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129 Cards in this Set
- Front
- Back
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pulse pressure is a function of what 2 things?
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SV (P=V/C, Where V = SV and c= compliance) and compliance (stiff aorta)
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Why does CO go up in pregnancy?
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SV increases
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During exercise, CO increases due to what?
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SV initially, HR in the long run
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Causes of increased preload?
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exercise (slightly), blood volume (transfusion), sympathetic innervation, AV shunt (congenital or acquired by dialysis)
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Velocity is slowest where? where is resistance highest?
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velocity slowest in capillaries, resistance highest in arterioles
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effect of hemorrhage or sympathetic block on CV function curves?
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decrease CO curve (loss of SV), decrease VR (TPR increases)
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Effect of decreasing TPR on CV function curves (seen in chronic AV fistula or exercise)?
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Increase VR curve (decrease TPR, increase venoconstriction) and increase CO
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during cardiac cycle, when is period of highest oxygen consumption?
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isovolumetric/isometric contraction
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To increase S3, what do you have patient do?
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Left lateral decubitus, exhale to bring heart closer to wall
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What does the C wave represent?
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RV contraction
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paradoxial splitting?
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LBBB or aortic stenosis
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wide splitting?
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pulmonic stenosis or RBBB
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when is aortic pressure the highest?
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during reduced ejection, not rapid ejection
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what are flow murmurs?
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ASD results in increased flow across TV and PV, so listen in pulmonic and tricuspid areas
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what do you listen for at left sternal border?
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aortic regurg, pulonic regurg, and hypertorphic cardiomyopathy
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what 2 murmurs are "blowing"
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aortic regurg, MVR
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What happens to V wave in MVR
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becomes prominent. S3 can also be heard. compliance of LA will increase chronically.
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Why is A-fib really bad in AS?
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loss of atrial kick suddenly decreases preload
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how do you augment murmur of AS?
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have them stand up suddenly
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what heart valve abnormality is seen with myxomatous degeneration?
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mitral valve prolapse
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In AR, what happens when patient given amyl nitrate? WHat happens in general to LVEDV (preload) and afterload?
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with nitrate - afterload dereases, so mrumur decreases. LVEDV increases in AR, and afterload increases initally (due to regurgitant afterload), but decreases if ventricle fails
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how do you decrease VR/load?
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stand up, valsalva
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how do you increase conduction velocity? how about HR
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To increase conduction velocity, need to increase calcium channel (verapamil blocks this Channel, which slows diastolic depolarization). to increase HR, need to increase the slope of phase 4 depolarization
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which channel activates first, T and L types?
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T type at -50, L type at .40
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what happens to pulse pressure in AS, MS?
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decreases, due to decreased SV. PDA increases SV, so it increases pulse pressure
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U wave causes?
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hypokalemia, bradycardia
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fastest speed of conduction?
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purkine>atria>ventricles>AV node
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In junctional rhythm, what is the EKG morphology?
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normal QRS, BPM 40-60
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Jervell and Lange-Nielsen syndrome?
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most common congenital LQTS, has sensorineural deafness. Autosomal recessive. K_ channel mutation
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Romano-Ward?
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AD, no deafness. K+ channel mutation
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treatment of A-fib?
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BB, CCB, warfarin. QRS is narrow (tachycardia). caused by alcohol consumtpion acutely, also increased symp tone and pericarditis
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mechanism of ANP?
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causes generalized vascular relaxation, is a diuretic, inhibits renin release. constricts efferent renal arterioles, dilates afferent arterioles
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What does the aortic arch baroreceptor respond to? what about carotid sinus baroreceptor?
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only to INCREASED BP for aortic arch. carotid sinus responds to both decreases and increases in BP.
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differences of peirpheral and central chemoreceptors?
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peripheralrespond to decreased PO2 (<60) or increased PCo2 or decreased pH. central - respond to pH and PCO2, not PO2.
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how is the cushing reflex regulated?
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increased ICP leads to cerebral ISCHEMIA-->HTN and reflex bradycardia. Also causes respiratory depression as a triad.
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what organ gets most of the blood? what about highest blood flow per gram of tissue?
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liver gets most blood, kidney has highest rate per gram of tissue
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autoregulation of heart, skeletal muscle, skin?
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heart - oxygen, adenosine (small arteries), NO (large arteries)
muscle - lactate, adenosine, potassium skin - sympathetic stimulation |
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in the starling equation, what affects the filtration stant Kf?
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toxins, infections, burns all increase Kf, increasing capillary permeability.
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what is the 4th cause of late cyanosis
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coarctation
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What else do ou see in truncus arteriosus
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VSD - cause there is no septum, which helps closed the ventricular septum off
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which type of coarctation is associated with notching?
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adult type. no cyanosis in this type (unlike infantile/PDA), just ischemia an dweak pulses
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which coarctation is Turners?
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preductal, infantile.
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supreme intercostal comes off of what?
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arch of the aorta, so coarctation has retrorade flow in all intercostals except supreme
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alprostadil?
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PgE - used for PDA maintenance
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22q11 syndromes are associated with what 2 heart defects?
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truncus arteriosus, tetralogy of fallot
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Down syndrome heart defects?
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ASD, VSD, endocardial cushion defect = AV septal defect (failure of neural crest migration)
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Rubella heart defects?
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septal defects, PDA, pulmonary artery stenosis
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What is coarctation of the aorta often associated with?
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bicuspid aortic valve (turner's syndrome
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Infant of diabetic mother gets what?
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transposition of great vessels
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what is corneal arcus?
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lipid deposit in cornea, nonspecific (arcus senilis). a white or gray opaque ring in the corneal margin (peripheral corneal opacity
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Monckeberg arteriosclerosis occurs where in arteries, and affects what arteries?
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calcifies the media, esp radial or ulnar. benign. "pipestem" arteries. Does not obstruct blood flow cause intima is spared
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what does the kidney look like in arteriolosclerosis?
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finelye granular
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in dissection, what is the BP finding? what heart valve anomaly does it cause?
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causes different arm BPs cause arterial branches are compressed. Also can cause AVR.
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what 2 growth factors cause smooht muscle cell migration?
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PDGF from platelets and FGF
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What is the ergonovine test?
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causes vasconstriction in Prinzmetal's variant. Often young women during night
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what happens in stable angina ECG? What about unstable?
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both show ST depression on ECG. in unstable/crescendo, there is thrombosis, but not totally occlusive, nor is there necrosis (no elevation of enzymes)
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Persistently low blood flow leads to what?
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loss of contractility (myocardial hibernation). becomes normal with reperfusion. irreversible damage occurs after 30 minutes
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What is ischemic preconditioning?
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resistance to infarcation by tissue previously exposed to nonlethal ischemia
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describe the external apperaance of the heart through an MI?
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First day = dark mottling, pale with tetrazolium stain. 2-4 days = hyperemia. 5-10 dyas = hyperemic border, centrally bellow brown. after 7 weeks - white
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when do you see contraction bands?
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after 12-24 hours post MI. coagulative necrosis occurs after 4 hours. see wavy fibers.
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when does coagulative necrosis peak?
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2-4 days
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when is the greatest risk for papillary muscle rupture, IV septal rupture?
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5-10 days, causes macorphages have eaten up tissue. granulation tissue starts to form in the outer zones, but more prominent in days 10-14
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what is the preferred vesself or CABG?
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left internal mammary or greater saphenous if multiple occlusions
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how do you diagnose an MI within 6 hours?
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EKG
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when do troponin I rise?
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after 4 hours. troponin I is most specific, cause CK-MB can also be released from skeletal muscle
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what 2 EKG findings are there in transmural infarct?
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ST elevation and Q wave
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What is the most common cause of death of an MI when reaching the hospital?
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LV failure, pulmonary edema, and cardiogenic shock
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why are aneurysms bad post MI?
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decrease CO, risk of arrhythmia, embolus
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what types of perciarditis are postinfarction and dressler's syndrome?
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fibrinous
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dilated cardiomyopathy genetic cause?
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genes for dysotrphin or mitochondrial enzymes.
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genetic causes of Hypertrophic cardiomyopathy? treatment?
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this is autosomal dominant, mutations in sarcomere proteins with an increase in ejection fraction, so treat with beta blocker or CCB to increase time for diastole filling. Anterior mitral leaflet has abnormal systolic motion toward septum
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what is endocardial fibroelastosis? loefler's syndrome?
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endocardial fibroelastosis - thick fibroelastic tissue in endocardium of young children, often seen in MUMPS.
lofflers - endoMYOcardial fibrosis with eosinophilic infiltrate, often seen in tropical altitudes |
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What is the most specific finding for CHF >40?
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S3
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what is cardiac cirrhosis?
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centrilobular hemorrhagic necrosis seen in nutmeg liver
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in diastolic HF, what is the EF and LVEDP and compliance? What about systolic?
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diastolic - normal EF, high LVEDP, low compliance
systolic - high EDV and high EDP, low EF |
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Which is tender, oslers nodes on the pads or janeway lesions on the sole/palm?
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oslers nodes
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in bacterial endocarditis, how is the diagnosis made?
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multiple blood cultures
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What 3 organisms are associated with tricuspid valve endocarditis in IVDU?
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pseudomonas, staph aureus, candida.
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what are 4 sequellae of bacterial endocarditis?
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chordae rupture, glomerulonephritis (immune complex deposition), suppurative percarditis, emboli
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libman sacks endocarditis can cause what valvular anomaly?
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mitral regurg more commonly, but also mitral stenosis
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what is the early lesion of rheumatic disease? late?
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early is MVP, late is mitral stenosis
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what are anitschkow cells?
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activated histiocytes. seen in acute infection, cause it's later replaced by fibrosis
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biopsy of subcutaneous nodules in rheumatic disease shows what?
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aschoff bodies
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what signs do you see in cardiac tamponade?
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pulsus paradoxus, no kusmaul sign, muffled heart sounds.
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what disease have pulsus paradoxus?
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asthma, tamponade, obstructive sleep apnea, percarditis, croup
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name the causes of serous pericarditis (4)
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SLE, rheumatoid arthritis, viral infection, uremia
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name causes of fibrinous percaditis?
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uremia, MI (dressler's), rheumatic fever, or cardiac muscle necrosis post STEMI
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What is a pericardial knock?
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seen in constrictive pericarditis. the knock happens earlier than S3. see calcification (dystrophic). remember pericarditis is relieved by leaning forward, worse when lying down
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hemorrhagic pericarditis?
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TB, malignancy (melanoma)
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What 2 diseases do you see Kussmaul's sign?
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cardiac tumors, constrictive pericarditis
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what is the cause of varicose veins?
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chronically icreased venous pressure. thromboemboli are rare, cause it's superficial. valves become incompetent
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What is a classic lung finding for wegner's?
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cavitating large nodular densities. other signs - otitis media, mastoiditis
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What is microscopic polyangiitis comprable to?
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wegener's, minus granulomas
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What are the pauci immune disorders?
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ANCA, wegeners, microscopic polyangiitis, churg strauss (all ANCA positive)
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Seizures, early onset glaucoma, and intracerebral AVM (leptomemningeal angiomatosis) are seen in what disease?
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sturge weber
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what disease is kown as thormoboangiitis obliterans?
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burger's disease. has segmental, thrombosing vasculitis. may extend contiguously to viens an dnerve
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what is the usual outcome of kawasaki's disease? treatment?
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self limiting in 2 weeks, though some get coronary aneurysms. need to give IVIG and aspirin
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what is the pathogenesis of PAN? what is the CT scan sign?
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immune complex mediated, fibrinoid necrosi. can have palpable purpura, neurologic dysufnction, abdominal pain. Leads to aneurysms and constriction of arteriogram
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2 vasculitides tha thave granulomas?
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takayasu's, temporal arteritis/giant cell arteritis. granulomas in both are in media
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pyogenic granuloma - causes and morphology?
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trauma and pregnancy
may ulcerate and bleed |
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what tumor does Kaposi's resemble?
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angiosarcoma (spindle shaped ENDOTHELIAL cells)
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what drug is contraindicated in decompensated CHF?
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beta blockers
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how does hydralazine work? what is a special indication? what should yo coadminister it with. side effects?
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indicated for pregnancy. give with bblocker. works via cGMP. causes fluid retention! also lupus like syndrome
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minoxidal side effects?
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salt retention, reflex tach, hypertrichosis, percardial effusion
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how does capsaicin work?
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reduces pain by decreasing substance P
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why don't CCbs work on skeletal muscle? what are special indications?
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doesn't depend on influx of calcium, it has it's intracellular pool
use for arryhthmias, esp A-fib. also prinzemtal's angina, raynauds |
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indication of fenoldopam?
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malignant HTN to relax renal vascular smooht muscle
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diazoxide MOA uses?
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increase K+ channel opener. thus used fo rmalginant hypertension and INSULINOMA. also can cause hyperglycemia
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what 2 partial beta agonists are contraindicated in angina?
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acebutalol, pindalol
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use of cilostazol?
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PDE inhibitor used for claudication cause it prevents platelet aggregation and direclty vasodilates. Note milrinone is also a PDE3 inhibitor
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effect of beta blockers on EDV? Ejection time?
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beta blockers increase EDV (more time for filling) and increase ejection time
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what stain isn't metabolized by CYP3A4?
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pravastatin. statins are good on LDL, HDL , and TG. inhibit mevalonate, the precursor
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what is the MOA of niacin? Side effects?
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reduces hepatic VLDL secretion/
SE - hyperglycemia, hyperuricemia, red flushed face |
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What is a bad effect of bile acids? What is a bad side effect?
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increases TG. also causes cholesterol gallstones
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how do fibrates work?
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upregulate LPL by increase PPAR alpha (PPAR gamma = thiazolidinediones). Also cause cholesterol gallstones, myositis, hepatotix
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how do B1 receptor increase calcium?
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2 ways - pohspohrylate L-type calcium channels nad phospholamban (which is inhibited, which means it can't inhibit calcium reuptake)
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What is the bioavailability of digoxin? how much is protein bound? what is the half life? how is it excreted? what drug has a bad interaction?
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bioavailability = 75%
20-40% protein bound half life - 40 hours urinary excretion watch out for quinidine (decreases digoxin clearance by displacing digoxin from tissue binding sites) |
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what do you give for digoxin toxicity -
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Magnsiusm, anti-dig FAb, cardia cpacer, lidocaine, isulin, kayexelate
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what are the Class IA drugs? Class IB?
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IA = procainamide, quinidine (headache, tinnitus, thromobocytopenia), disopyramide
IB - lidocaine, phenytoin, mexelitine, tocainid. Mexilitine is PO. These decrease AP duration, and are good for ischemic or depolarized ventricular tissue. they don't change Vmax unlike the others |
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IC drugs? Effect on VMAX, AP duration, QRS ?
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flecainide, propafenone, encainide. no effect on AP duration. Useful for atrial arrythmias. contraindicated post MI.
decreases Vmax, no change on AP duration (a funciton of repolarization), but increases QRS. |
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what are the drugs that increase AP duration?
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IA and III (K channel blockers)
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EKG effect of class II?
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prolongs PR interval
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class III drugs?
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sotalol, ibuitilide, bretylium, dofetilide, amiodarone (used in V-tach)
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which class III causes excessive beta block? Which cause new arrythmias?
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sotalol for b block. bretylium fo rnew arhythmias
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all side effects of amiodarone?
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hepatotoxic, pulmonary fiborsis, thyroid problems (hypo or hyper), corneal depsoits, blue discoloration, photodermatitis, neurologic effects, constipation, heart block
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what drug causes gingival hyperplasia, constipation, flushing, edema, AV block?
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verapamil
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drug for stress test?
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adenosine
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use of potassium ? use of magnesium/
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Potassium depresses ectopic pacemakers in hypokalemia.
Mg used in torsades and digoxin toxicity |
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what 2 EKG findings for Class IV blockers?
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prolonged PR, increased ERP
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