamation
What is the major danger of kawasaki disease and what is the tx? can develop coronary aneurysms, Tx: IV immunoglbulin and aspirin
What is the epidemiology and presentation of Buerger's disease (thromangitis obliterans)? heavy smokers, males <40 y/o. intermittent claudication may lead to gangrene, digit autoamputation, superficial nodular phlebitis
What other disease phenomena is Bueger's disease (thrombangitis obliterans) associated with? Raynaud's phenomenon (cold sensitivity) due to neural invovlement
What is the pathology and Tx for Buerger's disease (thrombangitis obliterans)? segmental thrombosing vascultis. tx: smoking cessatiuon
What is the epidemiology/presentation of microscopic polyangitis? pauci-immunie glomerular nephritis. palpable purpura
What is the pathology and key lab of microscopic polyangitis? no granulomas. +pANCA
What 3 body parts are most typically affected by Wegener's granulomatosis? URT, LRT, Renal
What does Wegener's granulomatosis present like in the URT? upper RT: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
What does Wegener's granulomatosis present like in the LRT? Lower RT: hemoptyisis, cough, dyspnea
What does Wegener's granulomatosis present like in the kidney? Renal: hematuria, red cell clasts?
What is the key pathological triad of Wegener's granulomatosis? 1. focal necrotizing vascultis 2. necrotizing granulomas in lung and upper airways 3. necrotizing glomerular nephritis
What is the key lab finding and CXR in Wegener's gramulomatosis? c-ANCA. CXR: large nodular densities
How do you Tx Wegener's granulomatosis? cyclophosphamide, corticosteroids
What is the epidemioloy/presentation of Churg-Strauss syndrome? ASTHMA, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop). can also involve heart, GI , kidneys
What is the pathology and key lab seen in Churg-strauss syndrome? pauci-immune. granulomatous vasculitis with eosinophilia. p-ANCA
What is Henoch-Schonlein purpura, How does it present? childhood systemic vasculitis following URIs. Triad: 1. skin: palpable purpura or buttocks/legs 2. arthralgia 3. GI: abdominal pain, melena, multiple lesions of same age
What causes Henoch-Schonlein purpura? IgA immune complexes. associted wiht IgA nephropathy
What is the presentation of Sturge-Weber disease? congenital vascular disorder affecting capillary BV. port wine (nevus flammeus) stain on face, ipsilateral leptomeningial angiomatosis (intracerbral AVM), seizures, early onset glaucoma
What vessels are most affected in Sturge-Weber disease? small ones
What is a strawberry hemangioma? benign capillary hemangioma of infancy. appears in first few weeks of life. grows rapidly and regresses at 5-8 y/o
What is a cherry hemangioma? benign capillary hemangioma of elderly. doesnt regress
What is a pyogenic granuloma? polypoid capillary hemangioma that can ulcerate and bleed. associted with trauma and pregnancy
What is a cystic hygroma? what is its associted with? cavernous lymphangioma of neck. associted with Turner syndrome
What is a Glomus tumor? beingn, patinful, red blue tumor under fingernails. arises from midifes SMM of glomus body
What is bacillary angiomatosis? When are they seen, What causes them, and what might it be confused for? benign capillary skin papules found in AIDs pt. caused by bartonella hensale. can be mistake for Karposi's sarcoma
What is anm angiosarcoma? highly lethal malignancy of liver. associted with vinyl choloride, arsenic, ThO2(throtrast exposure)
What is an lymphangiosarcoma? lymphatic malignancy associted with lymphedema (post radical mastectomy)
What is Kaposi's sarcoma? What causes it? endothelial malignancy of skin associted with HHV-8 and HIV. can be mistake for bacillary angiomastosis
What is the tx for essential HTN? diuretics, ACE I, angiotensin II receptor blockers, Ca++ channel blockers
What is used to treat HTN in CHF? diuretics, ACEI/ARBs, beta blocerks(if compensated, contra if cardiogenic shock), K+ sparing diuretics
What is used for HTN in DM? ACE I/ARB, Ca++ channel blockers, diuretics, Beta blockers, alpha blockers
Why are Ace I particulary useful in DM HTN management? they are protective against diabwetic neuropathy
What is the mech of hydralizine? incr cGMP--> SMM relaxation. vasodiates arterioles > veins. reduces afterload
What is the clinical use of hydralizine? severe HTN, CHF. 1st linefor HTN in pregnancy with methyldopa. adminstered with Beta blocker to prevent relfex tachy
What are the major SE of hydralizine? reflex tachy (so contraind in angina and CAD), fluid retention, nausea, HA, angina, lupus like syndrome
What is the mech of nifedipine, verapamil, diltiazam, amlodipine? Ca++ channels blockers, which block L type channels of CM and SMM reducing contractility
Which clacium channel blockers acts most on vascular SMM? nifedipine>diltiazem>verapamil
Which Ca++ channel blockers acts most on the heart? verapamil>diltiazem>nifedipine
What is the clinical use of nifedipine, verapamil, diltiazem, amlodipine? HTN, angina, arrythmia (NOT nifedipine), prinzmetal's variant angina, Raynaud's syndrome
What are the major SE of nifedipine, verapamil, diltiazem, amlodipine? cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
What can nitroprusside, fenoldopam, and diazoxide all be used for? malignant HTN
What is the mech and major SE of mitroprusside? short acting incr cGMP via release of NO. can cause cyanide toxicity(releases cyanide)
What is the mech of fenoldopam? dopamine D1 receptor agonist which relaxes renal vascular SMM
What is the mech and major SE of diazoxide? K+ channel opener, hyperpolarizes and relaxes vascular SMM. can cause hyperglycemia (reduce insulin release)
What is the mech of nitroglycerine, isosorbide dinitrate? vasodilate by releasing NO in SMM causing incr cGMP and SMM relaxion. work veins>>arteries. decr afterload
What is the clionical use of nitroglycerin, isosorbide dinitrate? angina, pulmonary edema. used also as aphrodesiac and erection enhancer
What are the major SE of nitroglycerin, isosorbide dinitrate? reflext tachycardia, hypoTN, flushing, HA.
What is Monday disease in assocition with nitroglycerin and isorbide dinitrate? industrial exposure develops tolerance over week and on weekedn gets tachycardia, dizziness, HA on rexposure after tolerance drops on weekends
What are the overall goals of antiangina therapy? reduce myocardial O2 consumption, by decr EDV, BP, HR, contractility, ejectionm time
What is the effect of nitrates on the variables in angina therapy? decr EDV, BP, ejection time, MVo2. incr HR and contractivitly via reflex response
What uis the effect of beta blockers on the variables targeted in angina? incr EDV, ejection time. decr BP, contractilty, HR, MVO2
What is the effect on the target variable in angina by a combined Nitrate and beta blocker? none or decr EDV, decr BP, HR. little to no effect on contractilty and ejection time. very decr MVO2
Which drugs are nifedipine and verapamil similar to in anginal mechanisms? Nifedipine similar to nitrates, verapamil to Beta blcokers
What 2 partial beta agonists are contra indicated in angina? pindolol, acebutolol
What is the mech of lovastatin, pravastatin, simvastain, atrovastatin, rosuvastatin? HMG-CoA reductase inhibitors. inhibit cholesterol precursor mevalonate
What cirulating lipid do statins have the most effect on? vastly decr LDL, also decr Tg, incr HDL
What are the major SE of the statins? hepatotoxicity (incr LFTs), rhabdomyolysis
What is the lech of niacin? inhibits lipolyisis in adipose tissue, reduces hepatic VLDL secretion into circulation
What is the major effect of niacin on circulating lipids? best at incr HDL, also decr LDL, TGs
What are the major SE of Niacin? red, flushed face (decr by aspirin), long term use hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbating gout)
What is the class and mech of cholestyramine, colestipol, colesevalam? bile acid resins. prevent intestinal reabsrobtion of bile acids, forcing the liver to use cholesterol to make more?
What are the effects of cholestyramine, colestipol, colesevalam on circulating lipids? decr LDL and slightly incr HDL and TGs
What are the major SE of cholestyramine, colestipol, colesevalam? pt hate it. tastes bad, cuases GI discomfort, decr absrobtion of fat soluble vitamins, cholesterol gallstones
What is the class and mech of ezetimibe? cholesterol absorbtion blocker, prevents cholesterol reabsorbtion at small intestine brush border
What is the major effect on circulating lipids by ezetimibe? decr LDL
What are the SE of ezetimibe? rarely incr LFTs
What is the class and mech of gemfibrozil, clofibrate, bezafibrate, fenofibrate? fibrates, upregualte LPL increasing TG clearance
What are the major effects of gemfibrozil, clofibrate, bezafibrate, fenofibrate on circulating lipids? most effective at decr TGs, also incr HDL, decr LDL
What are the major SE of gemfibrozil, clofibrate, bezafibrate, fenofibrate? myositis, hepatotoxicity(incr LFTs), cholesterol gallstones
What is the mech and T 1/2 of digoxin? direct inhibiton of Na+/K+ ATPase leads to direct inhibition of Na+/Ca++ exhanger causeing incr Ca++ and positive inotropy. stimulates vagus n.
What is the clinical use of digoxin? CHF (incr contractility), atrial fib (decr condcution at AV node
What are the major SE of digoxin? Cholinergic: n/v, diarrhea, blurry yellow vision (van Gogh).
What effects would digoxin have on the ECG? incr PR, decr QT, scooping, T wave inversion, arryhtmia, hyperkalemia
What conditions might worsen the effects of digoxin? renal failure ( decr excretion), hypokalemia (digoxin can bin to K+ site on ATPase), quinidine (decr digoxin clearance, displaces digoxin from tissue-binding sites)
What is the antidote to digoxin OD? slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragment,Mg2+
What is the mech of nesiritide? recombinant B-type natriuretic peptide. causes incr cGMP and vasodilation
What is the clinical use of nesiritide? acute decompensated HF
What is the major SE of nesiritide? hypoTN
Created by: tjs2123



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