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58 Cards in this Set

  • Front
  • Back
Normal Axis
upright QRS Lead I and aVF
Left Axis Deviation
Lead I UP aVF DOWN
Right Axis Deviation
Lead I DOWN aVF UP
Irregular Rhythm, ventricular rhythm
no P before each QRS
AV block
PR>200msec or P and NO QRS after
LBBB
QRS>120 no R in V1 tall R in I V5 and V6
RBBB
QRS>120 RSR' complex WIDE R in V1 QRS with S pattern in I V5 V6
Long QT syndrom
QTc>440 msec undiag. cong. disorder predisposes to VTACH
Wave forms Q > 40 (or >1/3 QRS)
= Old MI
Wave forms T inverted
Ischemia
Chamber enlargement RAA hypertrophy
P amp > 2.5 Lead I
Chamber enlargement LAA
P width Lead II > 120 msec
Chamber enlargement LVH
R in aVL+S in V3 >_24mm Men >_20 Women
Chamber enlargement RVH
rt axis dev and R wave V1.7mm
Treat afib is ABCD
Anticoag, BBB-rate, Cardioconvert-CCB, Digoxin
Dilated cardiomyopathy
Most common cardiomyopathy
Whats req for Dx of Dilated CM
LV dilation + Sys dysfx (Low EF)
Cause of DCM
most idiopathic, alcohol, wet beri beri, coxsackie, Chagas, parasites, cocaine myocarditis, doxorubicin, HIV AZT
2 MCC of 2nd DCM
ischemia and Long standing HTN
HX/PE DCM
gradual CHF, Cardiomegaly S3 gallop TVR and MVR
Dx DCM
Echocardiograph is Diagnostic
ECG changes in DCM
nonspecific ST-T , Low volt. QRS, Sinus Tachy, ectopy, LBBB common
CXR of DCM
enlarged, balloon like heart and Pulm congestion
S3 Gallop signifies
end of rapid ventricular filling in setting of fluid overload in DCM
Tx of DCM
stop OH, treat sx of CHF=diurectic, ACEIs, BB, Anticoags dec risk of thrombus, ICD if EF <35%
Hypertrophic CM
LVH cant relax and fill (diastolic dysfx)
Hypertrophy frequently involves
IV septum-->LV outflow obstruction and impaired ejection of blood
IHSS
idiopathic hypertrophic subaortic stenosis
IHSS inheritance
auto dominant 50% risk
IHSS is MCC of
sudden death in young, healthy athletes in US
Other causes of Marked Hypertrophy of heart
HT, AS
HX of HCM
asymptomatic, syncope, dyspnea, palpitation, angina, suddent cardiac death
PE of HCM
MR, sustained apical pulse, S4, Systolic ejection crescendo-decrescendo louder with dec preload (valsalva, squatting)
obstruction in HCM made worse by
inc. myocardial contractility or dec LV filling (exercise, valsalva, vasodilators, dehydration)
S4 signifies
stiff ventricle, and inc "atrial kick" assoc with HCM
Dx of HCM
Echocardiography is diagnostic shows THICKENED LV walls and dynamic obstruction of BF
ECG changes of HCM
LVH
CXR changes of HCM
LA enlargement from MR
Tx of HCM
BB first therapy for sx relief, CCB second line
TX of HCM
surg option for IHSS=dual chamber pacing, partial excision of myocard, ICD, avoid intense athletics
Restrictive CM
Dec elasticity of myocardium-->impair diastolic filling without significant systolic dysfunction (EF nl or slight dec)
Causes of RCM
infiltrative disease (sarcoid, hemochrom
Hx/PE of RCM
Left and Rt side HF, RHF sym (JVD, Peripheral edema) predominate
DX of RCM
CXR and Echo NON diagnostic, Cardiac Bx->show fibrosis or infiltrates
ECG changes with RCM
LBBB
Tx of RCM
symptoms, diuretics for fluid overload, vasodilators to dec filling pressure, Anticoags of no CI
CHF is a clinical syndrome caused by
inability of heart to pump enough blood for O2 needed by hrt and periph tissue
CHF risk factors
CAD, HTN, CM, valve disease, DB
Systolic dysfx leading to HF
dec EF by 50% and inc LVEDV
Cause of syst. dysfx HF
inadequate ventricular contractility or inc afterload
Mechanism of HF in syst dysfx HF
hrt compensates for low EF and inc PL through hypertrophy and ventricular dilation (FSlaw) then fail, lead to inc myocard work and worse sys fx
Hx/PE systol HF
dyspnea** MC and earliest sx, chronic cough, fatigue, PND, Cheyne-stokes, abd. fullness
CHF is a
CLINICAL Syndrome based on Sign and Sxs
Stages of CHF
ABCD
A of CHF
high risk for CHF NO structural or fx or SS
B of CHF
struct heart disease(MI hx, LVSys Dysfx, Valve disease) but NO sym of CHF
C of CHF
structure + sx (dyspnea, fatigue, dec exercise tol)
D of CHF
Marked sx of CJF despite max treatment