SINO-ATRIAL NODE IN HEART CONDUCTION
INITIATES HB
AV NODE IN HEART CONDUCTION
STRAIGHT LINE AFTER P WAVE (PR SEGMENT)
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
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
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
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
nL P WAVE ON ECG
nL UNIFORM FROM BEAT TO BEAT
nL PR INTERVAL ON ECG
CONSTANT FROM BEAT TO BEAT
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)
nL ST SEGMENT ON ECG
PLATEAU PHASE OF VENT CELLULAR ACTION POTENTIAL
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
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
PRINCIPLES FOR DETECTING HYPERTROPHY ON ECG
MORE MASS OF MYOCYTES --> INC ELEC ACTIVE TISSUE --> INC ECG DEFLECTIONS DURING DEPOLARIZATION OF LARGE OR THICK CHAMBER
LEFT ATRIAL ENLARGEMENT ON ECG
USUALLY w ABN VENT FUNCTION
RIGHT ATRIAL ENLARGEMENT ON ECG
USUALLY w ABN VENT FUNCTION
LEFT VENTRICULAR HYPERTROPHY IN ECG
INC TOWARD LEFT AND INF AND POST
RIGHT VENTRICULAR HYPERTROPHY IN ECG
VENT FORCES ARE INC TOWARD RIGHT AND INF AND ANT
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
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
RESTING ECG SIGNS OF INFARCTION
ST ELEV OR Q WAVE FORMATIONST ELEV IS A KEY SIGN --> ACUTE ONGOING MUSC INFARCTION AND REQUIRES IMMEDIATE ACTION
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")
ECG LEADS INVOLVED IN ACUTE OR RECENT/OLDER INFARCTION BASED ON LOCATION OF HRT DAMAGE
INFERIOR -- II, III, aVF
EXCERSIZE STRESS TEST ECG SIGN OF ISCHEMIA
ST SEG DEPRESSION
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
PROLONGED P WAVE DURATION ON ECG
INTRA-ATRIAL CONDUCTION ABN
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
PROLONGED QRS DURATION ON ECG
SLOW CONDUCTION THROUGH VENT
PROLONGED QT INTERVAL ON ECG
PROLONGED CELL ACTION POTENTIAL DUE TO ABN FUNC OF MYO CELL MEM ION CHAN POPULATION
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)
TACHYCARDIAS ON ECG
>100 BPMSINUS TACHYCARDIA -- FAST ATRIAL RATE AND nL P & QRSSUPRAVENT TACHY IF REGULAR RATE AND NARROW QRSWIDE-COMPLEX-TACHY IF REGULAR RATE AND WIDE QRS > .12secATRIAL FIBRILLATION IF IRREGULAR RATE
LIMITS OF ECG IN CARDIOVASCULAR Dx
1) NOT GOOD FOR MECHANICAL ABN
S3 AND S4 IN CARDIAC CYCLE
S3 -- END OF RAPID FILLING DURING VENT DIASTOLE -- AFTER S2
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
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
SPLITTING OF S1
USUALLY M1 BEFORE T1
EXAGERATED BY DELAYED T1 --RBBB --EBSTEIN'S ANOMALY
nL SPLITTING OF 2ND HRT SOUND
NORMALLY, P2 ALWAYS AFTER A2DURING EXPIRATION: A2 AFTER P2 PATHOLOGICAL
PATHOLOGICAL SPLITTING OF 2ND HEART SOUND
EARLY A2 -- MITRAL REGURGE (inc split)
FIXED SPLITTING OF S2
ASD -- L-R SHUNT
EJECTION CLICK
ATTEMPTED OPENING OF STENOTIC AORT OR PULM VALVE
OPENING SNAP
ATTEMPTED OPENING OF STENOTIC MITRAL/TRICUSPID VALVE
PERICARDIAL KNOCK
ATTEMPTED FILLING OF VENT THAT HAS THICKENED PERICARDIUM -> DEC DIALATION
MURMUR CAUSES AND R-L EFFECT OF RESPIRATION
VALVE STENOSIS
MURMUR INTENSITY RATING
1/6 BARELY AUDIBLE
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
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)
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
CAUSES OF MIDSYSTOLIC MURMURS
MITRAL VALVE PROLAPSE --FLOPPY LEAFLETS --AND/OR ELONGATED CHORDAE
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
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"
CAUSES OF MID DIASTOLIC MURMUR
MITRAL STENOSIS
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
SEQUENCE OF ELECTRICAL EXCITATION OF THE HEART
1) SINO-ATRIAL NODE --R TO L ATRIA; INFERIORLY
2) ATRIAL MUSCLE DEPOL
4) BUNDLE OF HIS --RAPID PURKINJE --ENDOCARDIUM
5) BUNDLE BRANCHES
6) VENTRICULAR DEPOL --ENDO TO EPICARDIUM
ORDER OF THE 4 MAJOR DIVISIONS OF THE CARDIAC CYCLE
SYSTOLE --ISOVOLUMIC CONTRACTION --VENTRICULAR EJECTION DIASTOLE --ISOVOLUMIC RELAXATION --VENTRICULAR FILLING
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
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
DEFINE PULMONARY VASCULAR RESISTANCE AND HOW CALCULATED
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
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
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
PHASES OF CARDIAC ACTION POTENTIAL
0 -- RAPID Na INTO CELL
DEFINITION OF SHOCK
GENERALIZED REDUCTION OF TISSUE PERF THAT MAY BE DUE TO VARIOUS ETIOLOGIES
SYMPTOMS OF SHOCK
SKIN -- COLD, CLAMMY
SIGNS OF SHOCK
VITAL -- HYPOTENSION, TACHYCARDIA
LAB RESULTS FOR SHOCK
LIVER -- INC AST, ALT, GGT
TYPES OF SHOCK
HYPOVOLEMIC --HEM, GI, DIURETIC, 3RD SPACING CARDIOGENIC --ACUTE MI --CHF DISTRIBUTIVE (profound arterial dilation) --SEPSIS --NEUROGENIC --ANAPHYLAXIS allergen
TREATMENT FOR SHOCK
IMMEDIATE Tx OF UNDERLYING CAUSE
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
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
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
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
SYMPTOMS OF CHFABN VENOUS CONGESTION
DYSPNEA ON EXERTION ORTHOPNEA PAROXYSMAL NOCTURNAL DYSPNEA
NY HEART ASSOC CLASSIFICATION SCHEME FOR CHF
I -- NO LIMITATIONS OF ACTIVITY
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
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
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
BICUSPID AORTIC VALVE
AORTIC STENOSIS
RHEUMATIC Dz OF AORTIC VALVE
AORTIC STENOSIS
SENILE DEGENERATIVE CALCIFIC Dz
AORTIC STENOSIS
NOT JUST DUE TO AGE -- RISK FACTORS SIMILAR TO ATHEROSCLEROSIS --MEN, AGE, SMOKING, HYPERCHOL
RARE CAUSES OF AORTIC STENOSIS
INFECTIVE ENDOCARDITIS
SLE
SUBVALVULAR --25% OF Pts w HYPERTROPHIC CARDIOMYOPATHY SUPRAVALVULAR --WILLIAMS SYND, ELFIN FACIES
SYMPTOMS OF AORTIC STENOSIS
LV HYPERTROPHY PULM CONGESTION CONCOMITANT CAD SYSTOLIC MURMUR (cresc-decresc, later peak more severe) PULSUS PARVUS ET TARDUS (small & late pulse)
*ECG
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
TREATMENT OF AORTIC STENOSIS
IF ANGINA SYNCOPE CHF --> SURGERY
AORTIC REGURGITATION ETIOLOGIES
VALVULAR OR ROOT PATHOLOGY
VALVE --CONG --RHEUM --CALCIFIC --ENDOCARDITIS --TRAUMA ROOT --HT --DISSECTION --SYPHILIS --MARFAN --WHIPPLE'S INF --SPONDYLOARTHROPATHIES
AORTIC REGURGITATION HEMODYNAMICS
VOL OVERLOAD OF LV --FILLED IN DIAST FROM LA & AORTA LV DIALATION --INC DIAST PRESSURE IN LV & LA --CHF & ANGINA
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
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
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)
ACUTE AORTIC REGURGITATION
2NDARY TO TRAUMA, INF, DISSECTION
NORMAL ANAT OF MITRAL VALVE
ANNULUS
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
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
SURGICAL MANAGEMENT OF MITRAL REGURGITATION
ACUTE -- AGGRESSIVE INTERVENTION
CHRON --TIMING IMPORTANT --LV-ESD >4.5cm --EF <.65
REPAIR IS FAVORABLE TO REPLACE
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
MITRAL VALVE PROLAPSE Tx
SURGERY --MILD -- FOLLOW-UP ONLY --SEVERE --CHF Sx, DEC LV FUNC
REPAIR RATHER THAN REPLACE RECOMMENDED
WHEN TO USE ECG vs. CXR
ECG -- ONGOING CHEST PAIN OR WITH DISTURBANCES IN HRT RHYTHM
2 INDICATIONS FOR ORDERING CARDIO STRESS TEST
Dx ISCH HRT Dz
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
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
CABG vs. PCI
CABG --BETTER OVERALL RESULTS IN DIABETES, MULTI CAD, AND TOTAL OBST --BUT, HIGHER PROCEDURAL MORTALITY AND MORB
WHEN IS CARDIAC ELECTROPHYSIOLOGIC ABLATION HELPFUL?
Tx FOR ARRHYTHMIAS
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
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
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
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
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
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
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
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
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
LIST COMMON ACYANOTIC CONGENITAL CARDIAC MALFORMATIONS
OBSTRUCTIVE: --PULM STENOSIS --AORTIC STENOSIS --COARCTATION OF AORTA LEFT-TO-RIGHT SHUNTS --VSD --ASD --PDA
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
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
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
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)
PATHOPHYS OF ACUTE CORONARY SYNDROME
PLAQUE RUPTURE (fibrous cap)
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
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
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
TRUE AORTIC ANEURISM vs. PSEUDOANEURISMTrue False
TRUE --LOCALIZED WIDENING OF AORTA OVER 50% --PRESENTS w PAIN! --LaPLACE T=(PxR)/2W PSEUDO --CONTAINED RUPTURE w OUTER ADVENTITIAL LAYER PREVENTING LEAKAGE
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
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)
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, miDESCENDING --STANFORD CLASS B --MEDICAL THERA PREFERRED (control bp) --SURGERY IF FAIL
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
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
ANKLE/BRACHIAL INDEX (ABI) IN CLASSIFICATION OF PERIPH VASC OBSTRUCTION
ANKLE SYSTOLIC PRESSURE / HIGHER OF 2 BRACHIAL PRESSURES
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
3 PRESENTATIONS OF VENOUS Dz
VARICOSE VEINS
VENOUS SKIN ULCERATION --MEDIAL MALLEOLUS OF ANKLE
LEG HEAVINESS
PALPABLE CORD
ABNORMAL FINDINGS IN PREGNANCY
DYSPNEA THAT INH ADL
4 MAJOR FACTORS IN REGULATION OF BLOOD PRESSURE
HEART
CLASSIFICATIONS OF BLOOD PRESSURE DEFINED BY SEVENTH JOINT NATIONAL COMMISION ON BP (JNC-7)
AVG OF BP RESULTS OVER 2 VISITS NEEDED FOR Dx
4 CLINICAL FACTORS THAT INC RISK FOR DEV ESSENTIAL HT
OVERWEIGHT
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
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
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
5 CONDITIONS WORSENED BY HT
ARTERIES
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
NON-PHARMACOLOGIC Tx OF HT
THERAPEUTIC LIFESTYLE CHANGE
GENERAL vs. DIABETIC IDEAL BP
GENERAL <140/90
LIST THE 3 TYPES OF CARDIOMYOPATHY
DIALATED (congestive)
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
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
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
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"
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
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%
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
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
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
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
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!!!
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
