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53 Cards in this Set
- Front
- Back
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aortic arch baroreceptors and chemoreceptors communicate to the medulla using what nerve?
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vagus nerve (CN X)
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aortic arch baroreceptor can sense what changes in BP?
carotid sinus baroreceptor can sense what changes in BP? |
aortic = only increase in BP
carotid = increase or decrease in BP |
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carotid sinus baroreceptors/chemoreceptors communicate with the solitary nucleus of the medulla via what nerve?
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glossopharyngeal (CN IX)
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crescendo-decrescendo following ejection click
diastolic or systolic murmur? |
aortic stenosis, sytolic murmur
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opening snap
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mitral stenosis
opening snap then delayed rumbling late diastolic murmur occurs secondary to rheumatic fever loudest at apex and radiates toward axilla |
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mid systolic click
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mitral prolapse
late systolic crescendo murmur with mid systolic click. can predispose to infective endocarditis. |
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harsh sounding holosystolic murmur
loudest where? |
VSD
loudest at tricuspid area |
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where do you hear hypertrophic cardiomyopathy murmur?
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left sternal border
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where do you hear atrial septal defect?
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tricuspid area (also where you hear VSD)
*defects are very "trying" |
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where do you hear aortic and pulmonic regurg?
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left sternal border
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8 characteristics of bacterial endocarditis
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1. Fever
2. Roth spots 3. Osler nodes - painful on palms/soles 4. murmur 5. janeway lesions - painless on palms, soles 6. anemia 7. nail bed hemorrhage 8. emboli |
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7 characteristics of rheumatic heart disease
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1. fevers
2. erythema marginatum (circular rash of redness around normal skin) 3. valvular damage (mitral > aortic >> tricuspid - first prolapse then stenosis) 4. elevated ESR 5. red hot joints - migratory polyarthritis 6. subcutaneous nodules 7. st vitus dance (chorea) |
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what are the 4 causes of pulsus paradoxus?
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1. cardiac tamponade
2. constrictive pericarditis 3. restrictive cardiomyopathy 4. severe obstructive lung disease |
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what are the 4 causes of pulsus paradoxus?
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1. cardiac tamponade
2. constrictive peridcarditis 3. restrictive cardiomyopathy 4. severe obstructive lung disease |
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Heart sound common in dilated ventricles, as well as healthy children and pregnant women
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S3- hear it in early diastole during rapid ventricular filling in an already filled ventricle.
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Heart sound associated with atrial kick
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S4 - late diastole. associated with ventricular hypertrophy; left atrium must push against stiff LV wall.
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What do the following waves mean in JVP?
a: c: x: v: y: |
a: atrial contraction (pressure spike) squirts last bit of blood in to RV
c: RV contraction (closed tricuspid valve bulges in into RA (pressure spike) x: tricuspid closed and inital blood fills RA (goes down) v: maximal RA filling (pressure rises) y: tricuspid valve opens right before, so pressure declines |
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generally in S2 splitting, what is the first of the two split sounds represent?
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Aortic valve closes before pulmonic so it goes (S1....A2, P2)
*inspiration will increase the S2 splitting --> increases pulmonary circulation, delays pulmonic valve closure even more |
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fixed S2 splitting
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ASD
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RCA becomes what two arteries
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Marginal: supplies RV
Posterior descending: supplies posterior septum/inferior LV |
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LCA becomes what two arteries
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circumflex: supplies posterior LV
LAD: supplies anterior septum |
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what is fick principal
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CO = rate of O2 consumption / (arterial O2 content - venous O2 content)
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what is the formula for resistance
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R = change in Pressure / Q
= (8 x viscosity x length)/ pi r^4 |
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late diastolic murmur, enhanced by expiration
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mitral stenosis, follows opening snap.
*almost always caused by rheumatic fever |
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machine like murmur, continuous . what is the mother suffer from?
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PDA, often due to congenital rubella or prematurity.
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what is the speed of conduction in atria, AV node, purkinje, and ventricles
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Speed of conduction-
purkinje (fastest) > atria > ventricles > AV node (slowest) best way to think about it: 1. purkinje is fastest 2. AV node is slowest 3. Atria > ventricular muscle speed |
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congenital long QT syndromes due to defects in cardiac Na+ or K+ channels.
Can present with severe congenital sensorinueral deafness. |
Jervell and Lange Nielsen syndrome.
*anything that prolongs QT interval can predispose to torsades de pointes (a type of V tach) |
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Atrial fibrillation
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irregularly irregular with no discrete P waves in between irregularly spaced QRS complexes
Rx: beta blocker, Ca channel blocker, warfarin (prevent emboli) |
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sawtooth appearance of waves
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atrial flutter- a rapid succession of identical, back to back atrial depolarization of waves
use clas IA, IC or III anti-arrhythmics |
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increase firing of carotid baroreceptor means what
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Increased baroreceptor firing means that there is increased pressure (occurs during carotid massage, valsalva).
Increased baroreceptor firing causes medulla to decreases SNS and increases PSNS which will decrease HR. |
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progressive lengthening of PR until a beat is dropped (no QRS follows)
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2nd degree AV block
Mobitz type I |
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dropped beats that are not preceded by a change in the PR interval (2:1 block - 2 P waves for 1 QRS)
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2nd degree AV block
Mobitz type II *may progress to 3rd degree complete block where the atria and ventricles beat independently, which is treated with a pacemaker |
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What are the normal pressures of the:
-LA -LV -Pulmonary capillaries -RA -RV |
-LA: 5
-LV:: 25/5 -Pulmonary capillaries: 25/10 -RA: 10 -RV: 130/10 *atria have one pressure because their sytole is just passive filling. *Also, notice that the diastolic pressure of an atria = the diastolic pressure of its respective ventricle, again because of the passive filling. |
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how does valsalava maneuver prevent paroxsymal SVT
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by increasing baroreceptor firing you decrease HR (decrease SNS and increase PSNS) specifically by prolonging AV node refractory.
Since most SVT is caused by reentrance through AV node, increasing the AV node refractory can prevent the SVT. |
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congenital cardiac defects with congenital rubella
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septal defects
PDA pulmonary artery stenosis |
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infant of diabetic mother congenital cardiac complications
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transposition of great cessles
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22q11 syndromes
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truncus arteriosus, tetralogy of fallot
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down syndrome cardiac complications
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All septal defects: ASD, VSD, AV septal defects (endocardial cushion defect)
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5 steps in the pathogenesis of atherosclerosis
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1. endothelial cell injury (from LDL, HTN, etc)
2. macrophage and platelets adhere to the damaged endothelium 3. fatty streaks (foam cells) are formed - don't obstruct flow, and present in all children over 10yo 4. smooth muscle cells migrate (PDGF, TGF-B) 5. smooth muscle cells make ECM (collagen, proteoglycans, elastin) --> fibrous plaque --> complex atheroma (with core of lipids0 |
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Evolution of an MI:
0-4hrs 4-12hrs 12-24hrs 1-5 days 5-10 days 10-14 days 2 weeks - 2 months: |
0-4hrs: no changes
4-12hrs: coagulation necrosis 12-24hrs: coagulation necrosis + contraction band necrosis 1-5 days: coagulative necrosis + neutrophil infiltrate (risk for arrhythmia) 5-10 days: macrophage phagocytosis of dead cells --> free wall rupture (tamponade risk) 10-14 days: granulation tissue, neovascularization 2 weeks - 2 months: collagen deposition/scar formation |
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difference between transmural and subendocardial infarcts on ECG
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transmural: ST elevation, Q waves
subendocardial: ST depression |
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Anterior wall (LAD) infarct
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V1-V4
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Anteroseptal (SALD)
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V1-V2
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Anterolateral (LCX)
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V4-V6
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Lateral wall (LCX)
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I, aVL
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Inferior wall (RCA)
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II, II, aVF
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Postinfarction fibrinous pericarditis: how many days out
Dressler's syndrome: how long out? |
1. friction rub 3-5 days post-MI
2. autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI |
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MI terms to remember:
- myocardial hibernation - myocardial stunning - ischemic preconditioning |
- myocardial hibernation: persistent ischemia that results in a chronic but reversible loss of contractile function
- myocardial stunning: breif, acute ischemic episodes that can be completely reversed with reperfusion - ischemic preconditioning: chronic nonlethal ischemia makes myocytes more resilient |
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1/3 of dilated cardiomyopathy is caused by
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mutation of dystrophin, mitochondrial enzymes
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6 causes of restrictive cardiomyopathy
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sarcoidosis
amyloidosis postradiation endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children) Loffler syndrome (fibrosis + eosinophils) hemochromatosis (can also be dilated) |
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eccentric vs concentric hypertrophy
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eccentric = dilated cardiomyopathy (sarcomeres added in series), can occur from volume overload (aortic regurg)
concentric = hypertophic, sarcomeres added in parallel, pressure overload like aortic stenosis or hypertrophic cardiomyopathy |
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immune complex mediated transmural vasculitis with fibrinoud necrosis
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polyarteritis nodosa
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5 systems affected in polyarteritis nodosum
*what is the organ system NOT affected? |
1. general: fever, weight loss, malaise, myalgia
2. GI: abdominal pain, melena (tarry feces from GI bleed) 3. renal failure 4. neuro dysfunction, headache 5. skin: cuteanus eruptions *see multiple aneurysms and constrictions on arteriogram Hepatitis B + in 30% NO pulmonary artery involvement |
