CARDIO_ICS

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soren101
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110755
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CARDIO_ICS
Updated:
2011-11-08 21:23:23
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CARDIOVASCULAR ICS MS2
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CARDIOVASCULAR ICS
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  1. SINO-ATRIAL NODE IN HEART CONDUCTION
    INITIATES HB

    PACEMAKER

    NOT SEEN ON ECG

    HIGH IN RA NEAR SVC
  2. AV NODE IN HEART CONDUCTION
    STRAIGHT LINE AFTER P WAVE (PR SEGMENT)

    SLOWEST CONDUCTION VEL IN HRT

    LONG REFRACT PERIOD

    ONLY ELEC CONNECTION FROM A TO V
  3. ISOVOLUMIC CONTRACTION ON ECG
    BEGINS w QRS (V DEPOL)

    INITIATES VENT CONTRACTION AND PRESSURE RISES

    ENDS AT THE END OF QRS

    • VENT PRESSURE EXCEEDED DIASTOLIC PRESSURE AND SEMILUNAR VALVES OPEN
    • --------------------------
    • CYCLE:

    ISOVOL CONTRACTION --> VENT EJECTION --> ISOVOL RELAXATION --> VENT FILLING --> REPEAT
  4. VENTRICULAR EJECTION ON ECG
    BEGINS AT END OF QRS COMPLEX

    • ENDS AT END OF T WAVE WHEN VENT CHAMBERS SMALLEST AND SEMILUNAR VALVES CLOSE
    • -------------------------------

    CYCLE:

    ISOVOL CONTRACTION --> VENT EJECTION --> ISOVOL RELAXATION --> VENT FILLING --> REPEAT
  5. ISOVOLUMIC RELAXATION ON ECG
    BEGINS AT END OF T WAVE

    ENDS ABOUT 0.08 sec LATER

    • NO CORRELATING ECG EVENT
    • --------------------------

    CYCLE:

    ISOVOL CONTRACTION --> VENT EJECTION --> ISOVOL RELAXATION --> VENT FILLING --> REPEAT
  6. VENTRICULAR FILLING ON ECG
    3 PHASES

    RAPID FILLING - NO ECG

    DIASTASIS - NO ECG

    ATRIAL KICK - BEGINS DURING P WAVE AS ATRIAL SYSTOLE ADDS TO VENT FILLING

    • ENDS w QRS COMPLEX
    • ---------------------------

    CYCLE:

    ISOVOL CONTRACTION --> VENT EJECTION --> ISOVOL RELAXATION --> VENT FILLING --> REPEAT
  7. nL P WAVE ON ECG
    nL UNIFORM FROM BEAT TO BEAT

    DURATION .06 - .10 sec (1.5 TO 2.5 mm)

    HEIGHT < 2.5 mm

    LEAD II: nL POS (UPGOING)

    V1: START POS AND END NEG
  8. nL PR INTERVAL ON ECG
    CONSTANT FROM BEAT TO BEAT

    DURATION .12 - .20 sec

    3-5mm ON nL PAPER SPEED
  9. nL QRS COMPLEX ON ECG
    DURATION .06 - .10sec

    1.5 - 2.5mm WIDE

    • R WAVES:
    • --INC V1 TO V4
    • --ALL LIMB LEADS < 20mm & ALL CHEST LEADS < 30mm
    • --AT LEAST ONE LIMB LEAD > 5mm
    • --CHEST LEAD > 10mm (R+S)
  10. nL ST SEGMENT ON ECG
    PLATEAU PHASE OF VENT CELLULAR ACTION POTENTIAL

    BEGINS HORIZONTALLY AT LEVEL OF PR AND TP SEGs

    MAY BE DISPLACED 1mm IN DIRECTION OF FOLLOWING T WAVE (early replarization)
  11. nL T WAVE ON ECG
    SMOOTH ROUNDED WAVE

    AMP USUALLY < 5 mm IN LIMB AND < 10mm IN CHEST LEADS

    • DIRECTION:
    • --SIMILAR TO QRS IN LIMB LEADS
    • --TRANSVERSE LEADS IT'S POS EXCEPT MAYBE IN V1
  12. R-PRIME AND QS COMPLEX ON ECG
    • R-PRIME:
    • --FIRST UPWARD DEFLECTION AFTER S WAVE
    • --MUST HAVE S WAVE TO HAVE R'

    • QS:
    • DOWNWARD DEFLECTION w/o ANY UPWARD DEFLECTION

    
  13. PRINCIPLES FOR DETECTING HYPERTROPHY ON ECG
    MORE MASS OF MYOCYTES --> INC ELEC ACTIVE TISSUE --> INC ECG DEFLECTIONS DURING DEPOLARIZATION OF LARGE OR THICK CHAMBER

    LOCATION OF HRT CHAMBERS(s) RELATIVE TO CHEST AND OTHER CHAMBERS DETERMINE THE DIRECTION FO THE LARGER ELEC FORCES --> DETERMINE WHICH ECG LEADS AFFECTED
  14. LEFT ATRIAL ENLARGEMENT ON ECG
    USUALLY w ABN VENT FUNCTION

    INC IN LEFTWARD AND POSTERIOR DIRECTION

    P WAVE HAS LARGE NEG DEFLECTION IN V1

    TIME FOR ATRIAL DEPOL IS PROLONGED (INC P WAVE DURATION) OFTEN WITH NOTCH SEEN IN LEAD II
  15. RIGHT ATRIAL ENLARGEMENT ON ECG
    USUALLY w ABN VENT FUNCTION

    INC INF AND SLIGHTLY RIGHTWARD AND ANT DIRECTION

    P WAVE TALL AND PEAKED IN LEAD II AND HAS TALL POS DEFLECTION IN V1

    TIME FOR ATRIAL DEPOL IS USUALLY NOT PROLONGED
  16. LEFT VENTRICULAR HYPERTROPHY IN ECG
    INC TOWARD LEFT AND INF AND POST

    LARGE S WAVE IN LEAD V1

    LARGE R WAVE IN LEADS I AND aVL AND V5-V6

    OFTEN ASSOC LAE

    OFTEN REPOL (st seg and t wave) IS ABN AND DIRECTED OPPOSITE FROM QRS COMPLEX
  17. RIGHT VENTRICULAR HYPERTROPHY IN ECG
    VENT FORCES ARE INC TOWARD RIGHT AND INF AND ANT

    OFTEN LARGE R WAVE IN LEAD V1

    OFTEN LARGE S WAVE IN LEAD I AND V5-V6

    MAY BE ASSOC RAE
  18. PRINCIPLES OF ISCHEMIA IN HRT AND CORONARY ARTERIES
    • MYOCARDIAL O2 SUPPLY
    • --RELATED TO MYOCARDIAL BLD FLOW AND BLD OXY CARRYING CAPACITY
    • --Hg CONC AND Hg OXY HANDLING CHARs AND OXY CONC IN BLD

    • MYOCARDIAL O2 DEMAND
    • --RELATED TO HR AND MYOCARDIAL MUSC MASS AND CONTRACTILITY
    • --CHANBER SIZE, THICKNESS, PRESSURE

    • BAD SUPPLY/DEMAND
    • --MYO CELLS BECOME SICK
    • --AEROBIC MET IMPAIRED (MYO ISCHEMIA)
    • --EXCESSIVE DEMAND DUE TO HT OR SEVERE TACHY
    • --INADEQ SUPPLY DUE TO NARROWING OF COR ARTs FROM ATHEROSCLEROSIS

    • DEGREES OF SEVERITY
    • --ISCHEMIA AND INJURY ARE REVERSIBLE
    • --INFARCTION MOST SEVERE --> PERMANENT
  19. RESTING ECG SIGNS OF ISCHEMIA AND SUBENDOCARDIAL INJURY
    • ISCHEMIA
    • --CHANGES IN T WAVE OR ST DEPRESSION
    • --T WAVE INVERSION (OPPOSITE from QRS)
    • ----------------------

    • SUBENDOCARDIAL
    • --ST SEG DEP
    • --MAY BE ASSOC w OTHER EVIDENCE OF OTHER MUSC DAMAGE
    • --DOES NOT LOCALIZE TO SPEC INJURED WALL
  20. RESTING ECG SIGNS OF INFARCTION
    ST ELEV OR Q WAVE FORMATION

    ST ELEV IS A KEY SIGN --> ACUTE ONGOING MUSC INFARCTION AND REQUIRES IMMEDIATE ACTION
  21. WHAT DOES Q WAVE FORMATION INDICATE ON ECG
    RECENT OR OLDER INFARCTION

    INF MYO CANT GEN ACTION POTENTIAL SO IS ELEC & MECH SILENT

    • QRS AFFECTED IN 2 WAYS:
    • 1) PATH Q WAVES (deep & wide) SEEN IN LEADS OF INFARCTED WALLS OF LV

    2) DEC R WAVE SEEN IN LEADS OF INF WALLS OF LV ("loss of r wave")
  22. ECG LEADS INVOLVED IN ACUTE OR RECENT/OLDER INFARCTION BASED ON LOCATION OF HRT DAMAGE
    INFERIOR -- II, III, aVF

    HIGH LAT OR LAT -- I, aVL

    ANTEROSEPTAL -- V1, V2

    ANTERIOR -- V3, V4

    ANTEROLATERAL -- V5, V6
  23. EXCERSIZE STRESS TEST ECG SIGN OF ISCHEMIA
    ST SEG DEPRESSION

    CONTRAST TO ST DEP IN RESTING ECG, IN STRESS TEST ALMOST ALWAYS COMPLETELY REVERSIBLE
  24. PRINCIPLES OF ABNORMAL CARDIAC CONDUCTION
    nL OCCURS IN PREDICTABLE AMOUNT OF TIME & MEASURED IN L-R DISTANCE

    • 4 COMMON TIME INTERVALS IN ECG
    • 1) P WAVE DURATION
    • 2) PR INTERVAL
    • 3) QRS DURATION
    • 4) QT INTERVAL

    PROLONGED IN ABN CONDUCTION
  25. PROLONGED P WAVE DURATION ON ECG
    INTRA-ATRIAL CONDUCTION ABN
  26. PROLONGED PR INTERVAL IN ECG
    AV BLOCK

    • 3 DEGREES
    • 1) PR CONSTANT DURATION PRODUCING QRS

    2) PR LONG OR nL AND CONSTANT OR VARIABLE, BUT SOME P FAIL TO GEN QRS

    • 3) PR DURATION VARIABLE AND NO P GENs QRS.
    • --PR DURATION RANDOM FROM BEAT TO BEAT.
    • --QRS GEN BY INTRINSIC VENT ACTIVITY OR LOWER AV NODE --> REGULAR DUR
  27. PROLONGED QRS DURATION ON ECG
    SLOW CONDUCTION THROUGH VENT

    LEFT BUNDLE BRANCH BLOCK

    RIGHT BUNDLE BRANCH BLOCK

    INTRAVENT CONDUCTION DELAY

    HYPERKALEMIA

    VENT ORIGIN BEAT

    WOLFF-PARKINSON-WHITE PATTERN OF VENT PRE-EXCITIATION
  28. PROLONGED QT INTERVAL ON ECG
    PROLONGED CELL ACTION POTENTIAL DUE TO ABN FUNC OF MYO CELL MEM ION CHAN POPULATION
  29. BRADYCARDIAS ON ECG
    1) IF LESS THAN 60 BPM w nL P AND QRS --> SINUS BRADYCARDIA

    2) IF ATRIAL RATE FASTER THAN VENT (p-p interval < r-r interval) --> AV BLOCK

    • 3) SLOW VENT RATE AND NO CLEAR P (abn sinus pacemaker) ORIGINATING IN:
    • *AV NODE --> JUNCTIONAL RHYTHM (narrow qrs)
    • *VENT --> VENTRICULAR RHYTHM (wide qrs)
  30. TACHYCARDIAS ON ECG
    >100 BPM

    1) SINUS TACHYCARDIA -- FAST ATRIAL RATE AND nL P & QRS

    2) FAST VENT RATE AND ABN P BEFORE EACH QRS THEN:

    *SUPRAVENT TACHY IF REGULAR RATE AND NARROW QRS

    *WIDE-COMPLEX-TACHY IF REGULAR RATE AND WIDE QRS > .12sec

    *ATRIAL FIBRILLATION IF IRREGULAR RATE
  31. LIMITS OF ECG IN CARDIOVASCULAR Dx
    1) NOT GOOD FOR MECHANICAL ABN

    2) NOT GOOD AND DETERMINING CHAMBER SIZE

    GOOD AT ACUTE ISCHEMIC PROBS w CHANGES IN REPOL (st seg and t wave)

    GOLD STANDARD FOR CONDUCTION ABN AND CARDIAC ARRHYTHMIAS
  32. S3 AND S4 IN CARDIAC CYCLE
    S3 -- END OF RAPID FILLING DURING VENT DIASTOLE -- AFTER S2

    S4 -- DURING ATRIAL CONTRACTION -- BEFORE S1

    CALLED GALLOPS, IF Pt TACHYCARDIC (>120 bpm) HARD TO HEAR AND CALLED SUMMATION GALLOPS
  33. S3 CHARACTERISTICS
    MAY BE nL IN KIDS, YOUNG ADULTS, PREGOs

    IMMEDIATELY AFTER S2 DURING RAPID FILLING (early diastole)

    • PATHOLOGIC STATES INVOLVING VOLUME LOAD ON VENTS:
    • --AORTIC/PULM REGURG
    • --DIALATED CARDIOMYOPATHY
    • --L-R SHUNTS (ASD AND VSD)
    • --PatDucArt

    LOCATION -- L OR R VENT

    LOW FREQUENCY -- USE BELL
  34. S4 CHARACTERISTICS
    ALWAYS PATHOLOGIC

    • TIMING -- JUST BEFORE S1
    • --ATRIAL CONTRACTION (late diastole)

    • ATRIUM CONTRACTING INTO NON-COMPLIANT VENT (stiff)
    • --SYSTEMIC OR PULM ARTERIAL HT
    • --ACUTE MYOCARDIAL INFARCTION
    • --HYPERTROPHIC CARDIOMYOPATHY
    • --AORTIC OR PULM VALVE STENOSIS
    • --DIALATED CARDIOMYOPATHY

    LOW FREQUENCY -- USE BELL
  35. SPLITTING OF S1
    USUALLY M1 BEFORE T1

    • EXAGERATED BY DELAYED T1
    • --RBBB
    • --EBSTEIN'S ANOMALY
  36. nL SPLITTING OF 2ND HRT SOUND
    NORMALLY, P2 ALWAYS AFTER A2

    DURING INSPIRATION:


    --FALL IN INTRATHORACIC PRESSURE

    --INC VENOUS RETURN TO RV AND DEC TO LV

    --LONGER RV EJECTION TIME -> GREATER SPLITTING

    DURING EXPIRATION: A2 AFTER P2

    --INC INTRATHORACIC PRESSURE

    --DEC VENOUS RETURN TO RV AND INC RETURN TO LV (bld "sponged from lungs")

    --LONGER LV EJECTION TIME -> LESS SPLITTING

    PATHOLOGICAL

    EARLY A2 -- MITRAL REGURGE

    DELAYED P2 -- RBBB, PULM HT, PULM VALVE STENOSIS
  37. PATHOLOGICAL SPLITTING OF 2ND HEART SOUND
    EARLY A2 -- MITRAL REGURGE (inc split)

    DELAYED P2 -- RBBB, PULM HT, PULM VALVE STENOSIS (inc split)

    DELAYED A2 -- LBBB, SYST ART HT, AORT VALVE STENOSIS, SEVERE LV FAILURE (dec split)

    EARLY P2 -- TRICUSPID REGURGE (dec split)
  38. FIXED SPLITTING OF S2
    ASD -- L-R SHUNT

    P2 LONGER THAN A2

    FIXED THROUGHOUT INSPIR AND EXPIR
  39. EJECTION CLICK
    ATTEMPTED OPENING OF STENOTIC AORT OR PULM VALVE

    OCCURS AFTER S1

    BEST HEARD OVER AORT/PULM AREAS
  40. OPENING SNAP
    ATTEMPTED OPENING OF STENOTIC MITRAL/TRICUSPID VALVE

    OCCURS AFTER S2

    BEST HEARD OVER MITRAL/TRICUSP AREA

    **EJECTION CLICK IS FROM AORT/PULM VALVE STENOSIS
  41. PERICARDIAL KNOCK
    ATTEMPTED FILLING OF VENT THAT HAS THICKENED PERICARDIUM -> DEC DIALATION

    OCCURS AFTER S2

    MID FREQUENCY

    BEST HEARD OVER APEX
  42. MURMUR CAUSES AND R-L EFFECT OF RESPIRATION
    VALVE STENOSIS

    VALVE REGURGE

    EXCESSIVE FLOW

    RIGHT SIDE MURMURS INC w RESPIRATION (CARVALLO'S SIGN)

    LEFT SIDE MURMURS NOT AFFECTED BY RESPIRATION
  43. MURMUR INTENSITY RATING
    1/6 BARELY AUDIBLE

    2/6 AUDIBLE

    3/6 LOUD

    4/6 LOUD w THRILL

    5/6 VERY LOUD w THRILL (heard w edge of steth)

    6/6 EXTREMELY LOUD w THRILL (heard w hovering steth)
  44. TYPES OF SYSTOLIC MURMURS AND THEIR TIMING / QUALITY
    • EJECTION
    • --AFTER S1 & BEFORE S2
    • --CRESCENDO/DECRESCENDO

    • PANSYSTOLIC/HOLOSYSTOLIC
    • --RIGHT AFTER S1 PAST S2
    • --CONSISTENT IN INTENSITY

    • MIDSYSTOLIC
    • --MID SYST AND INC 'TIL ENDING BEFORE S2
    • --CRESCENDO
  45. CAUSES OF SYSTOLIC EJECTION MURMUR
    • MAY BE nL "INNOCENT"
    • --SOFT
    • --DO NOT RADIATE

    VENT OUTFLOW OBSTRUCTION

    --VALVE STENOSIS w PLIABLE LEAFLETS (cong aort stenosis)

    --SEVERITY DETERMINED BY PEAK TIMING. MORE SEVERE IF LATER PEAK (loss of a2, delayed or dec carotid pulse)

    --POSS FOLLOWED BY OPENING CLICK

    --NO CLICK IF LEAFLETS SCLEROTIC & FIXED (rheumatic or calcif aort stenosis), OR SUB/SUPRA VALVE STENOSIS

    --RADIATE TOWARDS CAROTIDS, OR HRT APEX (GALLIVARDIN PHENOM)
  46. CAUSES OF PANSYSTOLIC / HOLOSYSTOLIC MURMURS (3)
    • MITRAL REGURGE
    • --HEARD AT APEX AND RADIATE TO AXILLA

    • TRICUSPID REGURGE
    • --HEARD OVER TRICUSP AREA
    • --INC DURING INSPIRATION

    • VSD
    • --HEARD BEST OVER LOWER LEFT STERNAL BORDER
    • --OFTEN w THRILL
  47. CAUSES OF MIDSYSTOLIC MURMURS
    • MITRAL VALVE PROLAPSE
    • --FLOPPY LEAFLETS
    • --AND/OR ELONGATED CHORDAE
  48. TYPES OF DIASTOLIC MURMURS AND THEIR TIMING AND QUALITY
    • EARLY
    • --BEGINS AT S2 AND ENDS BEFORE S1
    • --HIGH-PITCHED BLOWING
    • --DECRESCENDO MURMUR

    • MID
    • --SHORTLY AFTER S2
    • --SOFT
    • --LOW FREQ (bell)
    • --RUMBLING
    • --PRESYSTOLIC ATTENUATION
    • --POSS OPENING SNAP

    • PRESYSTOLIC
    • --ACCENTUATION BEFORE S1
    • --ATRIAL KICK
  49. CAUSES OF EARLY DIASTOLIC MURMURS
    • AORT/PULM REGURGE
    • --SEVERITY CORRELATED w DURATION
    • --SHORTER MORE SEVERE
    • --HEARD AT UPPER STERNAL BORDER
    • --MAY CAUSE PARTIAL CLOSE OF MITRAL WHICH MIMICS MITRAL STENOSIS -> RUMBLE "AUSTIN FLINT MURMUR"
  50. CAUSES OF MID DIASTOLIC MURMUR
    MITRAL STENOSIS
  51. CONTINUOUS MURMURS
    • CAUSES
    • --ARTERIOVENOUS CONNECTION
    • --CORONARY ARTERIOVENOUS FISTULAE
    • --RUPTURED SINUS OF VALSALVA (aorta into ra or rv)
    • --PDA
    • --SURGICAL

    • TIMING AND QUALITY
    • --BEGIN DURING SYSTOLE AND CONTINUE INTO DIASTOLE
    • --MAY NOT PROGRESS THOUGH DIASTOLE
    • --CRESCENDO / DECRESCENDO
  52. SEQUENCE OF ELECTRICAL EXCITATION OF THE HEART
    • 1) SINO-ATRIAL NODE
    • --R TO L ATRIA; INFERIORLY

    2) ATRIAL MUSCLE DEPOL

    • 3) AV NODE
    • --SLOW

    • 4) BUNDLE OF HIS
    • --RAPID PURKINJE
    • --ENDOCARDIUM

    5) BUNDLE BRANCHES

    • 6) VENTRICULAR DEPOL
    • --ENDO TO EPICARDIUM
  53. ORDER OF THE 4 MAJOR DIVISIONS OF THE CARDIAC CYCLE
    • SYSTOLE
    • --ISOVOLUMIC CONTRACTION
    • --VENTRICULAR EJECTION

    • DIASTOLE
    • --ISOVOLUMIC RELAXATION
    • --VENTRICULAR FILLING
  54. 9 CONDITIONS THAT MAY LIMIT CARDIAC OUTPUT
    1) SLOW HR

    2) INTRAVASCULAR VOL DEPLETION

    • 3) PERICARDIAL CONSTRAINT
    • --PERICARDIAL EFFUSION w/ TAMPONADE

    4) STIFF VENTRICULAR CHAMBERS

    5) OBSTRUCTION TO VENTRICULAR FLOW

    6) INADEQUATE TIME FOR VENTRICULAR FILLING

    7) POOR CARDIAC MYOCYTE FUNCTION

    • 8) EXCESSIVE PRESSURE LOAD OF VENTRICULAR CHAMBER
    • --HT OR SEMILUNAR STENOSIS

    • 9) INEFFECTIVE FLOW
    • --VALVE REGURGE, SHUNTS
  55. DEFINE SYSTEMIC VASCULAR RESISTANCE AND HOW CALCULATED
    PRESSURE IN THE ARTERIES

    • nL SVR
    • --15 mmHg/liter/min OR WOODS UNITS
    • --WOODS x 80 FOR DYNES-SEC-cm-5

    SVR = (MAP-CVP)/CO woods

    x80 FOR DYNES

    ELEVATION INDICATES SYSTEMIC ARTERIAL VASOCONSTRICTION
  56. DEFINE PULMONARY VASCULAR RESISTANCE AND HOW CALCULATED
    (mPAP-LAP) / CO

    • nL:
    • 1 WOODS
    • 80 DYNES
  57. LEFT CORONARY ARTERY BRANCHES
    • LMCA
    • --ORIGINATES IN LEFT CORONARY CUSP OF AORTIC ROOT

    • LAD
    • --ANT INTERVENTRICULAR GROOVE
    • --SUPPLIES ANT 2/3 OF INTERVENT SEPTUM w SEPTAL BRANCHES
    • --SUPPLIES ANT FREE WALL OF LV w DIAGONAL BRANCHES

    • LCX
    • --LEFT ATRIOVENT GROOVE
    • --SUPPLY LAT AND POST LV w OBTUSE MARGINAL BRANCHES
    • --MAY SUPPLY PDA
  58. RIGHT CORONARY ARTERY BRANCHES
    • RCA
    • --ORIGINATES IN RIGHT CUSP OF AORTIC ROOT
    • --SUPPLY RV w RV BRANCH

    • PDA (MAY BE FROM LCX)
    • --POST INTERVENT SEPTUM
    • --SUPPLY POST 1/3 OF INTERVENT SEPTUM
  59. CORONARY BLOOD SUPPLY TO THE CARDIAC CONDUCTION SYSTEM
    • SA NODE
    • --EITHER RCA 55%
    • --OR LCX 45%

    • AV NODE
    • --EITHER RCA 90%
    • --LCX 10%

    • HIS BUNDLE
    • --LAD SEPTAL BRANCHES
  60. PHASES OF CARDIAC ACTION POTENTIAL
    0 -- RAPID Na INTO CELL

    1 -- BRIEF MINOR REPOL

    2 -- PLATEAU

    3 -- MAJOR REPOL

    4 -- RESTING

    AP LASTS ~200 msec
  61. DEFINITION OF SHOCK
    GENERALIZED REDUCTION OF TISSUE PERF THAT MAY BE DUE TO VARIOUS ETIOLOGIES
  62. SYMPTOMS OF SHOCK
    SKIN -- COLD, CLAMMY

    BRAIN -- MILD RESTLESSNESS -> AGGITATION -> OBTUNDED -> LOSS OF CONSCIOUSNESS

    KIDNEY -- DEC URINE OUTPUT
  63. SIGNS OF SHOCK
    VITAL -- HYPOTENSION, TACHYCARDIA

    SKIN -- COLD, CLAMMY, PALLOR, CYANOSIS

    PULM -- TACHYPNEIC to compensate for metabolic acidosis

    HEART -- TACHYCARDIC
  64. LAB RESULTS FOR SHOCK
    LIVER -- INC AST, ALT, GGT

    KIDNEY -- INC BUN, CREATININE

    HEART -- INC TROPONIN, CREATINE KINASE

    MUSCLE/ORGANS -- LACTIC ACIDOSIS, COMPENSATORY RESP ALK
  65. TYPES OF SHOCK
    • HYPOVOLEMIC
    • --HEM, GI, DIURETIC, 3RD SPACING

    • CARDIOGENIC
    • --ACUTE MI
    • --CHF

    • DISTRIBUTIVE (profound arterial dilation)
    • --SEPSIS
    • --NEUROGENIC
    • --ANAPHYLAXIS allergen
  66. TREATMENT FOR SHOCK
    IMMEDIATE Tx OF UNDERLYING CAUSE

    HEMORRHAGIC -- TRANSFUSION

    PURE VOL DEPLETION -- IV FLUIDS

    CARDIAGENIC -- INOTROPIC DRUGS, VASODILATORS, HEART ASSIST DEVICE, TRANSPLANT

    MYOCARDIAL ISCHEMIA -- RESTORE BLD FLOW

    SEPTIC SHOCK -- SUPPORTIVE & ANTIBIOTICS

    ANAPHYLACTIC -- ANTI-INFLAM, FLUIDS, VASOPRESSORS
  67. RISK FACTORS FOR DEVELOPMENT OF ATHEROSCLEROSIS
    • CONSTITUTIONAL
    • --INC AGE (>40)
    • --MALES AND POST-MENOPAUSAL WOMEN
    • --FAM HIST, SINGLE GENE AND MULTIFOCAL

    • MODIFIABLE
    • --HYPERLIPIDEMIA / CHOLESTEROLEMIA
    • (ELEV LDL, LOW HDL)
    • --HT
    • --SMOKING
    • --DM

    OTHERS
  68. ECG INDICATIONS OF RIGHT AND LEFT ATRIAL ENLARGEMENT
    • LAE
    • --INC LEFTWARD AND POSTERIOR DIRECTION
    • --P WAVE DURATION INC, OFTEN w NOTCH SEEN IN LEAD II

    • RAE
    • --INC INFERIOR AND SLIGHTLY RIGHTWARD AND ANT DIRECTION
    • --P WAVE ALL AND PEAKED IN LEAD II
    • --TALL POS DEFLECTION IN V1
    • --ATRIAL DEPOL USUALLY NOT PROLONGED
  69. ECG INDICATIONS FOR LEFT/RIGHT VENTRICULAR HYPERTROPHY
    • LVH
    • --INC LEFT, INF, POST
    • --LARGE S WAVE IN V1
    • --LARGE R IN I, aVL, V5-V6
    • --OFTEN ASSOC w LAE
    • --ST SEG OFTEN ABN; DIR OPOSITE OF QRS

    • RVH
    • --INC RIGHT, INF, ANT
    • --LARGE R WAVE IN V1
    • --LARGE S IN LEAD I AND V5-V6
    • --POSS ASSOC w RAE
  70. DIFFERENCE IN PATTERN OF HYPERTROPHY BETWEEN PRESSURE-OVERLOADED AND VOLUME-OVERLOADED CONDITIONS
    • PRESSURE
    • --CONCENTRIC INC
    • --NEW SARCOMERES ADDED IN PARALLEL
    • --INC CROSS-SECTIONAL AREA

    • VOLUME
    • --VENTRICULAR DILATION
    • --NEW SARCOMERES ADDED IN SERIES
    • --LV THICKNESS MAY BE MORE/LESS THAN nL

    INC WEIGHT IS INDICATOR OF HYPERTROPHY

    IN PATH HYPERTROPHY ->NO COMPENS INC IN CAPILLARY DENSITY AS OPPOSED TO PHYSIOLOGIC HYPERTROPHY
  71. SYMPTOMS OF CHFABN VENOUS CONGESTION
    DYSPNEA ON EXERTION

    ORTHOPNEA

    PAROXYSMAL NOCTURNAL DYSPNEA

    EXERCISE INTOLERANCE

    FATIGUE AND WEAKNESS

    PERIPHERAL EDEMA

    PALPITATIONS
  72. NY HEART ASSOC CLASSIFICATION SCHEME FOR CHF
    I -- NO LIMITATIONS OF ACTIVITY

    II -- SYMPTS w ORDINARY ACTIVITY

    III -- SYMPTS w LESS THAN ORDINATY ACTIVITY

    IV -- SYMPTS AT REST

    RELATED TO MORTALITY
  73. NEUROHORMONAL RESPONSES TO HEART FAILURE
    • FLUID RETENTION
    • --ACT OF RAAS
    • --DEC GLOM FILT
    • --ACT OF SNS

    • LONG-TERM MALADAPTIVE EFFECTS
    • --Na AND H2O RETENSION --> CONGESTION

    --VASOCONSTRICTION --> PUMP DYSFUNC; INC ENERGY EXPENDITURE

    --SNS STIM --> INC ENERGY EXPENDITURE
  74. SYSTOLIC vs. DIASTOLIC HEART FAILURE
    • SYST
    • --IMPAIRED PUMP
    • --DEC EJECT FRAC
    • --DYSP, ORTHOP, PND

    • DIAST
    • --IMPAIRED FILLING
    • --STIFF VENT
    • --INC ATRIAL AND VENT FILLING PRESSURE
    • --VENOUS CONGESTION
    • --DEC OUTPUT
  75. AORTIC VALVE STENOSIS STATS
    ONE OF MOST COMMON VALVE Dz

    MOST COMMON FATAL VALVE Dz

    • 3 MAJOR Dzs
    • 1) CONGENITAL MALFORMATION
    • 2) RHEUMATIC Dz
    • 3) SENILE CALCIFIC DEGENERATIVE Dz

    DIFFER IN PATH, ONSET, AND SIGNS

    • >60 -- SENILE
    • <60 -- BICUSPID OR RHEUM
    • IN USA -- BICUSPID MOST LIKELY
  76. BICUSPID AORTIC VALVE
    AORTIC STENOSIS

    MOST COMMON ADULT CONGENITAL HRT Dz

    MOST COMMON ASSOC IS COARCTATION OF AORTA

    2-3% OF INFANTS

    2-3X MORE FREQ IN MALES
  77. RHEUMATIC Dz OF AORTIC VALVE
    AORTIC STENOSIS

    FUSED COMMISSURES w FIXED CENTRAL ORIFICE

    DECADES AFTER ACURE RHEUM FEVER

    STARTS IN MITRAL VALVE, SO IF AORTIC INVOLVED MUST ALSO HAVE MITRAL
  78. SENILE DEGENERATIVE CALCIFIC Dz
    AORTIC STENOSIS

    • NOT JUST DUE TO AGE -- RISK FACTORS SIMILAR TO ATHEROSCLEROSIS
    • --MEN, AGE, SMOKING, HYPERCHOL
  79. RARE CAUSES OF AORTIC STENOSIS
    INFECTIVE ENDOCARDITIS

    SLE

    • SUBVALVULAR
    • --25% OF Pts w HYPERTROPHIC CARDIOMYOPATHY

    • SUPRAVALVULAR
    • --WILLIAMS SYND, ELFIN FACIES
  80. SYMPTOMS OF AORTIC STENOSIS
    • CHF
    • ANGINA
    • SYNCOPE

    • LV HYPERTROPHY
    • PULM CONGESTION
    • CONCOMITANT CAD

    • SYSTOLIC MURMUR (cresc-decresc, later peak more severe)
    • PULSUS PARVUS ET TARDUS (small & late pulse)

    *ECG
  81. NATURAL HISTORY OF AORTIC STENOSIS
    • ONSET BETWEEN 50-80 yrs
    • --DOES REMARKABLY WELL BEFOREHAND

    THEN RAPIDLY DECLINES

    • AVG 5 yr SURVIVAL
    • --ANGINA 5 yrs
    • --SYNCOPE 3 yrs
    • --HF 2 yrs
  82. TREATMENT OF AORTIC STENOSIS
    IF ANGINA SYNCOPE CHF --> SURGERY

    MEDICAL THERAPY DOESN'T IMPROVE SURVIVAL

    Sx + SEVERE STENOSIS = SURGERY
  83. AORTIC REGURGITATION ETIOLOGIES
    VALVULAR OR ROOT PATHOLOGY

    • VALVE
    • --CONG
    • --RHEUM
    • --CALCIFIC
    • --ENDOCARDITIS
    • --TRAUMA

    • ROOT
    • --HT
    • --DISSECTION
    • --SYPHILIS
    • --MARFAN
    • --WHIPPLE'S INF
    • --SPONDYLOARTHROPATHIES
  84. AORTIC REGURGITATION HEMODYNAMICS
    • VOL OVERLOAD OF LV
    • --FILLED IN DIAST FROM LA & AORTA

    • LV DIALATION
    • --INC DIAST PRESSURE IN LV & LA
    • --CHF & ANGINA
  85. AORTIC REGURGITATION PHYSICAL SIGNS
    • WIDE PULSE PRESSURES (200/40)
    • --STRONG, WATER-HAMMER
    • --BOBBING, HEAD UVULA NAIL-CAPILLARIES

    • AUSTIN FLINT MURMUR
    • --REGURGE CAUSES EARLY CLOSURE OF MITRAL

    PMI DISPLACED LAT due to LV DILATION

    • MURMUR
    • --EARLY DIAST HIGH-PITCH
    • --MUST LEAN FORWARD & EXHALE TO HEAR
  86. AORTIC REGURGITATION NATURAL HISTORY
    LONG ASYMPT PERIOD

    DEC LV SYST FUNC (low ejec frac)

    • INITIALLY
    • --INC LV-EDV
    • --nL FUNC & EF due to FRANK STARLING

    • CHRON
    • --IMPAIRED SYST FUNC
    • --EF FALLS
    • --LV-EDV INC
    • --CHF
  87. Tx OF AORTIC REGURGITATION
    • MEDICAL
    • --DRUGS THAT DEC AORT PRESSURE (nifedipine dec afterload)
    • --DELAYS NEED FOR SURGERY

    • SURGERY
    • --CHF --> VALVE REPLACEMENT
    • --ASYMPT Pt w CHRON SEVERE AR AND DEC LV FUNC (EF <.55, OR LV-EDV >5.5cm)
  88. ACUTE AORTIC REGURGITATION
    2NDARY TO TRAUMA, INF, DISSECTION

    URGENT SURGERY

    LV DOESNT HAVE TIME TO DILATE

    ACUTE INC IN LV PRESSURE --> PULM EDEMA --> MASSIVE PULM EDEMA & DEATH

    WIDE PULSE PRESSURES ABSENT
  89. NORMAL ANAT OF MITRAL VALVE
    ANNULUS

    ANT & POST LEAFLETS

    CHORDAE TENDINEAE

    PAPILLARY MUSCs

    LV WALL
  90. MITRAL VALVE STENOSIS ETIOLOGY & PATHOPHYS
    MOST COMMONLY RESULTS FROM RHEUM HEART Dz

    FISH MOUTH

    FUSION OF LEAFLETS AT COMMISSURES, THICK SHORT CHORDAE, Ca DEPOT

    SEVERE STENOSIS @ <1cm, nL 4-6cm

    PROGRESSION CHRON & VARIABLE

    • INC LA PRESSURE DESPITE nL LV
    • --PULM CONG

    • LA DILATION
    • --FIBRILLATION

    *USE ECHO
  91. PATHOPHYSIOLOGY OF MITRAL REGURGITATION
    • PORTION OF LV OUTPUT BACK INTO LA
    • --INC LA PRESSURE AND DILATION
    • --INC LV DIASTOLIC VOL LOAD

    • LV EF SUPRA-nL (80-90%)
    • --FRANK STARLING
    • --OUTPUT TO LA & AORTA

    • ACUTE MR
    • --ACUTE PULM EDEMA

    • CHRON
    • --LA then LV DILATION
    • --DEC LV FUNC
    • --CHF

    HOLOSYSTOLIC MURMUR

    • *USE ECHO
    • --EF DEC TO 60%
  92. SURGICAL MANAGEMENT OF MITRAL REGURGITATION
    ACUTE -- AGGRESSIVE INTERVENTION

    • CHRON
    • --TIMING IMPORTANT
    • --LV-ESD >4.5cm
    • --EF <.65

    REPAIR IS FAVORABLE TO REPLACE
  93. MITRAL VALVE PROLAPSE
    FLOPPY VALVE SYND or BARLOW'S SYND

    COMMON -- 2% OF POP AND USUALLY ASYMPT FEM

    LEAFLETS BALLOONING & REDUNDANT

    CHORDAE ELONGATED

    • MYXOMATOUS DEGENERATION
    • --COLLAGEN DISSOLUTION -> EXCESS MUCOPOLYSACCHARIDES IN MID SPONGIOSA LAYER OF VALVE
    • --STRETCHING OF LEAFLETS & CHORD TEND
    • --GENETIC ABN FIBRILLIN, ELASTIC, COLL I&II

    • AUTOSOMAL DOMINANT
    • --ASSOC w MARFAN, EHLOR-DANLOS

    MID SYSTOLIC CLICK AND LATE SYST MURMUR

    *USE ECHO
  94. MITRAL VALVE PROLAPSE Tx
    • SURGERY
    • --MILD -- FOLLOW-UP ONLY
    • --SEVERE --CHF Sx, DEC LV FUNC

    REPAIR RATHER THAN REPLACE RECOMMENDED
  95. WHEN TO USE ECG vs. CXR
    ECG -- ONGOING CHEST PAIN OR WITH DISTURBANCES IN HRT RHYTHM

    CXR -- DYSPNEA, SOB, AND EXERCISE INTOLERANCE (think pulm probs)
  96. 2 INDICATIONS FOR ORDERING CARDIO STRESS TEST
    Dx ISCH HRT Dz

    STRATIFY MORTALITY RISK IN Pts w KNOWN ISCH Dz

    ASSESS FUNC CAPACITY

    OCCATIONALLY ASSESSS ARRHYTHMIAS
  97. CORONARY ANGIOGRAPHY vs. STRESS TEST
    • ANGIO -- MOST DEFINITIVE Dx IN MANY Dz & NEC BEFORE ART REVASC
    • --DISADVANTAGES
    • COST
    • RAD
    • DISCOMFORT
    • --RISKS
    • VASC INJ
    • ALLERGIC REACTION
    • ARRHYTHMIAS
    • MI OR STROKE

    USE FOR ACUTE MI OR REFRACTORY ISCH
  98. ELECTROPHYSIOLOGIC TESTING
    INVASIVE -- REQ CATH

    • INTRACARDIAC ELECTs PLACED ON HRT
    • --ACT RECORDED
    • --HRT STIMed BY TEMP PACING TO STRESS ELEC SYSTEM TO CAUSE AN ARRYTH OR COND ABN

    • INDICATIONS
    • --RECURRENT SYNCOPY OR UNCERTAIN CAUSE
    • --DETERMINE MECH OF OTHER TACHYs
  99. CABG vs. PCI
    • CABG
    • --BETTER OVERALL RESULTS IN DIABETES, MULTI CAD, AND TOTAL OBST
    • --BUT, HIGHER PROCEDURAL MORTALITY AND MORB
  100. WHEN IS CARDIAC ELECTROPHYSIOLOGIC ABLATION HELPFUL?
    Tx FOR ARRHYTHMIAS

    DESTROY FAULTY COND TISSUE
  101. PATHOGENESIS OF INFECTIVE ENDOCARDITIS
    • MICROBIAL
    • EXTRACELL POLYSACCH PROMOTES ADHERENCE

    CAP TO INDUCE PLATELET AGG

    COMPLEMENT RESISTANCE

    • HOST
    • VALVE ABN
    • --MVP w MR MOST COMMON b/c HIGH prevalence
    • --1/4 w NO KNOWN CAUSE
    • --DEGEN CALC VALVE LESION IN ELDERLY
    • --CHD
    • --RHEM VALVE Dz
    • --PREVIOUS ENDOCARDITIS

    TRICUSPID MOST COMMON IN IV DRUG users

    MITRAL IN REST
  102. COMPLICATIONS OF ENDOCARDITIS
    • 1) CARDIAC FAILURE MOST SERIOUS
    • --TRICUSPID LESS COMMON & LESS SERIOUS bc LOW PRESSURE

    2) CONDUCTION DEFECTS AND MYOCARDIAL RUPTURE

    3) DIFFUSE CARDIOMYOPATHY

    4) SEPTIC EMBOLI

    5) MYCOTIC ANEURYSM

    6) METASTATIC INF

    7) RENAL FAILURE
  103. COMMON PATHOGENS CAUSING ENDOCARDITIS
    • STAPH AUREUS MOST COMMON
    • --esp iv

    VIRIDANS STREP

    • S. EPIDERMIDIS (COAG NEG STAPH)
    • --MOST COMMON IN PROSTH VALVE w HEALTH-CARE ASSOC ENDOCARDITIS

    • "CULTURE NEG ENDOCARDITIS"
    • --CLINICAL & ECHO SIGNS BUT NEG BLD TEST
    • --MOST COMMON IN PREV ANTIBIOTIC USE
    • --FASTIDIOUS BUGS & OBLIGATE INTRACELL (chlam, coxiella) & FUNGI
  104. HOW ARE BLOOD CULTURES AND ECHOs USED APPROPRIATELY TO WORKUP ENDOCARDITIS
    • CULTURES
    • --AT LEAST 3 FROM SEPARATE SITES DRAWN AT LEAST 30mins APART

    • ECHO
    • --TTE ONLY 50% SENSITIVITY, SO CANNOT EXCLUDE
    • --TEE 90% SENSITIVE BUT INVASIVE
  105. GENERAL PRINCIPLES FOR ENDOCARDITIS THERAPY
    4-6 WEEK PARENTERAL ADMIN OF DRUGS

    • COMBO DRUGS FOR SYNERGISM
    • --ENTEROCOCCUS
    • --R. STREP
    • --PSEUDO etc

    • VALVE REPLACEMENT SURGERY
    • --REFRACTORY CHF MOST COMMON INDICATION
    • --UNRESPONSIVE INF
    • --EXT OF INF INTO PERIVALVULAR OR SEPTAL ABSCESS
    • --MULTIPLE EMBOLIC EVENTS
  106. SKIN MANIFESTATIONS OF ENDOCARDITIS
    • OSLER'S NODES
    • --"OUCHler's"
    • --PADS OF FINGERS/TOES
    • --SMALL, PAINFUL

    • JANEWAY LESIONS
    • --PAINLESS BLANCHING MACULES
    • --PALMS & SOLES

    • PETECHIAE
    • --RED PINPOINT NON-BLANCHING LESIONS
    • --BUCAL MUCOSA, PALATE, CONJUNCTIVE, OR EXTREMITIES
    • --MOST COMMON BUT NONSPEC

    • SPLINTER HEMMHOR
    • --RED STREAKS IN FINGERNAIL/TOE
    • --NONBLANCHING

    • RETINAL LESIONS
    • --ROTH SPOTS
    • --OVAL PALE
    • --SURROUNDED BY HEMORR
    • --NEAR OPTIC DISK
    • --RARE
  107. MODIFIED DUKE CRITERIA FOR Dx IE
    • CLINICAL
    • 2 MAJOR or
    • 1 MAJOR AND 3 MINOR or
    • 5 MINOR

    • POSSIBLE
    • 1 MAJOR AND 1 MINOR or
    • 3 MINOR

    • MAJOR
    • --POS BLD CULTURE OF TYPICAL BUG FROM 2 SEPARATE CULTURES
    • --EVIDENCE ON ECHO

    • MINOR
    • --PREDISPOSING HRT Dz OR IV DRUG USE
    • --TEMP >38/100.4
    • --VASC FINDINGS: EMBOLI, INFARCTs, ANEURYSM, JANEWAY
    • --IMMUNO: GLOM NEPH, OSLER'S, ROTH, Rh FACTOR
    • --MICROBIOLOGICAL EVIDENCE: POS BLD CULTURE NOT MEETING MAJ CRIT OR SERO ACTIVE INF w BUG CONSISTENT w IE
  108. STABLE ANGINA PECTORIS
    SQUEEZING PRESSURE-LIKE RETROSTERNAL CHEST PAIN

    • REPRUDUCIBLY INDUCED BY ACTIVITIES
    • --EXERCISE
    • --EMOTIONAL EXCITEMENT
    • --LARGE MEAL
    • --SMOKING

    OFTEN RADIATES TO LEFT AXILLA, SHOULDER, JAW, LEFT ARM

    RELIEVED BY REST
  109. THE 3 FETAL SHUNTS
    • DV
    • --UMBILICAL VEIN HAS HIGHEST O2
    • --1/2 BLD BYPASSES LIVER BY DV
    • --EMPTIES INTO IVC SO IVC HAS HIGHEST O2 CONC
    • --PASSIVELY COLLAPSE AT CLAMPING AND FULLY CLOSED AFTER 3 wks

    • FO
    • --MOST IVC BLD USES FO TO ENTER LA
    • --MOST SVC BLD GOES THRU TRI
    • --PASSIVELY CLOSES AT ~24hrs

    • DA
    • --90-92% OF COMBO BLD FROM VENTs ENTER SYSTEMIC CIRC w USE OF DA
    • --CLOSES AT 24 hrs
  110. LIST COMMON ACYANOTIC CONGENITAL CARDIAC MALFORMATIONS
    • OBSTRUCTIVE:
    • --PULM STENOSIS
    • --AORTIC STENOSIS
    • --COARCTATION OF AORTA

    • LEFT-TO-RIGHT SHUNTS
    • --VSD
    • --ASD
    • --PDA
  111. LIST THE 5 CYANOTIC CONGENITAL HEART Dzs
    ALL START w "T"

    • 1) TOF
    • 2) TGA
    • 3) TRICUSPID ATRESIA
    • 4) TAPVC
    • --TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION
    • 5) TA
    • --TRUNCUS ARTERIOSUS
  112. WHY IS TETROLOGY OF FALLOT CYANOTIC? HOW MANAGED?
    • VSD
    • --HOLE IN VS COMBINED w PULM STENOSIS --> INC PRESSURE IN RV --> RIGHT-TO-LEFT SHUNT
    • --OVERARCHING AORTA
    • --RVH

    CXR -- BOOT-SHAPED HRT, NOT SPECIFIC

    • NEED SURGERY
    • --CLOSURE OF VSD AND PS RELIEF
    • --IF ANAT UNFAV, ARTIFICIAL PDA FOLLOWED BY LATER TOTAL REPAIR
  113. WHY IS TGA CYANOTIC? HOW MANAGED?
    AORTA FROM RV AND PULOMARY FROM LV

    CIRCULATIONS IN PARALLEL RATHER THAN IN SERIES

    DIE IN EARLY INFANCY w/o SHUNTS

    • --PGE1 TO MAINTAIN PDA
    • --BALLOON ATRIAL SEPTOSTOMY IF F.O. RESTRICTIVE
    • --ARTERIAL SWITCH w REIMPLANT COR ARTERIES
  114. WHY IS TRICUSPID ATRESIA CYANOTIC? HOW MANAGED?
    NO DIRECT COMMUNICATION BETWEEN RA AND RV

    OBLIGATORY ASD

    CYANOSIS AFTER PDA CLOSES

    RV HYPOPLASTIC

    • --PGE1 FOR PDA
    • --SUBCLAV TO PULM ART (blalock-taussig)
    • --CONNECT SVC TO PULM ART (glen)
  115. PATHOPHYS OF ACUTE CORONARY SYNDROME
    PLAQUE RUPTURE (fibrous cap)

    PLATELETS ACTIVATED (collagen particularly activated)

    YOUNG IMMATURE PLAQUES ARE LIPID RICH --> PARTICULARLY VULNERABLE

    tPA AND PAI CONC DETERMINED GENETICALLY
  116. MORBIDITY AND MORTALITY OF ACUTE CORONARY SYNDROMES
    • LONG-TERM COMPLICATIONS
    • --ELECRICAL
    • --MECHANICAL

    HOSP MORTALITY IS 3-8%

    • SUBSEQUENT SURVIVAL DETERMINED BY:
    • --AGE
    • --LV SYSTOLIC FUNC
    • --EXTENT OF CAD
  117. HOW TO Dx UNSTABLE ANGINA AND non-ST SEG ELEVATION MI
    • ANGINA:
    • Sx OF ANGINA BUT NO EVIDENCE OF NECROSIS BY SERUM CONC OF TROPONIN OR CK-MB

    • non-ST:
    • NO ELEVATION ON ECG BUT ELEVATED SERUM TROPONIN AND CK-MB
  118. Tx OF ACUTE CORONARY SYNDROMES
    • ACUTE
    • --HOSPITALIZE
    • --CONTINUOUS ECG MONITORING
    • --PLATELET INHIBITOR (low-dose asp) and THROMBIN (heparin)
    • --DRUGS TO DEC MYOCARDIAL O2 DEMAND (b-blockers)
    • --IF ST-SEG ELEV, REPERFUSION THERAPY
    • --PRIMARY PCI
  119. TRUE AORTIC ANEURISM vs. PSEUDOANEURISM
    • TRUE
    • --LOCALIZED WIDENING OF AORTA OVER 50%
    • --PRESENTS w PAIN!
    • --LaPLACE T=(PxR)/2W

    • PSEUDO
    • --CONTAINED RUPTURE w OUTER ADVENTITIAL LAYER PREVENTING LEAKAGE
  120. ABDOMINAL AORTIC ANEURYSM
    MOST COMMON TYPE

    • ETIOLOGY ATHEROSCLEROSIS
    • --SMOKING

    USUALLY BELOW RENAL ARTERIES

    USUALLY ON LEFT SIDE

    • SCREEN USING ULTRASOUND
    • --MEN >60 WITH POS FAM HIST
    • --MEN 65-75 WHO EVER SMOKED
    • --NO WOMEN
  121. ASCENDING (thoracic) AORTIC ANEURYSM
    • USUALLY CONNECTIVE TISSUE DEFECT
    • --MARFANS (auto dom assoc w fibrillin-1 gene)

    • ABN ELASTIC AORTIC WALLS
    • --SMC SHOW DEGENERATION OR DROP-OUT "CYSTIC MEDIAL DEGENERATION"

    • DILATION OFTEN GREATEST NEAR HRT
    • --ANNULO-AORTIC ECTASIA (valve ring)
  122. AORTIC DISSECTION
    TEAR IN INTIMAL LAYER

    MEDIAL LAYER SUBJECT TO AORTIC PRESSURES

    BLD FLOWS ALONG MEDIAL LAYER (ante or retro) CREATING FALSE LUMEN

    BLD RE-ENTERS TRUE LUMEN THRU 2ND TEAR

    • PRESENTATION
    • --SUDDEN EXCRUCIATING CHEST PAIN
    • --MAX AT ONSET
    • --MAJOR EMERGENCY (mortality 1% per hr and 25% per day)
    • --POSS LOSS OF PULSE DUE TO EXTERNAL OBST

    • ASCENDING
    • --STANFORD CLASS A
    • --SURGERY PREFERRED
    • --COMPLICATIONS: aortic regurge, tamponade, mi

    • DESCENDING
    • --STANFORD CLASS B
    • --MEDICAL THERA PREFERRED (control bp)
    • --SURGERY IF FAIL
  123. 4 RISK FACTORS FOR PERIPH VASC Dz AND COMPARE w CAD
    VASOSPASMS

    • ATHEROSCLEROSIS (same as cad)
    • --HT, HYPERLIPID, POS FAM HIST, SMOKING DIABETES

    MORE SEVERE IMPACT OF SMOKING AND DIABETES ON PVD
  124. OBSTRUCTIVE PERIPH VASC Dz
    ACUTE VASC EMERGENCY

    • ATHEROSCLEROTIC LESION
    • --MOST LIKELY IF PRIOR CLAUDICATION Hx

    • EMBOLISM
    • --MOST LIKELY IF NO CLAUDICATION Hx
    • --FROM PROXIMAL AORTIC LESION
    • --CARDIAC THROMBOEMBOLISM: from la in afib or lv in prior myocardial infarction
    • --VEGITATION FROM ENDOCARDITIS
    • --CARDIAC TUMOR SEGMENT esp myxoma
    • --PARADOXICAL EMBOLISM in pt w asd or patent f.o.

    • CLINICAL PRESENTATION
    • --5 P's and a C
    • PAIN
    • PALLOR
    • PARALYSIS
    • PARESTHESIA
    • PULSELESSNESS
    • COOLNESS
  125. ANKLE/BRACHIAL INDEX (ABI) IN CLASSIFICATION OF PERIPH VASC OBSTRUCTION
    ANKLE SYSTOLIC PRESSURE / HIGHER OF 2 BRACHIAL PRESSURES

    > 1.3 IS NON-COMPRESSIBLE (prob calcified)

    1-1.29 nL

    .91-.99 EQUIVOCAL nL

    < .41 SEVERE Dz
  126. 4 VASCULITIC SYNDROMES
    • 1) TAKAYASU'S ARTERITIS
    • --PULSELESS Dz
    • --GRANULOMAS IN LRG ARTS
    • --YOUNG WOMEN esp asians

    • 2) TEMPORAL
    • --GIANT CELL
    • --IMMUNE MEDIATED
    • --OLDER MEN
    • --40% w POLYMYALGIA RHEUMATICA

    • 3) THROMBOANGIITIS OBLITERANS
    • --AFFECTS ART, VEIN, & NERVE
    • --HEAVY TOBACCO ADDICTION
    • --MEN <45
    • --INTRAMURAL THROMBI

    • 4) REYNAUD'S SYND
    • --VASOSPASM RELADED TO COLD TEMPS
  127. 3 PRESENTATIONS OF VENOUS Dz
    VARICOSE VEINS

    • VENOUS SKIN ULCERATION
    • --MEDIAL MALLEOLUS OF ANKLE

    LEG HEAVINESS

    PALPABLE CORD
  128. ABNORMAL FINDINGS IN PREGNANCY
    DYSPNEA THAT INH ADL

    ORTHOPNEA: prog or severe

    PND

    HEMOPTYSIS

    SYNCOPE

    CHEST PAIN

    JVP INC BEFORE 20 wks

    CYANOSIS, CLUBBING

    PULM RALES
  129. 4 MAJOR FACTORS IN REGULATION OF BLOOD PRESSURE
    HEART

    VASCULAR SYSTEM

    INTERACTION OF HEART AND VESSELS

    KIDNEY

    ENDOCRINE

    PRESSURE REGULATED TO A SET POINT -- ABN IN HT
  130. CLASSIFICATIONS OF BLOOD PRESSURE DEFINED BY SEVENTH JOINT NATIONAL COMMISION ON BP (JNC-7)
    AVG OF BP RESULTS OVER 2 VISITS NEEDED FOR Dx

    nL -- <120 SYST and <80 diast

    PRE-HT -- 120-139 syst or 80-89 diast

    STAGE 1 -- 140-159 syst or 90-99 diast

    STAGE 2 -- >160 syst or >100 diast

    IF SYST AND DIAST IN DIFF STAGES -- USE HIGHER
  131. 4 CLINICAL FACTORS THAT INC RISK FOR DEV ESSENTIAL HT
    OVERWEIGHT

    SEDENTARY

    EXCESS DIETARY Na

    LOW DIETARY K

    EXCESS ALC

    DIABETES
  132. VASCULAR PATHOLOGY OF SYSTEMIC HT
    INC ATHEROGENESIS

    DEGENERATIVE CHANGES IN MED LGR ARTS

    • HYALINE ARTERIOLOSCLEROSIS
    • --PLASMA PROT LEAKAGE
    • --INC MATRIX SYNTH
    • --NEPHROSCLEROSIS

    • HYPERPLASTIC ARTERIOLOSCLEROSIS
    • --SEVERE HT
    • --ONION SKINNING
    • --THICKENED SMC; REDUPLICATION OF BM
    • --FIBRINOID DEPOTS; NECROT ART esp in kidney
  133. PATHOLOGY OF SYSTEMIC (left-sided) HYPERTENSIVE HEART Dz
    HYPERTROPHY w NO INC IN CAPILLARY PERF

    • MORPHOLOGY
    • --LV HYPERTROPHY wo DILATION
    • --MAY BECOME STIFF
    • --PARALLEL THICKENING
  134. PATHOLOGY OF PULMONARY (right-sided) HYPERTENSIVE HEART Dz
    • CORPULMONALE -- ISOLATED RT SIDE PULM HHD
    • --PULM HT
    • --ACUTE OR CHRON (embolism vs. parench dz)

    • MORPHOLOGY
    • ACUTE
    • --DILATION OF RV wo HYPERTROPHY
    • --OVOID rather than CRESCENT
    • CHRON
    • --RV WALL THICK
    • --THICKENING OF OUTFLOW TRACT OR MODERATOR BAND
    • --STOCHASTIC MYOCYTE ARRANGEMENT
    • --ABSENT TRANSMURAL FAT
  135. 5 CONDITIONS WORSENED BY HT
    ARTERIES

    EYE

    KIDNEY

    HEART

    CNS -- HT MOST IMP FACTOR IN RISK OF ARTERY RUPTURE
  136. 4 CAUSES OF 2NDARY HT
    • CHRON RENAL PARENCHYMAL Dz
    • --PROTEINURIA
    • --GFR < 60

    • RENAL ARTERY STENOSIS
    • --USUALLY ATHEROSCLEROSIS

    • ADRENAL ABN
    • --HYPERALDO MOST COMMON (conn's)
    • --CUSHINGS inc acth
    • --PHEOCHROMOCYTOMA

    • COARCTATION
    • --PRESSURE DROP ACROSS COARCH
    • --INC RENIN
    • --LEG PULSES WEAKER THAN ARM
  137. NON-PHARMACOLOGIC Tx OF HT
    THERAPEUTIC LIFESTYLE CHANGE
  138. GENERAL vs. DIABETIC IDEAL BP
    GENERAL <140/90

    DIABETIC <130/80
  139. LIST THE 3 TYPES OF CARDIOMYOPATHY
    DIALATED (congestive)

    HYPERTROPHIC

    RESTRICTIVE
  140. DIALATED (congestive) CARDIOMYOPATHY PRESENTATION AND FINDINGS ON PHYSICAL EXAM
    IMPAIRED SYSTOLIC FUNC AND DILATION

    • PRESENTATION
    • LH FAILURE
    • --DOE 86%, PND, ORTHOPNEA, SOB

    • RH FAILURE
    • --PEDAL EDEMA 30%, ANOREXIA, NAUSEA, INC ABDOM GIRTH

    • LOW OUTPUT STATE
    • --FATIGUE, EXERTIONAL DYSPNEA

    • PHYSICAL EXAM
    • --TACHY, NARROW PULSE PRESSURE
    • --JVD
    • --PLEURAL EFFUSIONS
    • --LAT DISPLACED PMI, S3, MR and/or TR, Rt Hrt FAIL ABSENT IN 50%
    • --ENLRG LIVER, ASCITES, PITTING EDEMA
    • OFTEN IDIOPATHIC
    • --ETHANOL MOST COMMON IN WEST
    • --CHAGAS IN SOUTH/CENTRAL AMERICA (protoxoa trypanosuma cruzi)

    • COMPLICATIONS
    • --TACHYARRHYTHMIAS
    • --HRT BLOCK (stretched condiction system)
    • --STOKES ADAMS (SYNCOPE)
    • --CNS and/or PULM EMBOLISM
  141. DIALATED (congestive) CARDIOMYOPATHY CLINICAL COURSE AND PROGNOSIS
    50% CHANCE OF BEING ALIVE 5 yrs LATER

    • LV DYSFUNCTION IS PROGRESSIVE
    • --SEVERE CASES 50% CHANCE OF BEING ALIVE 1 yr LATER
    • --GOOD PROGNOSIS IF ETIOLOGY IDed (hypothyroid, pheo etc)

    • LV EF NOT RELIABLE FOR PROGNOSIS
    • --O2 CONSUMPTION BEST PREDICTOR (at peak excersize)
    • --NYHA CLASS
    • --HEMODYNAMIC DERANGEMENT

    • 40% DEATHS OCCUR SUDDENLY
    • --VENT ARRHYTHMIA MOST COMMON
    • --PROG HRT FAIL AND THROMB TO PULM OR SYSTEMIC CIRC
  142. ETIOLOGIES OF DIALTED (congestive) CARDIOMYOPATHY
    MOST IDIOPATHIC

    • H&P AND OCCASIONALLY BLD/URINE ANALYSIS
    • ---------------------

    • INFECTIONS
    • --VIRAL COXACKIE, CMV, HIV
    • --BAC DIPTHERIA, GAS
    • --CHAGAS

    • TOXINS
    • --ETHANOL
    • --MEDICATIONS

    • METABOLIC
    • --NUTRITION THIAMINE, VIT C, NIACIN
    • --ENDOCRINE HYPOTHYROID, PHEO

    • INFLAM
    • --PERIPARTUM CARDIOMYOPATHY
    • --COLLAGEN VASC Dz SLE, SARCOID,

    • INHERITED
    • --20% HAVE PRIMARY RELATIVE
  143. DEFINITION AND TYPES OF HYPERTROPHIC CARDIOMYOPATHY
    INC LV THICKNESS IN ABSENCE OF APPARENT ETIOLOGY

    nL SYSTOLIC FUNC BUT DIASTOLIC SEVERELY IMPAIRED

    • TYPES
    • --MOST CONCENTRIC DIFFUSE
    • --25% Pts ASYMETRIC and are:
    • ----OBSTRUCTIVE (25%) OR NONOBST (75%)

    • OBSTRUCTION CAUSES
    • --"ASH AND SAM"
    • --ASYMMETRIC SEPTAL HYPERT
    • --SYSTOLIC ANTERIOR MOTION of mv
    • --SYSTOLIC MURMUR
    • ----INC DURING VALSALVA & NITRATES (lv cavity dec)
    • ----DEC DURING SQUATTING, HANDGRIP, b-BLOCKER (lv cavity inc)

    "THE SMALLER THE CHAMBER SIZE, THE GREATER THE OBSTRUCTION"
  144. HYPERTROPHIC CARDIOMYOPATHY PRESENTATION AND FINDINGS ON PHYSICAL EXAM
    • PRESENTATION
    • --ASYMPT 10-15%
    • --PULM CONG/DYSPNEA 90%
    • --CHEST PAIN 75%
    • --SYNCOPE due to arrythmias and/or dec co
    • --SUDDEN DEATH (often w sports/exercise)

    • PHYSICAL EXAM
    • --BRISK CAROTID PULSE w bisfiriens (obst form)
    • --RALES
    • --LAT & FORCEFULL PMI, SYSTOLIC THRILL & MURMUR, S4

    DISTINGUISH FROM SYSTOLIC MURMUR OF AORTIC STENOSIS (same crescendo-decrescendo) WHICH RADIATES TO CAROTIDS AND HAS EJECTION CLICK
  145. HYPERTROPHIC CARDIOMYOPATHY CLINICAL COURSE AND PROGNOSIS
    • CLINICAL COURSE
    • --VARIED
    • --Sx STABLE OR ABSENT IN MANY Pts
    • --SEVERITY INC w AGE:
    • *WORSENING HYPERT
    • *PROG TO DIALATED MYOPATHY
    • *WORSE MR
    • *A.FIB
    • *INF ENDOCARDITIS
    • --SUDDEN DEATH INCIDENCE 1-3% and inc w hx of syncope, family hx, vent arryth, athletes. risk not related to presence of outflow obstruction

    ANNUAL MORTALITY HIGHER IN CHILDREN 6% vs. ADULTS 3%
  146. RESTRICTIVE CARDIOMYOPATHY DEFINITION AND ETIOLOGIES
    LEAST COMMON OF 3 TYPES (dialated and hypertrophic)

    INFILTRATION OF MYOCARDIUM LEADING TO EXCESSIVE STIFFNESS OF RV AND LV w MARKED IMPAIRMENT OF DIASTOLIC FILLING

    nL VENT SYSTOLIC FUNC AND WALL THICK KEY DIFFERENCES FROM OTHER 2 TYPES

    • ETIOLOGIES
    • --AMYLOIDOSIS
    • --HEMOCHROMATOSIS
    • --SARCOIDOSIS
    • --EOSINOPHILS (in tropic & temperate regions)
    • --CARCINOID TUMORS OF LIVER secrete vasoactive agent that fibroses the right hrt
    • --GENETIC
    • --IDIOPATHIC

    AMYLOID AND SARCOID MAY ALSO CAUSE DIALATED MYOPATHY
  147. RESTRICTIVE CARDIOMYOPATHY SYMPTOMS AND FINDINGS ON CLINICAL EXAM
    • Sx
    • PREDOM RIGHT SIDED HRT
    • --ABDOM GIRTH INC
    • --RUQ PAIN (LIVER CONG)
    • --NAUSEA, ANOREXIA
    • --PEDAL EDEMA
    • LOW OUTPUR STATE
    • --FATIGUE w EXERTION
    • --DOE

    • PHYSICAL EXAM
    • --TACHY, NARROW PULSE PRESSURE
    • --INSP INC IN JVD (kussmaul)
    • -- +/- PLEURAL EFFUSION
    • --RT-SIDED S3 & S4 mitral or tri regurge
    • --ASCITIES, PERIPH EDEMA

    • LOFFLER'S ENDOCARDITIS
    • --FIBROSIS OF AV VALVE AND SUBVALVE

    • CARCINOID HRT Dz
    • --THICK PULM VALVE STENOSIS

    ECHO AND ENDOCARDIAL BIOPSY EXTREMELY HELPFUL
  148. RESTRICTIVE MYOCARDITIS PROGNOSIS AND COMPLICATIONS
    • PROGNOSIS
    • --EXTREMELY POOR
    • --MOST DIE wi 1-2 yrs from rt hrt fail

    • COMPLICATIONS
    • --A.FIB
    • --VENT ARRHYTH
    • --DIGOXIN BINDS TO AMYLOID FIBRILS IN HRT CAUSING TOX AT LOWER CONC
    • --RESEMBLES CHRON CONSTRICTIVE PERICARDITIS
  149. ACUTE PERICARDITIS ETIOLOGIES AND PRESENTATIONS
    • DEFINITION: INFLAM OF THE PERICARDIUM
    • --w or wo EFFUSION

    • CAUSES
    • --IDIOPATHIC most common
    • --ACUTE MI
    • --INFECTION
    • --TRAUMA
    • --TUMOR
    • --IRRADIATION
    • --UREMIA
    • --CARDIAC SURGERY
    • --MEDICATIONS
    • --CONNECTIVE TISSUE Dz

    • PRESENTATIONS
    • --RETROSTERNAL CHEST PAIN worsened by deep insp and lying supine
    • --DYSPNEA
    • --COUGH
    • --HOARSENESS
    • --DYSPHAGIA
    • (compression of bronchi, recurrent laryngeal nerve, and esoph)

    • PHYSICAL EXAM
    • --PERICARDIAL FRIC RUB

    • EKG
    • --DIFFUSE ST SEG ELEV & PR SEG DEPRESSION
  150. ACUTE PERICARDITIS COURSE AND COMPLICATIONS
    • MUST ID UNDERLYING Dz PROCESS
    • --REMEDIATED IN DAYS/WEEKS IF FOUND

    • COMPLICATIONS
    • --RECURRENT PERICARDITIS 10-40%
    • --TAMPONADE
    • --CONSTRICTIVE PERICARDITIS

    IDIOPATHIC RESPONDS TO NSAIDS

    • SIGNS OF TAMPONADE
    • --DEC BP
    • --NARROWED PULSE PRESSURE
    • --TACHY
    • --INC JVP
    • --PULSUS PARADOXUS
    • --FAINT HRT SOUNDS
    • --CLEAR LUNG FLUIDS

    Dx w ECHO!!!

    Tx BY DRAINING!!!
  151. CONSTRICTIVE PERICARDITIS
    THICKENED FIBROTIC PERICARDIUM WHICH RESTRICTS DIASTOLIC FILLING

    • CAUSES
    • --ACUTE VIRAL --> scarring & contraction
    • --TB most common in underdeveloped countries
    • --PURULENT, FUNGAL, OR PARASITIC INFECTION OF PERICARIUM
    • --CONNECTIVE TISS DISORDERS rhum arth, sle
    • --RENAL FAILURE
    • --IRRADIATION

    • PRESENTATION
    • --INSIDIOUS ONSET ABDOM SWELLING from ascities
    • --PERIPH EDEMA
    • --DEC CO --> FATIGUE; DISPNEA
    • --PULM VENOUS CONG -> orthop, pnd

    PHYSICAL EXAM SIMILAR TO RESTRICTIVE CARDIOMYOPATHY

    MILD Sx Txed w DIURETICS

    REFRACTORY --> TOTAL PERICARDIECTOMY

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