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183 Cards in this Set
- Front
- Back
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CK-MB/CK-MM looks at
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heart vs other muscle damage in cardiac contusion
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heart failure with biopasy shows lymphocytic infiltrate of subendocardium
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coxasccie
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from rt sternum to inches left of left sternum at 4th intercostal
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RV
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RA makes what boarder of the heart...LV
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rt boarder and left border
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MI which results in compete heart block and requires pacemaker
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LAD which gets the anterior IV septum which is where condution through budle of his occurs
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MI with sinus bradycardia and problems with posterior medial papillary muscles
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RCA which gets the posterior heart and posterior IV septum where the AV and SA nodes are
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MI which results in new holosytolic muruor
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mitral reg...caused by rupture of the posterior medial pappilary muscle supplied by RCA
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supplied inferior LV 80% of the time...what does it the other 20%
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RCA...left circumflex
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supplies the posterior left ventricle...
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circumflex
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MAP equals...
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2/3 diastolic + 1/3 systolic
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pulse pressure is proportional to...
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CO this is why with AR you have huge pulse pressure
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decreases in contractility caused by
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ACIDOSIS, hypoxia or hypercapnia
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with the stavling curve (preload X CO)... what is an up or down
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changes in contractility ...rememeber there is a "sweet spot" for
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why dont you want to volume overload or dehyrate a patient with CHF?
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they have a sweat spot which is a EDV that maximizes their CO...over or under that the CO starts to go down
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normal ejection fraction
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55%
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increase resistence with increase length and viscosity... what increased blood viscosity?
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polycythemia, hyperprotein states like MM, hereditary spherocytosis
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what is the X intercept on the venous return sterling curve
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MAP (when CO is zero...whats the pressure in the system)
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irrreg-irreg pulse with no A wave
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a fib
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giant A wave
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tricsupid stenosis
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giant C and V waves
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tricuspid regurg
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associated with increased filling pressures, dilated ventricles and is normal in woman who are preg and children
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S3 (CHF and dilated CM)
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left atrium must push against a stiff LV wall...LV hypertrophy
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S4 "atrial kick"
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dicrotic notch...
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shows the elasticity of the aorta...this is ruined in marfanns and syphillis
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wide splitting on both experiation and even more on inspiration...
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exaggerated right side late...RBBB or pulmonic stenosis
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splitting of s2 where the sounds get closer together with inspiration
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this means the A is closing after the P, taking longer to close... LBBB or AS
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At Carters X-ossing vehicles yield
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AC (buldge with iso contraction) XV (filling)Y
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whats heard at left sternal border...
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the regurg of AR and PR ...hypertrophic cardio too
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which two systolic heart sounds are heard at lower left sternal boarder
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VSD and TR
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t or f... sounds for ASD come from flow across the actual ASD
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false... ASD murmor is usually pulmonic or diasolic rumble wih split S2
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flash pulm edema...
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a fib
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difference between AS and hypertrophic cardiomyopathy when listening?
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location (aortic vs left sternal boarder) ... AS louder with expiration
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ejection click
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AS after isometric contraction
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pulses parvus et tardus with BP of 95/80
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AS...where the pulses sound much weaker than the heart sounds (bicupid)
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mid systolic click
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MP (most common heart lesion)...due to sudden tensing of the chordae tendon
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increased preload does what to mid click of MP...
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moves it toward S2...patient is supine, more blood means it will take longer for the balloon to snap
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decreased preload (anxiety) does what to midsystolic click of MP
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moves it close to S1... if there is less blood pushing on the ballon it will take less time to click
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mitral prolapse predisposed to...
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infective endcarditis, sudden death...think marfans or elhers danlos
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opening snap
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mitral stenosis...due to tnesing of the choardae tendon
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difference between mitral stenosis and aortic regurg
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both are diastolic but MS is delayed because there is the iso relaaxation before the opening of the valve, whereas the AR is holo
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where is PDA loudest
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S2
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phase 0 upstoke in pacemaker cells (AV node)
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Ca conduction...results in slow conduction velocity through the AV node for prolonged transmission from A to V
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phase 4 in pacemaker
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If with Na..
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what determines heart rate in pacemaker
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phase 4..If channels, Na conduction
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Ach effects which part of pacemaker
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slope of 4... decreased slope
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adenosine effects which part of pacemaker AP
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slope of 4...decreased slope
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catecholamine effect which part of AP pacemaker
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slope of 4... increase slow therefore increasing heart rate
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beta blockers work on which part of pacemaker AP?
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slope of phase 4 by decreasing slope they decrease heart rate and increase PR interval
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where do CCB work in the pacemaker AP?
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slope of phase 0... by decreasing the slope they prolong the AP and increase PR interval through the conduction AV node
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which congential prolonger QT has assocated deafness?
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autorecessive defect in K channel....AD not deaf but defect in either K or Na
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length of normal...PR interval and QRS
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200ms (one bold box), 120msec (3 small box)
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where is atrial repolarization?
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masked in the QRS complex
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which are the fastest and which are the slowest conducting heart cells?
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fastest pukinje>atrial>V>AV node
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what is the sequence of pacemakers?
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SA>AV>his>ventricles
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how does each electrolyte balence effect conduction?
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increased Ca- shorter QT (vomitting)
increased Mg- longer QT, hypotension, resp distress increase Na- nausea, twitch, delirum |
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drugs that can cause prolonged QT and thus torsades?
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macrolides/erythromycin, cloroquine/mefloquine, haloperidol, respiriodone, methadone, protease inhibitor, class1A, class 3 K
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bypass AV node with decreased PR interval and lengthening of QRS...add in a delta wave
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premature ventricular excitation with WPW (preexcitation from accessory pathway)
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the worry with WPW is reentrant SVT...how would you treat SVT with WPW and contraindication with SVT WPW
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procainamide and amioderone...NO ADENOSINE
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no P waves...often caused by too large od atrium which doesnt give enough time for 1 pacemaker to run the show (spread is too slow)
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a fib (predisposes to SVT)
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treat a fib
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b blocker and CCB for rate control...rhythem control use sodalol and amioderone
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treat for A flutter
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class 1A or 1C or III (for the saw tooth)
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PR is longer than one bold block...200msec
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1st degree heart block
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sinus rhythem then no P and wide QRS with cannon "A" wave
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premature ventricular contraction
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progressive lengthening of PR until a beat is dropped and no QRS is seen...usually asymptomatic
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2nd degree heart block (mobitz 1 /wenkebach)
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2:1 or 3:1 P for every QRS...no changes in PR length, just abrupt drop
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mobitz 2 sendond degree heart block...MUST get pacemaker because this can become 3rd degress
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P waves and QRS are compleltly indep of eachother... p waves have no realtion to qrs
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3rd degree heart block... bust get a pacemaker
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effect of ANP on the kidney
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effecert constriction and afferet dilation to increase GFR
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aortic arch only responds to ____ while the carotid sinus responds to both_____ and ______
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hypertension....sinus both low and high
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chemo receptors in the brain respond defferently to chemo receptors in the aorta and carotid...whats the difference?
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brain is only CO2 and pH mediated while the peripheral chemo receptors respond to decreased PO2 when it drops below 60... (this is why you dont give O2 to a COPD pateint
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what is the cushing reaction (hypertension, bradycardia, resp depression)
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pressure--- hypertension, bradykardia, and respirtory depression....caused when intracranial pressure rises, the arterioles become constriced which makes the central receptors think its hypoxic so sympathetics go out causing hypertension, then reflex bradykardia
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pressures in the PA and in the LA
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25/10 and less than 12
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autoregulation of the heart vs the skeltal muslces?
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heart is adenosine, O2, NO...skeletal muscles is lactate adenosine and K
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pitting vs nonpitting edema...
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pitting is with decreased colloid (increased fluid without shit inside caused by fgravity) and non pitting is with increased colloid (lymph onstruction)
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what increases cappilary permiability and causes ypovolemia because of loss of plasma into the intersittium...
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burns, infection toxins (Kf increased)
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absence of tricuspid valve with hypoplasic RV...needs ASD and VSD to survive
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tricuspid atresia
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eisenmangers can cause which other porblems besdies cyanosis?
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clubbing, systemic sepsis, polucythemia, IE
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anteriorsuperior displacement of the infundicbular septum causes
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T of F
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with T of F worry about...
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polycythemia and infective endocarditis and spesis and cerebal abcess
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what is needed for a patient with transpositon of the great vessels to stay alive?
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need mixing of blood so ASD or VSD or PDA...do this with misoprostol
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worry about berry anyeusm, see notching of the ribs, AORTIC REGURG, hypertension of the upper extremities with no pulse lower, claudication/calf pain, increase RAAS
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post ductal coarctation of the aorta
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collateral flow in coarctation...
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superficial epigastric to mammry...anterior intercostal internal thoracic,...posterior intercostal to aorta
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ebsteins anomaly worry about...
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SVT and WPW
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mechanism of hypertension is
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cant get rid of Na thus increase Na causes increse Ca which causes increase TPR...number one complication is LVH
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death in HTN
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MI, stroke, renal dieease
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effects of HTN on the system
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decrease number of arterioles, thickened walls (hyaline or hyperplasic), increase TPR with RAAS
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plasma proteins cross the endothelium and ECM is produced by SMC...
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hylane ateriol
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progression of athrosclerosis...
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enothelial, macrophages with LDL, foam cells smooth musle cell across internal elastic lamina and into intima (PDGF and TGF-beta)
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A corn pop car
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if you have carotid then ur coronary are already gone
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why is b-blocker good for aortic dissection?
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decreases the RATE of rise in MAP...decreases the "hitting" of the tear
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angia of ST depression and which of elevation...
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elevation with prinz metal...depression with stable and unstable
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coronary spasm is induced by what drug
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ergonovine
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patient which MI...autopsy shows no coronary artery athrosclerosis...
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cocaine use
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common cause of heart transplant... over time heart is replaces by fibrous tissue which doesn contract and leads to heart failure
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chronic heart disease
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number one risk factor for CAD?
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age... then HDL/LDL/smoke DM...not cholestrol
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patient post MI lost abaility to pump for significant time... brain shows necrosis between anterior and middle cerbal
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global ischemia... purkinje cells are most sensitive... so are hippo
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time of MI cell...0-4 hours
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nothing
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post MI 4-24 hours...
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contraction bands (can still see on echo)...dark and motling
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2-4 days post MI
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neutorphils, hyperemia with coagulative necrosis...worry about arrhythmia
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5-10 days post MI
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macrophages have come in and granulation tissue is seen...looks brown and yellow in the middle with hyperemia boarder...worry about rupture (new murmor)
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over 2 weeks post MI
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fibrosis and scarring...this is when you worry about aneurysm... patient would half pulsating puldge in chest
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what two patients dont have normal presentaions of MI?
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old bitches and DM
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rupture of the heart 7 days after MI can present with...
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tamponade, new murmor of MR , new murmor of VSD... of there is the free wall rupture
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what do you use troponin 1 vs CK MB for...
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CKMB only stays around 72 hours... any longer means re infacrtion...troponin rises after 4 hours and is specific but stays
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look for the LDH flip...and what is the earliest but no specific
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1>2 to 2>1...myoglobin
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St elevation means...depression...Q wave
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elevation is tranumural along with Q wave....depression is sunendocardial
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why is subendocardium vulnerable?
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fewer collaterals and higher pressure
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q waves seen in V4-V6
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lateral LV is the circumflex
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q waves in I and aVL
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lateral LV is the cicumflex
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q waves in II, III and aVf
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posterior and inferior this is RCA
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3-5 days post MI...muffled heart sounds and neck veins disteneded?
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free wall rupture causing tamponade
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7 days post MI and theres and new sytolic murmor...which leaflet?
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medial posterior pappillary muscle... or could be a VSD
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weird causes of dilated cardiomyopathy (posible genetic mysosite or mitochonrial dysfunction)...
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cocaine, hemochromatis, and peripartum
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S3 heart sound... with sarcomeres in series
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dialted cardio
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anterior leaflet of the mitral valve comes close to IV settum ...assocaited with fredrichs ataxia...caused by point mutation in beta-myosin...causes s4 heart sound with apical impluse and systolic murmor
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hypertrophic cardiomyopathy...give bblocker and CCB
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death from hypertrophic cardiomypthy
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conduction defect because bundle of his is in the IV septum
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resirictive cardiomayopathy in children and adults
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child- fibroelastosis adult is amyloidosis
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restricive heart disease with eosinophiic infiltrae and fibrosis
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loefflers syndrome
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most common cause of ISOLATED right heat failure
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tamponade
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drugs for CHF and why?
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loop- volume depletion
ACEi- decrease RAAS dig-contractility spiranolactone- decrease cardiac removeling b-blocker- decrease sympathetics |
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acute heart failure therapy
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LMNOP...loop, morphine, nitro, ocygen, presser
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complications of IE...
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chordae rupture, embolism, glomerulonephritis, supperitive pericarditis...ANEMIA (dont forget gram negative HACEK)
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most common heart defects in lupus...
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pericarditis and liebman sac causing MR...on both sides
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area of fibrinoif necrosis surrounded by necrosis and mutlinucleated giant cells... with activated histoicytes...type two hypersensitiveity to M protein
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rheumatic fever
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early death by myocarditis, early is MP then MS...what are the jones criterian
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J(heart)NES...joints, heart (pancarditis), subcutaneous nodules, erythema rash, chrea
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QRS beat to beat variation (electrical alternans), eqilibrium in all 4 heart chambers...causes?
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tamponade of blood or effusion or exaggerated inspiration (copd/asthma/sleep apea)
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radial pulse disappears...what can send this person into cardiogenic shock?
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tamponade from collapse of atria with asthma, croup
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pericardial pain, friction rub, pulus paradoxis...causes?
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serous- lupus, RA, Viral, uremia
fibrinous- uremia, post MI, rhematic hemorragic- melanoma and TB |
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adult heart tumor myxoma can cause what...
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kushmalls sign also VEGF release and fever because it embolizes shit everywhere
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treatment for raynauds...
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aspirin, CCB, sildenafil (pulm htn)
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mastoiditis with vasculitis
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wegeners
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same as wegeners but with P anca
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micoscopic polyangitis
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capillary sized vessels with leptomeningeal angiomatosis...can cause seizures and early onset glaumcoma
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sturge webber... post vein on V1
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pain in the hands or claudication with vasculitis in veins artery and nerves
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bueger...thrombotis obliterans
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only give aspirin to children for
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kawaski
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lesions of different ages and transmural fibrinoid necrosis...can have melana and cutaneous erruptions
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polyaretitis nodosa (30% hep B)
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granulomatous thinkening of aortic arch with elevated ESR..differential pulses.night sweats, eyes probelsm, and skin/muscle
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large vessel TAKAYSU
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poor perfusion of the scalp with trouble getting up from chair and climbing stair...opthalmic artery invovled
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check ESR... temp arteritis (bracnhes of carotid)
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red lesion in pregnancy or after trauma, polypoind hemangioma the ulcerates and bleeds
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pyogenic granulosum
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painful red/blue benign tumor arising from smooth muscles cells of...
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glmous
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treat for essential hypertension...
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thiazide, ace, ccb, no bblock
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diabetics with hypertension
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get acei to protect against kindy disease
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this drug uses cGMP to dilate arteries and is used in pregnant woman...usually give with b block to prevent reflex tachy
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hydralazine (reflex tachy)...lupus
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side effects of AV block, edema, flushing, dizzi and CONSTIPATION...five for any spams
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CCB
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significant tolerance owing to "monday disease", plus reflex tachy and significant headaches... must have drug free interval during the day
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nitroglycerine (mononitrate is most bioavailable)
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three drugs for maligant hypertension...
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nitroprusside (like acei decreases both pre and after but risk CN poisen)
fenoldopam (D1 agonist which relaxes renal vascular diazoxide (opens K channels to relax and decrease insulin secretion causing hyperglycemia) |
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what b blockers are contraindicated for angina...
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pindolol and acebutolol because they are partial B agonists
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minoxidil
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severe HTN and hairloss... helps grow hair and decreases BP by opening K channels
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lipid drugs that cause hepatitis and myositis...
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statin in fibrates
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lipid drugs that cause gallstones...
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fibrates and cholystyraimen
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best for LDL...
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statins with ezetimbibe
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best for TG...
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fibrates because they increase LPL which increases clearence
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which one slightly increase TG levels and should not be given to patients with high TG...
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cholystramine (also binds c diff)
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flush caused by PG can be decreased with aspirin and causes reduced VLDL secretion... acanthosis nigrcan and gout
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niacin for HDL
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what blocked volatge gated L-gated calcium channels...
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b blockers by dephosphylation and CCB (phosphylation increases Ca)
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lower extracellular Na would cause...
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increased contractility because it blocked Na/Ca excahnge and makes it so calium stays in the cell longer
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renally excreted, increasesintercellular calcium to increase contractitity, increases vagal parapympathetic to decrease AV conduction,
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dgioxin
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toxicity is colinergic, blurry vision, EKG changes, hyper K and bradicardia (increase PR, decrease QT, t wave inversion,
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digoxin
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what makes digoxin toxicity worse?
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renal failure, hypo K (no competetion for na/k, quinidine with decreased clearence
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heart block drug causes...
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if dig...cholinergic side effects
if CCD...look for constipation if b-block- worsen COPD athma |
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police departmetn questioned, the little man, for pushing ecstasy
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Na channel blocking class one antiarrthmics...all decrease slope of phase O and increase the threshold...all are state dependant which means they select frequently depolarized tissue
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BCA is order of?
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prolong or shortening of ERP
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increase AP duration, increase ERP, increase QT interval...for both atrial and ventricular also SVT
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quinidine (dig), procainamide (WPW), DIsco
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class what has toxicity of tinnitus+heachache=cinchonism...thrombocytopenia...TORSADES DE POINTS...
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quinidine causes cinchonism... PDQ can cause torades and thrombo
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DECREASE AP duration (BCA)...like ischmic tissue, use for Varrythemia post MI and digitalis
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1B..lido, taco, mex..
these have side effects of local anethetic, CNS, and CV depression |
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no effect on AP (BCA)...used with VT that progressto VF...LAST resport for last letter ...patients without sturutureal structural abnormalities
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FPE...flec, encaine, propafenone
IC- Contraindicated post MI |
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what causes increased toxcity in all class antiarrhythmics
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hyperkalemia (BCA...because ASS)
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decreased cAMP and Ca...decreases slope of phase 4 in pace maker cells particularly in the AV node causing INCREASED PR interval (decreased slope of phase 4)
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b-blockers (class 2)
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rate control for afib, v tach, SVT with toxicity of (metoprolol) causing dyslipidemia and AV block
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b blocker with esmolol being the shortest acting one...treat OD with glucagon to increase cAMP
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sotalol
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causes torasdes, excessive bblock (brady)
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ibutilide
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K channel (clas3) blocker that causes torsades
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bretylium
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class 3 K blocker causing new arrthmias and hypotension
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dofetilide (ilide or bret)
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class 3 K blocker
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tox is LFTS, PFTS, TFTs...corneal deposits (eyese, blue grey skin, photodermatisit (SAT), heart block and consitpation NOT TORSADES
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amioderone (alters lipid mebrane therefor can be all 4 classes)
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treat for WPW
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procainamide and amioderone...no adenosine
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1A and 3 classes cause
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torsades from porlonged QT
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decrease conduction velocity, increase PR interval by selectivly acting at same node as B blockers...increase PR, increase ERP
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CCB...works at phase zero of the AV node
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prevention of SVT causing gingival hyperplasia, constipation, flushing, edema and AV block
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CCB (verapamil and diltizam)
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what is contraindicated in a CHF pateint already on B-blocker
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CCB... due to bradycardia and decreased iontropic
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used for diagnosis and abolishing SVT...very short acting... causes K out of cell causing HYPERPOLARIZTION and decreased Ca conduction
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adenosine
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SVT given drug that causes flushing, hypotension, chest pain due to bronchospam...
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adenosine
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pateint with COPD given adenosine and nothing happend...what ahppend?
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theophyllin blocks the effects of adenosine
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K and Mg used for arrthemia...
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K-depresses ectopic pacemakers
Mg- effective in torsades and dig toxicity |
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patient with MI give a drug and CV gets better but eye probelms...
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atropine and bblocker can cause actue glaucoma
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contraindicated in digoxin toxicity...
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Ca gluconate
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