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cardiology

Eric Zhang Organ modules Inglés 130 fichas

cardiology

Fichas del conjunto (130)

  1. 1Truncus arteriosus (gives rise to...)1. Ascending aorta
    2. Pulmonary trunk    Truncus arteriosus (gives rise to...)
  2. 2Bulbus cordis (gives rise to...)Smooth parts (outflow tract) of left and right ventriclesBulbus cordis (gives rise to...)
  3. 3Endocardial cushion (gives rise to...)1. atrial septum
    2. membranous inter ventricular septum
    3. AV and semilunar valves    Endocardial cushion (gives rise to...)
  4. 4Primitive pulmonary vein (gives rise to)Smooth part of left atrium
  5. 5Sinus venosus (left horn vs right horn....gives rise to)Sinus venosus precedes the atria on the venous side of the chordate heart
    Left horn - coronary sinus (receives venous blood from the heart)
    Right horn - smooth part of right atrium
  6. 6Right common cardinal vein + right anterior cardinal vein (gives rise to)Superior vena cava (SVC)
  7. 7When does the heart starts beating1. starts beating by week 4
    2. first functional organ in vertebrate embryo
  8. 8Cardiac loopingPrimary heart tube loops to establish left-right polarity --> begins in week 4 of gestation
    Defect in left-right dynein -->
    1. Dextrocardia (Kartagener syndrome)
  9. 9Septation of the atria (all the steps)1. Septum primum grows toward endocardial cushions --> narrows foramen primum
    2. Foramen secundam forms in septum premum
    3. Septum secundum develops as foramen secundum maintains right-to-left shunt
    4. Septum secundum expands and covers most of foramen secundum --> residual foramen is foramen ovale
    5. Remaining portion of septum premium forms valve of foramen ovale    Septation of the atria (all the steps)
  10. 10Patent foramen ovale- Failure of septum premium and septum secundum to fuse after birth
    - Most are left untreated
    1. paradoxical emboli (venous thromboemboli that enters systemic arterial circulation)
  11. 11Morphogenesis of the ventricles1. Muscular interventricular septum forms --> opening is inter ventricular foramen
    2. Aorticopulmonary septum rotates and fuses w/ muscular ventricular septum to form membranous interventricular septum --> closing interventricular foramen
    3. Growth of endocardial cushions separate separate atria from ventricles --> contributes to atrial separation + membranous inter ventricular septum    Morphogenesis of the ventricles
  12. 12Ventricular septal defect (VSD)Most common congenital cardiac anomaly --> usually occurs in membranous septum
  13. 13Outflow tract formation (and assoc. abnormalities)Neural crest, endocardial cell migration --> truncal + bulbar ridges spiral --> fuse --> formation of aorticopulmonary septum --> ascending aorta + pulmonary trunk
    Conotruncal abnormalities assoc. w/ failure of neural crest cells to migrate:
    1. Transposition of great vessels
    2. Tetralogy of Fallot
    3. Persistent truncus arteriosus    Outflow tract formation (and assoc. abnormalities)
  14. 14Valve development (aortic/pulmonary vs mitral/tricuspid)Aortic/pulmonary: from endocardial cushions of outflow tract
    Mitral/tricuspid: from fused endocardial cushions of the AV canal
  15. 15Fetal circulation- Blood in umbilical vein has PO2 of 30 mmHg, 80% saturated
    - Blood in umbilical artery have low O2 saturation
    1. Oxygenated blood of umbilical vein --> ductus venosus --> IVC (bypass hepatic circulation)
    2. IVC + SVC --> right atria --> foramen ovale --> descending aorta
    3. Right atria --> right ventricle --> main pulmonary artery --> patent ductus arteriosus --> descending aorta
    - this shunt^ is due to high fetal pulmonary artery resistance (due to low O2 tension)
    At birth: infant breaths --> lowers resistance in pulmonary vasculature --> higher left atrial pressure --> foramen ovale closes    Fetal circulation
  16. 16Patent ductus arteriosus (what closes it? what keeps it open?)1. PGE1 + PGE2 kEEp PDA open
    2. Indomethacin help close PDA --> ligament arteriosum
  17. 17Allantois --> Urachus --> ? Ductus arteriosus --> ? Ductus venosus --> ? Foramen ovale --> ? Notochord --> ? Umbilical arteries --> ? Umbilical vein --> ?1. MediaN umbilical ligament (urachus is part of allantoic duct between bladder and umbilicus)
    2. Ligamentum arteriosum
    3. Ligamentum venosum
    4. Fossa ovale
    5. Nucleus pulposus
    6. Medial umbilical ligaments
    7. Ligamentum teres hepatis (contained in falciform ligament)
  18. 18Coronary artery anatomy (what each supplies: RCA, RMA, PDA, LCA, LCX, LAD)RCA:
    1. SA and AV nodes (infarct = arrhythmia)
    RCA --> PDA (if right dominant) OR
    LCA --> PDA (if left dominant) OR
    Codominant:
    1. Posterior 1/3 of inter ventricular septum
    2. Posterior walls of ventricles
    3. Posteromedial papillary muscle
    LCA --> LCX:
    1. Lateral + posterior walls of left ventricle
    2. Anterolateral papillary muscle
    LCA --> LAD (most affected by occlusion):
    1. Anterior 2/3 of inter ventricular septum
    2. Anterolateral papillary muscle
    3. Anterior surface of left ventricle    Coronary artery anatomy (what each supplies: RCA, RMA, PDA, LCA, LCX, LAD)
  19. 19What is the most posterior part of heart? What happens when it enlarges?Left atrium
    Enlargement
    1. dysphagia
    2. hoarseness (compression of left recurrent laryngeal nerve (a branch of vagus))
  20. 20Cardiac output (= ?.....2 ways to measure) (......how is it maintained during exercise?)CO = stroke volume (SV) X heart rate (HR)
    CO = rate of O2 consumption/[arterial O2 content - venous O2 content]
    SV = end-diastolic volume (EDV) - end-systolic volume (ESV)
    During exercise:
    1. Early --> Increase HR and SV
    2. Late --> Increase HR (SV maxed out)
    Diastole shortens as HR increases --> less filling time --> less CO --> ventricular tachycardia
  21. 21Mean arterial pressure (MAP) (2 ways to measure)MAP = CO x total peripheral resistance (TPR)
    MAP = 2/3 diastolic pressure + 1/3 systolic pressure
  22. 22Pulse pressure (1. measurement.....2. proportionalities....3. changed by what?)1. PP = Systolic P - Diastolic P
    2. Pulse pressure proportional to SV, inversely proportional to arterial compliance
    Pulse pressure increased by:
    1. Hyperthyroidism
    2. Aortic regurgitation
    3. Aortic stiffening (isolated systolic hypertension in elderly)
    4. Obstructive sleep apnea (high sympathetic tone)
    5. Exercise (transient)
    Decreased by:
    1. Aortic stenosis
    2. Cardiogenic shock
    3. Cardiac tamponade
    4. Advanced heart failure (HF)
  23. 23Stroke Volume (affected by?)SV CAP
    Increased SV from
    1. Increased contractility (anxiety, exercise)
    2. Decreased afterload
    3. Increased preload (early pregnancy)
    Failing heart has low SV
  24. 24Contractility (increased by (4), decreased by (5))Contractility (and SV) Increased by:
    1. Catecholamines (phospholamban inhibition --> Ca entry into SR --> Ca-induced Ca release --> high [Ca])
    2. Increased intracellular [Ca]
    3. Decreased extracellular Na (less Na/Ca exchanger activity)
    4. Digitalis (blocks Na/K pump --> increases intracellular Na --> decreases Na/Ca exchanger --> higher intracellular Ca)
    Contractility (and SV) decreases w/:
    1. B1-blockage (less cAMP)
    2. HF w/ systolic dysfunction
    3. Acidosis (less Ca)
    4. Hypoxia/hypercapnia (less Ca)
    5. Non-dihydropyridine Ca channel blockers
  25. 25Myocardial oxygen demand (increased by....? Laplace....?)myoCARDial O2 demand increased by:
    1. Inc. Contractility
    2. Inc. Afterload
    3. Inc. heart Rate
    4. Inc. Diameter of ventricle (inc. wall tension)
    Laplace's law:
    Wall tension = P x R / (2 x wall thickness)
  26. 26Preload (how to measure? depends on?)Preload:
    - approximated by ventricular EDV
    - Depends on:
    1. Venous tone
    2. Circulating blood volume - ventilators (nitroglycerin) decreases Preload
  27. 27Afterload (how to measure? depends on?)Afterload: approx. by MAP
    Inc. afterload --> inc. pressure --> inc. wall tension (per Laplace's law)
    -Afterload is the pressure in LV after ejection
    -LV compensates for increased afterload by thickening (hypertrophy) in order to reduce wall tension
    - Vasodilators decrease afterload
    - ACE inhibitors and ARBs reduce both preload AND afterload
    -Chronic hypertension --> inc. MAP --> LV hypertension
  28. 28Ejection fraction (how to calculate? what's normal? decreased when?)EF = SV / EDV = (EDV - ESV) / EDV
    Left ventricular EF = index of ventricular contractility. Normal EF > 55%
    Dec. in systolic HF
    Norm. in diastolic HF
  29. 29Starling curve (what's it about?)Contraction force proportional to end-diastolic length of cardiac muscle fiber (preload)
    Inc. contractility w/
    1. catecholamines
    2. Positive inotropes (digoxin)
    Dec. contractility w/
    1. Loss of myocardium (MI)
    2. B-blockers (acutely)
    3. Non-dihydropyridine Ca channel blockers
    4. dilated cardiomyopathy    Starling curve (what's it about?)
  30. 30Resistance, pressure, flowQ = volumetric flow rate
    v = flow velocity
    A = cross sectional area
    n = viscosity (depends on hematocrit, inc. in proteinemic states, dec. in anemia)
    d(P) = Q x R
    Q = v x A
    R = d(P)/Q = (8n x length)/(pi x r^4)
    Total resistance of vessels in series
    R(T) = R1 + R2 + R3 .....
    Total resistance of vessels in parallel
    1/R(T) = 1/R1 + 1/R2 + 1/R3 ....
    - Capillaries have highest total cross-sectional area and lowest flow velocity
    - Arterioles account for most of TPR. Veins provide most of blood storage capacity
  31. 31Cardiac and vascular function curves (inotropy)Changes in contractility --> altered CO for a given RA pressure (preload)
    1. Inc. by catecholamines, digoxin
    2. Dec. by uncompensated HF, narcotic overdose    Cardiac and vascular function curves (inotropy)
  32. 32Cardiac and vascular function curves (venous return)Changes in circulating volume or venous tone --> altered RA pressure for a given CO
    MAP (x-intercept) changes w/ volume/venous tone
    3. Inc. by fluid infusion, sympathetic activity
    4. Dec. by acute hemorrhage, spinal anesthesia    Cardiac and vascular function curves (venous return)
  33. 33Cardiac and vascular function curves (TPR)At a given MAP (x-intercept) and RA pressure, changes in TPR --> altered CO
    5. Inc. by vasopressors
    6. Dec. by exercise, AV shunt    Cardiac and vascular function curves (TPR)
  34. 34Pressure-volume loops (inc. contractility? afterload? preload?)1. Isovolumetric contraction (after mitral valve closing, before aortic valve opening), highest O2 consumption
    2. Systolic ejection - between aortic valve opening and closing
    3. Isovolumetric relaxation - between aortic valve closing and mitral valve opening
    4. Rapid filling (after mitral valve opening)
    5. Reduced filling (before mitral valve closing)    Pressure-volume loops (inc. contractility? afterload? preload?)
  35. 35Cardiac cycle (heart sounds)S1 - mitral and tricuspid valve closure (loudest at mitral area)
    S2 - aortic and pulmonary valve closure (loudest at left upper sternal border)
    S3 - in early diastole during rapid ventricular filling phase. Assoc. w/ inc. filling pressure (mitral regard, HF) and more common in dilated ventricles (can be normal in children and young adults)
    S4 - in late diastole (atrial kick). Best heart at apex with patient in left lateral decubitus. High atrial pressure. Assoc. w/ ventricular noncompliance (hypertrophy). Left atrium must push against stiff LV wall (abnormal regardless of age)    Cardiac cycle (heart sounds)
  36. 36Cardiac cycle (jugular venous pulse)a wave - atrial contraction. Absent in atrial fibrillation (AF)
    c wave - RV contraction (closed tricuspid valve bulging into atrium)
    x descent - atrial relaxation and downward displacement of closed tricuspid.
    Absent in tricuspid regurgitation.
    Prominent in tricuspid insufficiency and right HF
    v wave - inc. right atrial pressure due to filling against closed tricuspid valve
    y descent - RA emptying into RV.
    Prominent in constrictive pericarditis
    Absent in cardiac tamponade    Cardiac cycle (jugular venous pulse)
  37. 37Normal splitting (how?)Inspiration --> dec. in intrathoracic pressure --> inc. venous return --> inc. RV stroke volume --> inc. RV ejection time --> delayed closure of pulmonic valve
    Dec. pulmonary impedance (inc. capacity of pulmonary circulation) also occurs during inspiration --> contribute to delayed closure of pulmonic valve    Normal splitting (how?)
  38. 38Wide splitting (how?)Seen in conditions that delay RV emptying
    1. Pulmonic stenosis
    2. Right bundle branch block
    Causes delayed pulmonic sound (esp. on inspiration).    Wide splitting (how?)
  39. 39Fixed splitting (how)Heart in ASD (atrialseptal defect)
    Left to right shunt --> inc. RA and RV volumes --> inc. flow through pulmonic valve --> regardless of breast, pulmonic closure is greatly delayed    Fixed splitting (how)
  40. 40Paradoxical splitting (how?)Heard in conditions that delay aortic valve closures
    1. Aortic stenosis
    2. Left bundle branch block
    Normal order of valve closure is reversed, so that P2 sound occurs before delayed A2 sound. On inspiration, P2 closes later and moves closer to A2 --> paradoxically eliminating the split (usually heart in expiration)    Paradoxical splitting (how?)
  41. 41Auscultation of heartAuscultation of heart
  42. 42Bedside maneuvers (4 of them...what they do....etc)Inspiration: inc. venous return to RA
    1. inc. intensity of right heart sounds
    Hand grip: inc. afterload
    1. inc. intensity of MR, AR, VSD murmurs
    2. Dec. hypertrophic cardiomyopathy murmurs
    3. later onset of click/murmur in MVP (mitral valve prolapse)
    Valsalva, standing up: dec. preload
    1. Dec. intensity of AS, PS, TR
    2. Inc. intensity of hypertrophic cardiomyopathy murmur
    3. earlier onset of click/murmur in MVP
    Rapid squatting: inc. venous return, inc. preload, inc. afterload
    1. Dec. intensity of hypertrophic cardiomyopathy murmur
    2. inc. intensity of AS murmur
    3. later onset of click/murmur in MVP
  43. 43Aortic stenosis (heart murmurs, characteristics, causes)- systolic murmur
    - crescendo-decrescendo
    - radiates to carotid
    - pulsus parvus et trades (weak and delay)
    - Can lead to (SAD):
    1. syncope
    2. angina
    3. dyspnea
    - due to aging calcification OR bicuspid aortic valve    Aortic stenosis (heart murmurs, characteristics, causes)
  44. 44Mitral/tricuspid regurgitation (heart murmurs, characteristics, causes)- holosystolic
    - high-pitched "blowing murmur" loudest at apex
    - MR radiates toward axilla
    - MR due to ischemic heart disease, MVP, LV dilatation
    - TR radiates to right sternal border
    TR due to RV dilatation
    - Rheumatic fever can cause either    Mitral/tricuspid regurgitation (heart murmurs, characteristics, causes)
  45. 45Mitral valve prolapse (heart murmurs, characteristics, causes)- late systolic crescendo murmur w/ mid systolic click
    - most frequent valvular lesion
    - usually benign
    - due to:
    1. Marfan
    2. Ehlers-Danlos syndrome
    3. Rheumatic fever
    4. Chordae rupture    Mitral valve prolapse (heart murmurs, characteristics, causes)
  46. 46Ventricular septal defect (heart murmurs, characteristics, causes)- holosystolic, harsh-sounding murmur
    - loudest at tricuspid area    Ventricular septal defect (heart murmurs, characteristics, causes)
  47. 47Aortic regurgitation (heart murmurs, characteristics, causes)- high pitched blowing
    - early diastolic decrescendo murmur
    - if severe and chronic --> head bobbing
    - wide pulse pressure
    - Due to:
    1. Aortic root dilation
    2. bicuspid aortic valve
    3. Endocarditis
    4. Rheumatic fever
    Progresses to left HF    Aortic regurgitation (heart murmurs, characteristics, causes)
  48. 48Mitral stenosis (heart murmurs, characteristics, causes)- late diastolic murmur
    - rumbling
    - follows opening snap
    - LA pressure > LV pressure during diastole
    Due to rheumatic fever    Mitral stenosis (heart murmurs, characteristics, causes)
  49. 49Patent ductus arteriosusContinuous machine-like murmur
    often due to congenital rubella or prematurity    Patent ductus arteriosus
  50. 50Myocardial action potential (phases 0 - 4, compare to skeletal muscle)Phase 0 = rapid upstroke + depolarization
    --> V-gated Na channels open
    Phase 1 = initial depolarization --> inactivation of V-gated Na channels. V-gated K channels begin to open
    Phase 2 = plateau: Ca influx through V-gated Ca channels balances K efflux. Ca influx triggers Ca release from SR and myocyte contraction
    Phase 3 = rapid depolarization - massive K efflux due to opening of V-gated slow K channels + closure of V-gated Ca channels
    Phase 4 = resting potential - high K permeability through K channels
    In contrast to skeletal muscle:
    1. Cardiac muscle Ap has a plateau due to Ca influx and K efflux
    2. Cardiac muscle contraction requires Ca influx from ECF for Ca release from SR
    3. Cardiac myocytes are electrically coupled to each other by gap junctions    Myocardial action potential (phases 0 - 4, compare to skeletal muscle)
  51. 51Pacemaker action potentialOccurs in the SA and AV nodes
    Phase 0 = upstroke - opening of voltage-gated Ca channels. Fast voltage-gated Na channels are permanently inactivated because not eh less negative resting potential of these cells --> slow conduction velocity --> used by AV node to prolong transmission from atria to ventricles
    Phase 1 absent
    Phase 2 absent
    Phase 3 = inactivation of Ca channels, activation of K channels --> K efflux
    Phase 4 = slow spontaneous diastolic depolarization due to I-funny (funny current - slow, mixed Na/K inward current). This accounts for the automaticity of SA and AV nodes. Slope of Phase 4 determines HR.
    ACh/adenosine dec.
    1. rate of diastolic depolarization
    2. HR
    Catecholamines inc.
    1. Depolarization
    2. HR
    Sympathetic stimulation inc. chance that I-f channels are open --> inc. HR    Pacemaker action potential
  52. 52Conduction pathwaySA node --> atria --> AV node --> bundle of His --> right + left bundle branches --> purkinje fibers --> ventricles --> left anterior and posterior fascicles
    SA node pacemaker inherent dominance w/ slow phase of upstroke
    AV node - posteroinferior part of interatrial septum. Blood supply from RCA. 100 msec delay allow time for ventricular filling
    Pacemaker rates - SA > AV > bundle of his/others
    Speed of conduction - Purkinje > atria > ventricles > AV nodes    Conduction pathway
  53. 53—P wave - atrial depolarization
    PR interval - start of atrial depolarization to ventricular depolarization (< 200 msec)
    QRS complex - ventricular depol. (< 120 ms)
    QT interval - ventricular depolarization + mechanical contraction of ventricle + ventricular repolarization
    T wave - ventricular repolarization. T-wave inversion = recent MI
    J point - QRS + ST (junction)
    ST segment - isoelectric, ventricles depolarized
    U wave - prominent in hypokalemia, bradycardia    P wave - atrial depolarization PR interval - start of atrial depolarization to ventricular depolarization (&lt; 200 msec) QRS complex - v...
  54. 54(what it is? what causes it? treatment?)Polymorphic ventricular tachycardia w/ shifting sinusoidal waveforms on ECG
    - can progress to ventricular fibrillation (VF)
    - long QT interval predisposes to torsades de pointes
    - Causes: drugs, low [K], low [Mg]
    - treat w/ MgSO4
    Drug-induced long QT (ABCDE)
    1. AntiArrhythmics (IA, III)
    2. AntiBiotics (macrolides)
    3. AntiCychotics (haloperidol)
    4. AntiDepressants (TCAs)
    5. AntiEmetics (ondansetron)    (what it is? what causes it? treatment?)
  55. 55Congenital long QT syndrome (2 types, and what about)- inherited disorder of myocardial repolarization, typically due to ion channel defects
    - inc. risk of sudden cardiac death due to torsades de pointes
    Romano-Ward Syndrome - AD, pure cardiac phenotype (no deafness)
    Jervell and Lange-Nielsen syndrome - AR, sensorineural deafness
  56. 56Brugada syndromeAD, most common in asian males
    Pseudo-right bundle branch block and ST elevations in V1-V3
    Inc. risk of ventricular tachyarrhythmias and SCD (sudden cardiac death) --> prevent SCD w/ cadioverter-defibrillator
  57. 57Wolff-Parkinson-White syndrome- most common type of ventricular pre-excitation syndrome
    - abnormal fast accessory conduction pathway from atria to ventricle (bundle of kent) bypasses the rate-slowing AV node --> ventricles begin to partically depolarize earlier --> characteristic delta wave with widended QRS complex and shortened PR interval
    May result in re-entry circuit --> supraventricular tachycardia    Wolff-Parkinson-White syndrome
  58. 58—Atrial fibrillation
    Chaotic and erratic baseline w/o discrete P waves in between irregular QRS
    Irregularly irregular heartbeat
    Risk factors:
    1. Hypertension
    2. Coronary artery disease (CAD)
    Can lead to thromboembolic event/stroke    Atrial fibrillation Chaotic and erratic baseline w/o discrete P waves in between irregular QRS Irregularly irregular heartbeat Risk facto...
  59. 59—Atrial flutter
    rapid succession of identical, back to back atrial depolarization waves
    "sawtooth" appearance
    Treat like atrial fibrillation
    Definitive treatment: catheter ablation    Atrial flutter rapid succession of identical, back to back atrial depolarization waves "sawtooth" appearance Treat like atrial fibrillati...
  60. 60—Ventricular fibrillation
    Completely erratic rhythm w/o identifiable waves
    Fatal arrhythmia w/o immediate CPR and defibrillation    Ventricular fibrillation Completely erratic rhythm w/o identifiable waves Fatal arrhythmia w/o immediate CPR and defibrillation
  61. 61—1st degree AV block
    PR interval is prolonged (> 200 ms)
    Benign and asymptomatic
    No treatment    1st degree AV block PR interval is prolonged (&gt; 200 ms) Benign and asymptomatic No treatment
  62. 62—2nd degree AV block
    mobitz type 1
    Progressive lengthening of PR interval until a beat is dropped (P wave not followed by QRS complex)
    Usually asymptomatic
    Regularly irregular    2nd degree AV block mobitz type 1 Progressive lengthening of PR interval until a beat is dropped (P wave not followed by QRS complex) Usu...
  63. 63—2nd degree AV block
    mobitz type II
    Dropped beats that are not preceded by a change in the length of the PR interval
    May progress to 3rd degree block - treat with pacemaker    2nd degree AV block mobitz type II Dropped beats that are not preceded by a change in the length of the PR interval May progress to 3rd d...
  64. 64—3rd degree AV block (complete)
    - Atria and ventricles beat independently of each other
    - P waves and QRS complexes not rhythmically associated
    - Atrial rate > ventricular rate
    Treat with pacemaker
    Can be caused by Lyme disease    3rd degree AV block (complete) - Atria and ventricles beat independently of each other - P waves and QRS complexes not rhythmically assoc...
  65. 65Atrial natriuretic peptide- released from atrial myocytes in response to inc. blood volume and atrial pressure
    - acts via cGMP
    1. Vasodilation
    2. Dec. Na reabsorption at renal collecting tubule
    3. Dilates afferent/constrict efferent renal arterioles
    4. promotes diuresis --> "aldosterone escape"
  66. 66B-type natriuretic peptide (brain)- Released from ventricular myocytes in response to inc. tension
    - Acts via cGMP (similar mechanism to ANP)
    - Longer half-life than ANP
    - BNP blood test used for diagnosing HF (very good negative predictive value)
    1. Vasodilation
    2. Dec. Na reabsorption at renal collecting tubule
    3. Afferent dilation/efferent constriction in renal arterioles
    4. Promotes diuresis --> "aldoesterone escape"
  67. 67Afferent and efferent baro/chemoreceptors (part 1: the two receptors)Receptors:
    1. Aortic arch --> change in BP --> vagus nerve (X) --> solitary nucleus of medulla
    2. Carotid sinus --> change in BP --> glossopharyngeal nerve (IX) --> solitary nucleus of medulla    Afferent and efferent baro/chemoreceptors (part 1: the two receptors)
  68. 68Afferent and efferent baro/chemoreceptors (part 2: baroreceptor response to hypotension, carotid massage, etc)Baroreceptors:
    1. Hypotension --> low arterial pressure --> low stretch --> less afferent baroreceptor firing --> inc. sympathetic firing + dec. parasympathetic firing --> vasoconstriction + inc. HR + inc. contractility + inc. BP
    2. Carotid massage --> pressure on carotid sinus --> stretch --> inc. afferent baroreceptor firing --> inc. AV node refractory period --> dec. HR
    3. Cushing reaction (hypertension + bradycardia + respiratory depression):
    inc. intracranial P constricts arterioles --> cerebral ischemia --> inc. pCO2, dec. pH --> central reflex sympathetic --> inc. perfusion pressure --> inc. stretch --> peripheral reflex baroreceptor-induced bradycardia
  69. 69Afferent and efferent baro/chemoreceptors (part 3: chemoreceptor actions)Chemoreceptors:
    1. Peripheral: carotid and aortic bodies stimulate by low PO2 (< 60 mmHg), high pCO2, low pH of blood
    2. Central: stimulated by changes in pH, pCO2 of brain interstitial fluid (which are influenced by arterial CO2)
    *do not respond directly to PO2
  70. 70Normal cardiac pressures (RA, RV, PCWP, LA, LV, in mitral stenosis?)- Pulmonary capillary wedge pressure (PCWP) is a good approx of LA pressure [4-12 PCWP]
    - In mitral stenosis, PCWP > LV end diastolic pressure
    - PCWP is measured with pulmonary artery catheter
    - RA < 5 mmHg
    - RV 25/5 mmHg
    - LA: < 12 mmHg
    - LV: 130/10 mmHg
  71. 71Autoregulation (heart, kidneys, lungs)Heart - Local metabolites (vasodilatory)
    1. adenosine
    2. No
    3. CO2
    4. Dec. O2
    Kidney - Myogenic and tubuloglomerular feedback
    Lungs - Hypoxia --> vasoconstriction
  72. 72Autoregulation (brain, skeletal muscle, skin)Brain - local metabolites (vasodilatory)
    1. CO2 (via pH)
    Skeletal muscle - local metabolites during exercise: CHALK
    1. CO2
    2. H
    3. Adenosine
    4. Lactate
    5. K
    - sympathetic tone at rest
    Skin - sympathetic stimulation most important --> temperature control
  73. 73Right to left shunts (how? symptoms?)- Early cyanosis "blue babies"
    - Require urgent medical treatment AND/OR maintenance of a PDA
    5 T's
    1. Truncus arteriosus (1 vessel)
    2. Transposition (2 switched vessels)
    3. Tricuspid atresia (3 = Tri)
    4. Tetralogy of Fallot (4 = tetra)
    5. TAPVR (5 letters in name)
    Total anomalous pulmonary vein return: all four pulmonary veins return to the right atrium.
  74. 74Persistent truncus arteriosus- No aorticopulmonary septum --> Truncus arteriosus fails to divide into pulmonary trunk and aorta
    - most patients also have VSD
  75. 75D-transposition of great vessels- failure of aorticopulmonary septum to spiral --> aorta leaves RV and pulmonary trunk leaves LV --> separate systemic and pulmonary circulations
    - not compatible w/ life unless there's a shunt (VSD, PDA, patent foramen ovale)    D-transposition of great vessels
  76. 76Tetralogy of FallotAnterosuperior displacement of the infundibular septum (conus arteriosus) --> early childhood cyanosis
    PROVe
    1. Pulmonary infundibular stenosis (prognostic factor)
    2. Right ventricular hypertrophy (boot shaped heart on CXR)
    3. Overriding aorta
    4. VSD
    Pulmonary stenosis --> VSD --> RVH    Tetralogy of Fallot
  77. 77Ebstein anomaly- tricuspid valve leaflet displaced downward into RV --> atrialized ventricle
    assoc. w/:
    1. Tricuspid regurgitation
    2. Right HF
    Lithium exposure in utero
  78. 78Ventricular septal defectMOST COMMON congenital cardiac defect
    - asymptomatic at birth --> manifest weeks later OR asymptomatic through life
    - most self-resolve
    [O2] higher in RV and pulmonary artery
  79. 79Atrial septal defectDefect in interatrial septum
    1. Loud S1
    2. wide, fixed split S2
    3. Asymptomatic or HF
    4. O2 saturation inc. in RA, RV, AND pulmonary artery
    Due to ostium secundum defect (isolated)
    Ostium primum defect (assoc. w/ others)    Atrial septal defect
  80. 80Patent ductus arteriosus- Continuous machine-like murmur
    - Patency maintained by PGE and low O2 tension
    - If uncorrected --> late cyanosis in lower extremities
    ENDomethacin (indomethacin) ends patency of PDA
  81. 81Eisenmenger syndromeUncorrected left-to-right shunt (VSD, ASD, PDA) --> inc. pulmonary blood flow --> pathologic remodleing of vasculature --> pulmonary arterial hypertension
    - RVH --> Shunt becomes right to left
    1. Late cyanosis
    2. Clubbing
    3. Polycythemia    Eisenmenger syndrome
  82. 82Coarctation of aorta- Aortic narrowing near insertion of ductus arteriosus
    - Assoc. w/
    1. Bicuspid aortic valve
    2. Turner syndrome
    1. hypertension in upper extremities
    2. weak, delayed pulse in lower extremities
    3. Intercostal arteries enlarge due to collateral circulation --> rib notching on CXR
    Complications:
    1. HF
    2. Cerebral hemorrhage (berry aneurysm)
    3. Aortic rupture
  83. 83Congenital cardiac defect (alcohol exposure in utero, congenital rubella, down syndrome, infant of diabetic)Alcohol exposure -
    1. VSD/ASD
    2. PDA
    3. Tetralogy of Fallot
    Congenital Rubella
    1. PDA
    2. Pulmonary artery stenosis
    3. VSD/ASD
    Down syndrome
    1. ASD + VSD (endocardial cushion defect)
    Infant of diabetic
    1 Transposition of great vessels
  84. 84Congenital cardiac defect associations (marfa, prenatal lithium exposure, turner syndrome, williams syndrome, velocardiofacial syndrome - 22q11)Marfan
    1. MVP (mitral valve prolapse)
    2. Aortic aneurysm --> dissection
    3. Aortic regurgitation
    Lithium
    1. Ebstein anomaly
    Turner syndrome
    1. Bicuspid aortic valve
    2. Coarctation of aorta
    Williams
    1. Aortic stenosis
    Velocardiofacial
    1. Truncus arteriosus
    2. Tetralogy of Fallot
  85. 85HypertensionSystolic BP > 140 mmHg
    Diastolic BP > 90 mmHg
    Risk factors: age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history
    Blacks > whites > asians
    90% of hypertension is primary
    10% secondary
    Hypertensive urgency - (>180/120 mmHg), severe hypertension w/o acute end-organ damage
    Hypertensive emergency - severe hypertension w/ evidence of acute end organ damage
    Predisposition:
    1. CAD (coronary artery disease)
    2. LVH (left ventricular hypertrophy)
    3. HF (heart failure)
    4. AF (atrial fibrillation)
    5. Aortic dissection/aneurysm
    6. Stroke
    7. Hypertensive nephropathy
    8. Retinopathy
  86. 86Hyperlipidemia signs1. Xanthomas
    plaques/nodules composed of lipid-laden histiocytes in skin, esp. the eyelid (xanthelasma)
    2. Tendinous xanthoma
    Lipid deposit in tendon, esp. achilles
    3. Corneal arcus
    Lipid deposit in cornea, common in elderly, but appears earlier in life in hypercholesterolemia    Hyperlipidemia signs
  87. 871. Arteriosclerosis 1a. Arteriolosclerosis 1b. Monckeberg sclerosis (medial calcific sclerosis)1. Hardening of arteries w/ arterial wall thickening and loss of elasticity
    1a. Affects small arteries and arterioles
    Type 1 - Hyaline --> thickening of vessel walls in essential hypertension or diabetes mellitus
    Type 2 - Hyperplastic --> onion skinning in severe hypertension w/ proliferation of smooth muscle cells
    1b. Affects medium-sized arteries. calcification of internal elastic lamina and media of arteries --> vascular stiffening w/o obstruction --> "pipestem" on xray    1. Arteriosclerosis 1a. Arteriolosclerosis 1b. Monckeberg sclerosis (medial calcific sclerosis)
  88. 88Atherosclerosis (definition, pathophys, risk factors, symptoms, complications)- Disease of elastic arteries and large/medium sized muscular arteries
    - a form of arteriosclerosis due to buildup of cholesterol plaques
    - inflammation --> endothelial cell dysfunction --> macrophage + LDL accumulation --> foam cell formation --> fatty streaks --> smooth muscle cell migration (PDGF, FGF) + ECM deposition --> fibrous plaque --> complex atheromas
    Risk factors (modifiable):
    1. Smoking
    2. Hypertension
    3. Hyperlipidemia
    4. Diabetes
    Risk factors (nonmodifiable)
    1. Sex
    2. Age
    3. Family history
    Location:
    Abdominal aorta > coronary artery > popliteal artery > carotid artery
    Symptoms:
    1. Angina
    2. Claudication
    3. Asymptomatic
    Complications:
    1. Aneurysms
    2. Ischemia --> infarcts
    3. Thrombus --> emboli
  89. 89Aortic aneurysm (definition, 2 types + manifestations, etc)- Localized pathologic dilatation of aorta
    - May have abdominal/back pain --> sign of leaking, dissection, or imminent rupture
    Abdominal aortic aneurysm
    - assoc. w/ atherosclerosis
    - risk factors:
    1. Tobacco use
    2. Age
    3. Male
    4. Family history
    consider - pulsatile abdominal mass
    Thoracic aortic aneurysm
    - Assoc. w/ cystic medial degeneration
    - Risk factors:
    1. Hypertension
    2. Bicuspid aortic valve (turner)
    3. Marfan syndrome
    4. Tert. syphpilis    Aortic aneurysm (definition, 2 types + manifestations, etc)
  90. 90Traumatic aortic ruptureTrauma/deceleration injury
    Commonly at aortic isthmus (proximal descending aorta just distal to origin of left subclavian artery)
  91. 91Aortic dissection- Longitudinal intimal tear forming a false lumen
    - Assoc. w/
    1. Hypertension
    2. Bicuspid aortic valve
    3. Inherited connective tissue disorder (marfan's)
    - presentation
    1. Tearing chest pain (sudden)
    2. Radiating pain to back
    3. MAYBE different right/left arm BP
    CXR: widened mediastinum
    Result:
    1. Organ ischemia
    2. Aortic rupture
    3. Death
    Stanford type A: involving ascending aorta
    - Treat with surgery
    Stanford type B: involes descending aorta and/or aortic arch
    - Treat with B-blockers THEN vasodilators    Aortic dissection
  92. 92Angina- Chest pain due to ischemic myocardium from coronary artery narrowing/spasm
    - no myocyte necrosis
    1. Stable
    - exertional chest pain
    - ST depression on ECG
    - resolve w/ rest/Nitroglycerin
    2. Variant (prinzmetal)
    - occurs at rest from coronary artery spasm
    - transient ST elevation on ECG
    - triggers: tobacco, cocaine, triptans
    - Treat w/ Ca channel blockers, Nitrates, Smoke cessation
    3. Unstable
    - thrombosis w/ incomplete coronary artery occlusion
    - +/- ST depression, +/- T inversion
    - No cardiac biomarker elevation
    - inc. frequency/intensity of chest pai
  93. 93Coronary steal syndromeDistal to coronary stenosis, vessels are maximally dilated at baseline --> administration of vasodilators --> normal vessels dilate and shunt blood towards them --> ischemia in poststenotic region
    *principle of pharmacologic stress test*
  94. 94Sudden cardiac deathDeath from cardiac causes within 1 hour of onset of symptoms
    - most common: lethal arrhythmia (VF)
    - assoc. w/
    1. CAD >
    2. Cardiomyopathy (hypertrophic, dilated)
    3. Hereditary ion channelopathies (long QT, Brugada)
    Prevent w/ inplantable cardioverter-defibrillator (ICD)
  95. 95Chronic ischemic heart diseaseProgressive onset of HF over many years due to chronic ischemic myocardial damage
  96. 96Myocardial infarction (how? types? labs?)Most often: acute thrombosis due to rupture of coronary artery atherosclerotic plaque
    Diagnostic labs:
    1. inc. cardiac biomarkers (CK-MB, troponins)
    STEMI
    - transmural infarcts
    - full thickness of myocardial wall involved
    - ST elevation on ECG, Q waves
    NSTEMI
    - subendocardial infarcts
    - subendocardium (inner 1/3) esp. vulnerable to ischemia
    - ST depression on ECG
    LAD > RCA > circumflex
    Symptoms:
    1. Diaphoresis
    2. Nausea/vomiting
    3. Severe retrosternal pain
    4. Pain in left arm/jaw
    5. Shortness of breath + fatigue    Myocardial infarction (how? types? labs?)
  97. 97MI between 0-24 hrs Gross? micro? complications?Gross: none
    Micro:
    1. early coagulative necrosis
    2. edema, hemorrhage
    3. neutrophils appear
    Reperfusion injury due to free radicals --> hypercontraction of myofibrils through high free Ca influx
    Complications:
    1. Ventricular arrhythmia
    2. HF
    3. Cardiogenic shock
  98. 98MI between 1-3 days Gross? micro? complications?Gross: hyperemia
    Micro:
    1. extensive coagulative necrosis
    2. tissue surrounding infarct shows acute inflammation w/ neutrophils
    Complications:
    Postinfarction fibrinous pericarditis
  99. 99MI between 3-14 days Gross? micro? complications?Gross: hyperemic border, central yellow-brown softening. Max yellow and softening by 10 days
    Micro:
    1. Macrophages then:
    2. Granulation tissue at margins
    Complications:
    Free wall rupture --> tamponade
    Papillary muscle rupture -> mitral regurg
    LV pseudoaneurysm --> risk of rupture
  100. 100MI after 2 weeks Gross? micro? complications?Gross:
    1. Recanalized artery
    2. Gray-white scar
    Micro:
    1. Contracted scar complete
    Complications
    1. HF
    2. Arrhythmias
    3. True ventricular aneurysm (mural thrombus)
  101. 101Diagnosis of MIfirst 6 hrs:
    ECG
    - gold standard
    Cardiac troponin I
    - rises after 4 hrs (peaks at 24), up for 7-10 days (more specific than other markers)
    CK-MB
    - rises after 6-12 hrs (peaks at 16-24), return to normal at 48 hrs
    - found in myocardium
    - useful for reinfarction diagnosis
    STEMI
    NSTEMI (depressed ST)
    Hyperacute T waves (peaked T waves)
    T-wave inversion
    left bundle branch block
    Pathologic Q waves/poor R wave progression
  102. 102ECG localization of STEMI Anteroseptal? Anteroapical? Anterolateral? Lateral? inferior? posterior?Anteroseptal (LAD) - V1-v2
    Anteroapical (distal LAD) - V3-V4
    Anterolateral (LAD, LCX) - V5-V6
    Lateral (LCX) - I, aVL
    InFerior (RCA) - II, III, aVF
    Posterior (PDA) - V7-V9, ST depression in V1-V3 with tall R waves
  103. 103Myocardial infarction complications (14 days and before)1. Cardiac arrhythmia
    - occurs within first few days post MI
    - Important cause of death before getting to hospital
    2. Postinfarction fibrinous pericarditis
    - 1-3 days after MI
    - Friction rub
    3. Papillary muscle rupture
    - 2-7 days after MI
    - Posteromedial papillary muscle rupture -> mitral regurgitation
    - inc. due to single blood supply from PDA
    4. Interventricular septal rupture
    - 3-5 days after MI
    - Macrophage-mediated degradation --> VSD
    5. Ventricular pseudoaneurysm formation
    - 3-14 days after MI
    - Contained free wall rupture
    - Dec. CO
    - risk of embolus from mural thrombus
    6. Ventricular free wall rupture
    - 5-14 days after MI
    - Free wall rupture --> cardiac tamponade
  104. 104Myocardial infarction complications (after 2 weeks)1. True ventricular aneurysm
    - after 2 weeks after MI
    - outward bulge w/ contraction (dyskinesia)
    - assoc. w/ fibrosis
    2. Dressler syndrome
    - Occurs weeks after MI
    - Autoimmune phenomenon --> fibrinous pericarditis
    3. LV failure and pulmonary edema
  105. 105Acute coronary syndrome treatments (Unstable angina/NSTEMI, STEMI)NSTEMI
    1. Anticoagulation (i.e. heparin)
    2. Antiplatelet therapy (i.e. aspirin) + ADP receptor inhibitors (i.e. clopidogrel)
    3. B-blockers
    4. ACE-i
    6. Statins
    7. Nitroglycerin (symptomatic)
    8. Glycine (symptomatic)
    STEMI
    - the above
    9. Reperfusion therapy (interventional > fibrinolysis)
  106. 106Dilated cardiomyopathy (etiology, findings, treatment)90% of all cardiomyopathies
    - problem with systolic dysfunction
    - eccentric hypertrophy
    Etiology (ABCCCD:
    - familial
    - chronic Alcohol abuse
    - wet Beriberi
    - Coxsackie B viral myocarditis
    - chronic Cocaine
    - Chagas
    - Doxorubicin (cancer)
    - Hemochromatosis
    - Sarcoidosis
    Findings:
    - HF
    - SE
    - Systolic regurgitation
    - Dilated heart
    Treatment:
    - Na restriction
    - ACE-i
    - B-blockers
    - Diuretics
    - digoxin
    - ICD
    - Heart transplant
  107. 107Hypertrophic cardiomyopathy (etiology, findings, treatment)- Diastolic dysfunction
    - Marked ventricular hypertrophy
    Etiology:
    - Familial (AD: B-myosin heavy chain mut.)
    - Friedreich ataxia
    Manifestations:
    - Syncope during exercise
    - Sudden death in young athletes (from ventricular arrhythmias)
    Findings:
    - S4
    - Systolic murmur
    - Mitral regurgitation (impaired mitral valve closure)
    Treatment:
    - Cessation of high-intensity athletics
    - Use of B-blocker
    - Use of non-dihydropyridine Ca channel blockers (verapamil)
    - ICD if high risk patient
  108. 108Restrictive/infiltrative cardiomyopathyCauses:
    1. Sarcoidosis
    2. Amyloidosis
    3. Post-radiation fibrosis
    4. Endocardial fibroelastosis
    5. Loffler syndrome (end-myocardial fibrosis w/ a prominent eosinophilic infiltrate)
    6. Hemochromatosis (dilated cardiomyopathy is more common)
    Diastolic dysfunction ensues
  109. 109Heart Failure (general)Cardiac pump dysfunction --> congestion + low perfusion
    Symptoms
    1. Dyspnea
    2. Orthopnea
    3. Fatigue
    Signs:
    1. Rales
    2. JVD
    3. Pitting edema
    Systolic dysfunction: reduced EF, high EDV, low contractility 2nd to ischemia/MI or dilated cardiomyopathy
    Diastolic dysfunction: preserved EF, normal EDV, low compliance 2nd to myocardial hypertrophy
    Cor pulmonale - isolated right HF from pulmonary causes
    Right HF most often from Left HF
    To decrease mortality:
    1. ACE-i
    2. Angiotensin II receptor blockers
    3. B-blockers (not in acute decomp. HF)
    4. Spironolactone
    Symptomatic relief:
    1. Thiazide/loop diuretics
    2. Hydralazine + nitrate
  110. 110Left heart failure (clinical signs)1. Orthopnea (supine --> inc. venous return --> pulmonary vascular congestion)
    2. Paroxysmal nocturnal dyspnea
    - breathless awakening from sleep
    - inc. venous return: blood redistribution
    - reabsorption of peripheral edema
    3. Pulmonary edema
    - from inc. pulmonary venous pressure
  111. 111Right heart failure (clinical signs)1. Hepatomegaly (nutmeg liver)
    2. JVD
    3. Peripheral edema
  112. 112Hypovolemic shockinadequate organ perfusion
    caused by:
    1. hemorrhage
    2. dehydration
    3. burns
    Cold, clammy skin
    Dec. PCWP (preload)
    Dec. CO
    Inc. SVR (afterload)
    Treat w/ IV fluids
  113. 113Cardiogenic, obstructive shockInadequate organ perfusion
    Due to:
    1. Acute MI (cardiogenic)
    2. HF (cardiogenic)
    3. Valvular dysfunction (cardiogenic)
    4. Arrhythmia (cardiogenic)
    5. Cardiac tamponade (obstructive)
    6. Pulmonary embolism (obstructive)
    Cold, clammy skin
    Inc. PCWP (preload)
    Dec. CO
    Inc. SVR (afterload)
    Inotropes, diuresis (cardiogenic)
    Relieve obstruction (obstructive)
  114. 114Distributive ShockInadequate organ perfusion
    Due to:
    1. Sepsis
    2. Anaphylaxis
    3. CNS injury
    Warm, dry skin
    Dec. PCWP (preload)
    Inc. CO (1, 2), Dec. CO (3)
    Dec. SVR (afterload)
    Treat with:
    1. IV fluids
    2. Pressors
  115. 115Bacterial endocarditis (acute? subacute? IV D? Colon cancer? prosthetic valve? culture neg? symptoms?)If acute: S. aureus (large vegetations on normal valves)
    If subacute: Strep viridian.
    If IV-D: S aureus, Pseudomonas, Candida
    Colon cancer: S. bovis
    Prosthetic valves: S. epidermis
    2nd: malignancy, hyper coagulability, lupus
    Culture neg (CB-HACEK)
    1. Coxiella
    2. Bartonella
    3.. Haemophilus
    4. Aggregatibacter
    5. Cardiobacterium
    6. Eikenella
    7. Kingella
    Symptoms:
    FROM JANE
    1. Fever
    2. Roth spots (white spots on retina)
    3. Osler nodes (pain, finger/toes)
    4. Murmur
    5. Janeway lesions (painless, palm/soles)
    6. Anemia
    7. Nail-bed (splinter) hemorrhage
    8. Emboli    Bacterial endocarditis (acute? subacute? IV D? Colon cancer? prosthetic valve? culture neg? symptoms?)
  116. 116Rheumatic fever (etiology, presentation, findings, etc)- Group A B-hemolytic strep infection
    - Late sequelae --> rheumatic heart disease (early --> mitral valve regurg, late --> mitral valve stenosis)
    - Aschoff bodies (granuloma w/ giant cells)
    (blue arrows)
    - Anitschkow cells (large macrophages w/ ovoid, wavy, rod-like nucleus)
    (red arrows)
    - high anti-streptolysin O (ASO) titers
    - Type II hypersensitivity reaction (antibodies to M protein cross react)
    JONES
    Joint (migratory polyarthritis)
    O (heart --> peri/myocarditis, valve probs)
    N --> nodules in skin (subcutaneous)
    E --> erythema marginatum
    S --> Sydenham chorea
    Treat: penicillin    Rheumatic fever (etiology, presentation, findings, etc)
  117. 117Acute pericarditis (etiology, presentation, findings, etc)Inflammation of the pericardium
    Causes:
    - Idiopathic (probably viral)
    - Infections (coxsackie virus)
    - Neoplasia
    - Autoimmune (SLE, RA)
    - Uremia
    - Radiation therapy
    - Most MI complication (i.e. Dressler)
    Signs:
    - Sharp pain, aggravated by inspiration, relieved by sitting up and leaning forward
    - Complicated by pericardial effusion (pic)
    - Friction rub
    - ECG: widespread ST-elevation and/or PR depression    Acute pericarditis (etiology, presentation, findings, etc)
  118. 118Cardiac tamponade1. Compression of heart by fluid --> dec. CO
    2. Equilibriation of diastolic pressures in all 4 chambers
    beck triad:
    1. Hypotension
    2. Distended neck veins
    3. Distant heart sounds
    4. Inc. HR
    5. Pulsus paradoxus - dec. amplitude of systolic BP by > 10 mmHg during inspiration (also in asthma, obstructive sleep apnea, pericarditis, croup)
    ECG:
    1. low-voltage QRS
    2. electrical alternans (from swinging mvmd of heart)    Cardiac tamponade
  119. 119Syphilitic heart disease3rd syphilis disrupts vasa vasorum of aorta --> atrophy of vessel wall --> dilatation of aorta + valve ring
    May see calcification of aortic root and ascending aortic arch -->
    1. Tree bark appearance of aorta
    2. Aneurysm of ascending aorta
    3. Aortic insufficiency
  120. 120Cardiac tumorsMost common - metastasis
    Myxomas
    - most common 1* cardiac tumor in adult
    - most in atria (left)
    - "ball valve" obstruction
    - May hear early diastolic "tumor plop"
    Rhabdomyoma
    - most frequent 1* cardiac tumor in children (assoc. w/ tuberous sclerosis)    Cardiac tumors
  121. 121Kussmaul sign (where seen?)inc. in JVP on inspiration instead of a normal dec.
    inspiration --> high pulmonary pressure (normally relieved by lower intrathoracic pressure) --> impaired filling of right ventricle --> blood backs up --> JVD
    1. Constrictive pericarditis
    2. Restrictive cardiomyopathies
    3. Right atrial/ventricular tumors
  122. 122Giant Cell (temporal arteritis)- Usually elderly females
    - Assoc. w/ polymylagia rheumatica
    - Common affects carotid artery branches
    Signs:
    1. Unilateral headache (temporal artery)
    2. Jaw claudication
    3. Irreversible blindness (ophthalmic artery occlusion)
    Lab:
    1. Focal granulomatous inflammation
    2. Inc. ESR
    Treatment
    1. High-dose corticosteroids prior to temporal artery biopsy    Giant Cell (temporal arteritis)
  123. 123Takayasu arteritis- Asian females < 40 years old
    - Pulseless disease (weak upper extremities)
    Signs:
    1. Fever
    2. Night sweats
    3. Arthritis
    4. Myalgias
    5. Skin nodules
    6. Ocular disturbances
    Lab:
    1. Granulomatous thickening + narrowing of aortic arch AND proximal vessels
    2. Inc. ESR
    Treat w/ corticosteroids    Takayasu arteritis
  124. 124Polyarteritis nodosa- Young adults
    - Hepatitis B seropositivity in 30%
    - Typically involves renal/visceral vessels
    - Immune complex mediated
    - Transmural inflammation of arterial wall: fibrinoid necrosis
    Symptoms:
    1. Fever
    2. Weightloss
    3. Malaise + headache
    4. Abdominal pain --> melena
    5. Renal damage
    6. Neurological dysfunction
    7. Cutaneous eruptions
    Treatment
    1. Corticosteroids
    2. Cyclophosphamide    Polyarteritis nodosa
  125. 125Kawasaki disease*mucocutaneous lymph node syndrome*
    - Asian children < 4 years old
    - CRASH and burn
    C-onjunctival injection
    R-ash (polymorphous --> desquamating)
    A-denopathy (cervical)
    S-trawberry tongue
    H-and foot change (edema, erythema)
    fever
    Can develop coronary artery aneurysms --> thrombosis/rupture --> death
    IV-Ig and aspirin treatment    Kawasaki disease
  126. 126Buerger disease"thromboangiitis obliterates"
    - Heavy smokers
    - Males < 40 years old
    - Gangrene (intermittent claudication)
    - superficial nodular phlebitis
    Raynaud phenomenon is often present
    Treat with smoking cessation
  127. 127Granulomatosis w/ polyangiitis"wegener's granulomatosis"
    Upper respiratory tract:
    1. perforation of nasal septum
    2. chronic sinusitis
    3. otitis media
    4. mastoiditis
    Lower respiratory tract
    1. Hemoptysis
    2. Cough
    3. Dyspnea
    Renal:
    1. Hematuria
    2. Red cell casts
    Triad:
    1. Focal necrotizing vasculitis
    2. Necrotizing granulomas in lung and upper airway
    3. necrotizing glomerulonephritis
    Lab:
    1. p-ANCA (PR3)
    2. c-ANCA
    3. CXR: large nodular densities
    Treatment
    1. Cyclophosphamide
    2. Corticosteroids    Granulomatosis w/ polyangiitis
  128. 128Microscopic polyangiitisNecrotizing vasculitis commonly involving:
    1. Lung
    2. Kidneys (pauci-immune glomerulonephritis)
    3. Skin (palpable purpura)
    - Like wagerer's but NO NASOPHARYNGEAL INVOLVEMENT
    Lab:
    1. No granulomas
    2. MPO-ANCA (myeloperoxidase)
    3. p-ANCA
    Treatment:
    1. Cyclophosphamide
    2. Corticosteroids    Microscopic polyangiitis
  129. 129Eosinophilic granulomatosis w/ polyangiitis*churg-strauss*
    1. Asthma
    2. Sinusitis
    3. Skin nodules/purpura
    4. Peripheral neuropathy (wrist/foot drop)
    5. Heart, GI, kidney (pauci-immune glomerulonephritis)
    Lab:
    1. Granulomatous necrotizing vasculitis w/ eosinophilia
    2. MPO-ANCA/p-ANCA
    3. Inc. IgE levels    Eosinophilic granulomatosis w/ polyangiitis
  130. 130Henoch-Schonlein purpura- Most common childhood systemic vasculitis
    - Often follows URI
    - Classic triad
    1. Skin - palpable purport on butt/legs
    2. Arthralgias
    3. GI: abdominal pain
    - Vasculitis 2* to IgA immune complex deposition
    - Assoc. w/ IgA nephropathy    Henoch-Schonlein purpura

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Organ modules Fichas sobre cardiology, creado por Eric Zhang el 31/01/2017.
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Eric Zhang
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