ACEi/ARB for patients with IHD + HTN and/or DM
Class I Indication
Features associated with adverse prognosis in PE
Echo: RV Dilation (RV/LV > 0.9), septal flattening and paradoxical leftward septal motion, RV enlargement, TR, PH, McConnell’s sign (RV free wall hypokinesis with apical sparing)
Biomarkers: Elevated CTnT, BNP
CT: RV dilation, ventricular septal bowing from R to L
ECG: new atrial arrhythmias, new RBBB (even incomplete), T wave inv in V-V4
normal P wave axis
up in I, II and down in avR
Type I CRCD
anthracyclines (Doxorubicin) resulting in myocyte destruction and clinical heart failure from iron-based oxygen free radicals
Dose related
Type II CRCD
Loss of myocardial contractility but not myocyte death, usually reversible. Seen with mAB
Not dose related
Clue against athletic heart in enlarged RV
Pulmonary HTN
Imaging test of choice for hemochromatosis
cMR- heart and liver with decreased T2 compared to skeletal muscle
DAPT after CVA
NIHSS </= 3 and no lytics = 21 days then lifelong ASA
1st step w/u of asymptomatic WPW
GXT to look for abrupt loss of pre-excitation
TIMI Score Components
Age >65
multiple risk factors
ST deviation on admission
multiple episodes over 24 hours
ASA in past 7 days
Elevated biomarkers
known stenosis > 50%
Class I indication for bi-v ICD
LVEF < 35%, sinus rhythm, NYHA II +, LBBB and QRS > 150ms
Nervous response after MI
increase in sympathetic nervous system via norepi and beta-1-adrenergic activity. Decrease in parasympathetic via acetylcholine signaling
Later RAAS system is activated, leading to increased renin and angiotensin II levels
Indications for immediate invasive (<2h) NSTEMI
refractory angina
s&s of HF or new/worsening MR
hemodynamic instablitiy
recurrent angina at rest despite meds
sustained VT/VF
Hyperaldosteronism causes
Primary hyperaldosteronism from tumor
hyperplasia (almost always bilateral)
LFLG AS
AVA < 1, mean gradient < 40
low-dose dobutamine stress echo or invasive hemodynamic assessment, looking for gradient to increase over 40 with area < 1
or DI (<0.25 severe)
Calc scoring >1300 women or > 2000 men
MVP murmur
Standing will decrease pre-load as more blood is in LE, leading to earlier click and more intense murmur
Duration to call persistent a-fib
7 days
Longstanding persistent = > 12 months
Increase the MVP murmur
mid-systolic click and late systolic murmur at apex
Valsalva/handgrip increased intrathoracic pressure and decreased venous return /preload and decreased LV cavity size, leading to earlier fail and earlier click/murmur
also increases HCM, so click differentiates
Decreased with things that increase LV volume/size so laying down, inspiration, passive leg lift and squatting as they increase venous return
MOA of P2y12i
inhibit p2y12 receptor conformational change and G-protein activation induced by ADP, which inhibits platelet activation and aggregation
Class Ic antiarrhythmics use dependence
more effective at faster heart rates; makes flecainide good pill in pocket
Indications to intervene on ASYMPTOMATIC carotid stenosis before CABG
- Recent symptoms (<6 mo)
- Bilateral >80%
- Unilateral >70% with contralateral total occlusion
Medical therapy of vasospastic angina
Long acting nitrates or CCB
ECG changes associated with prior MI
- Any q wave in leads V2-V3 at least 0.02 sec or QS complex in V2and V3
- Q wave at least .03 seconds and 0.1 mV deep or QS comples in I, II, aVL, aVF or V4-V6 in any two leads of a contiguous grouping
- R wave at least 0.04 seconds in V1-V2 and R/S at least 1 with a concordant positive t wave in absence of conduction defect
MV PPM
Severe is EOA index < 0.9
