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50 Cards in this Set
- Front
- Back
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Lower Mortlity in ACS |
Aspirin Alteplase Angioplasty (90 mins) Metoprolol Statin Clopidogrel |
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When Clopidogrel |
Aspirin allergy in chest pain before Angioplasty Acute MI |
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Post MI Discharge |
Aspirin + Clopidogrel ACEI Metoprolol Simvastatin (Zocor)/ Atorvastatin (Lipitor) Add eplerenone (aldos antagonist) to ACEI/BB if EF<40%
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Acute Pul Edema |
S3
Furosemide Nitrates 30 -60 mins Dobutamine |
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Systolic dysfunction |
Low EF ACEI Metoprolol Spironolactone / eplerenone Digoxin (dec hospitalizations) |
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Diastolic Dysfunction |
Metoprolol Diuretic
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Regurg Murmurs |
ACEI Nifedipine Furosemide |
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Pericarditis |
ST elev PR dep Aspirin 1-2 d add pred
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Dissect Aorta |
Beta then nitroprusside
CXR move CT angio |
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PAD |
Initial test - ABI (N 1.01-1.40) (Abn <0.90) if borderline and high suspicion - do exercise ABI Aspirin Acei (same efficacy as ARBs) Cilostazol Statins Duplex to localize and follow up Do invasive angio if revascularization is considered
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A Fib |
Meto/diltiazem/digoxin noacarin (CHADS 2) |
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Q and T wave inversion |
Evaluate for MI with ECHO (TTE) |
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No beta blockers if |
Hypotension bradycardia COPD Overt CHF |
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Asystole |
CPR Epi
No defib No atropine |
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HF diagnosis |
Major - PND/orthop/JVD/S3/CXR inc vasc or heart Minor - edema/noct cough/tachy/Pl effu/ dysapn/hepatospleno
2 major or 1 major+ 2 minor |
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CHADS2 |
CHF HTN >75 DM Stroke/TIA |
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Very high risk pts Step 1 add statin Step 2 If LDL > 70 add ezetimibe Step 3 If still >70 add PCSK9 inhibitors |
LDL-C goal <70 Non HDL-C goal <100 clinical benefits of incremental LDL-C lowering with ezetimibe when used in combination with statins results suggest that lower LDL-C levels are better |
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Risk and LDL-C goal Non-HDL-C goal |
Low, moderate, or high <100 <130 Very high <70 <100 |
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High intensity Statins Atorva - 40 - 80mg Rosuva - 20 - 40mg |
clinical ASCVD and age ≤75 years LDL-C ≥190 mg/dL diabetes and estimated 10-year risk for ASCVD events ≥7.5% many patients aged 40-75 years with estimated 10-year risk for ASCVD events ≥7.5%. |
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Moderate intensity statins Atorvastatin 10-20 mg Fluvastatin 40 mg bid Fluvastatin XL 80 mg Lovastatin 40 mg Pitavastatin 2-4 mg Pravastatin 40-80 mg Rosuvastatin 5-10 mg Simvastatin 20-40 mg |
clinical ASCVD, but are >75 years of age or not candidates for high-intensity therapy LDL-C ≥190 mg/dL who are not candidates for high-intensity therapy diabetes and estimated 10-year risk for ASCVD events <7.5% some patients aged 40-75 years with 10-year risk for ASCVD events ≥7.5%. |
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PCSK9 inhibitors alirocumab and evolocumab in pts with clinical ASCVD or heterozygous familial hypercholesterolemia (Evolo can be used in homo familial hyperchol) only small to medium trials so far |
MOC - inhibit PCSK9 by binding to it in ECM. Normaly PCSK9 reduce the availability of LDL-R (receptor) at the cell surface and decrease the amount of LDL-C that can attack to receptor and is cleared from the circulation. Use in conjunction with diet and maximally tolerated statins in patients who require additional lowering of LDL-cholesterol (LDL-C) |
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Familial Hypercholesterolimia |
autosomal dominant disorder caused by mutations in genes for the LDL receptor, PCSK9, or apolipoprotein B (apoB) Target - >50% reduction in LDL-C or LDL-C <100 mg/dL). 2-drug regimens (statins plus ezetimibe) 3-drug regimens (statins, ezetimibe, plus either PCSK9 inhibitor, bile acid sequestrant, or niacin) 4-drug regimens (statins, ezetimibe, plus 2 of the 3 drugs in step 2) and LDL apheresis. |
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Cocaine Heart Pain |
Nitrate / CCB Aspirin BZD no improv Angiograph for thrombus |
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Change in O% detect heart defect (L - R shunt)
SVC/IVC to RA
RA to RV
RV to Pul A |
ASD / VSD with TR
VSD / PDA with Pul regurg
PDA |
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Pt with ED and 3 athero risk factors |
do stress test for CVD
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Vasovagal syncope |
<60 - emotional / orthostasis >60 - micturation / cough/ defecat
no tilt test if cliniclly clear |
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Carotid sinus hypersenstivity |
with neck mvm = falls positive carotid massage |
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Dilated cardiomyopathy+prog hearing loss+peripheral neuropathy+renal failure in pt with total hip replacement |
consider cobalt toxicity |
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Dominant R and St depression V1 - V3 |
Acute Posterior Wall MI |
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HFrEF pts |
Give ACEI or ARB and a beta blocker Class II-IV patients add aldosterone antagonist/mineralocorticoid receptor antagonist (MRA) (eg, spironolactone) when estimated creatinine clearance is >30 mL/min and K+ <5.0 mEq/L Renal function and potassium levels should be monitored serially |
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Acute SOB + High RR + High BP + No murmurs + Edema + Rales + Elevated Filling Pressure + Normal LV EF |
Acute heart failure preserved ejection fraction Risk - elderly, H/o HTN DM |
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Aspirin for stroke prevention (USPSTF) |
Pts 50 - 69 with 10% CVD Contraindication: bleeding risk Reduction in heart attacks, stroke, colorectal ca be careful in pts in 60s since higher risk of bleeding |
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Outcomes in pts with stroke and elevated sbp in ED |
No significant difference if lower to 140-179 or lower to 110 - 139 use IV nicardipine |
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Allopurinol's effect on hypertensive pts |
dec stroke and cardiac events in more than 65 yrs pts |
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Role of natriuretic peptides in heart |
The natriuretic peptides (NP), including ANP, BNP, and CNP, have cardiorenal protective properties, including multiple effects on vascular tone, intravascular volume, neurohormonal activity, and cardiovascular remodeling Levels of circulating BNP and CNP are normally very low, and only become elevated in certain disease states contribute to the regulation of vascular tone through direct effects on vascular smooth muscle cells and by suppressing the RAAS, thereby reducing sympathetic tone and inhibiting secretion of vasoconstrictors. In the kidney, the NPs inhibit sodium reabsorption in the proximal and distal nephron, further reducing intravascular volume Promoting these effects is the goal of using neutral endopeptidase inhibitors in the treatment of patients with heart failure |
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Sacubitril/valsartan |
Combination of the angiotensin receptor blocker (ARB) valsartan and sacubitril, an inhibitor of the neutral endopeptidase neprilysin Compared to enalapril more symptomatic hypotension, less cret, K, cough Neprilysin (neutral endopeptidase) is the principal enzyme responsible for degradation of the natriuretic peptide catalyzes the conversion of angiotensin I to Ang, which acts in opposition to angiotensin II which is beneficial to heart |
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Omapatrilat |
a dual inhibitor of angiotensin converting enzyme (ACE) and neutral endopeptidase higher risk of angioedema than enalapril associated with a significantly greater reduction in systolic blood pressure at 8 weeks and reduced use of adjunctive antihypertensive drugs at 24 weeks compared to enalapril |
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RAAS AT1 and AT2 |
Renin made by the kidney converts angiotensinogen to angiotensin I which is the converted to angiotensin II by angiotensin converting enzyme in the lungs. (Angio II acts regulate blood pressure, release of hemodynamic mediators (aldosterone, vasopressin, catecholamines, endothelin), and sodium reabsorption) Angiotensin II binds to AT1 and AT2. AT1 receptors vasoconstriction, increased cardiac contractility, and cardiomyocyte hypertrophy. AT2 receptors mediate opposing effects, including vasodilation and inhibition of MAPK. Release of vasopressin/antidiuretic stimulated by angiotensin II and arterial underfilling. |
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Vasopressin |
vasopressin can vc (via V1 receptors) and vd (via V2 receptors) inhibiting diuresis. main effect on bp is mediated by the V1 receptors, contributing to vasoconstriction |
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AT receptor changes in HF |
AT2 receptors expression is increased in cardiac tissue in adults with heart failure, a decrease in cardiac AT1 receptor expression. Change in receptor correlates with progression of interstitial fibrosis, cardiac remodeling, and increased intracardiac filling pressures. |
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Bradykinin and ACEI |
modulates vd response through cNOS, phospholipase A2, and adenyl-cyclase. (Also a substrate for angiotensin converting enzyme (ACE) Inactivates bradykinin in addition to production of angiotensin II from the inactive angiotensin I) ACE inhibitors have a two-fold effect: reducing angiotensin II production and potentiating the activity of bradykinin. |
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Chronic effects of LV systolic dysfunction sympathetic/adrenergic (short term - increased adrenergic activity improve overall cardiac contractility and hemodynamics) |
Chronic adrenergic stimulation leads to desensitization to norepi, downreg b1 recp left ventricular remodeling, myocardial cell death, changes in gene expression, and positive chronotropic effects, contributing to increased heart rate which increase stress on the heart and foster progression to advanced heart failure. |
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Eplerenone |
Significant reduction in deaths due to cardiovascular causes or hospitalization for heart failure Hyperkalemia is more common |
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stage C heart failure (characterized by structural heart disease with prior or current heart failure symptoms) patients with volume overload African American patients who are persistently symptomatic |
an ACE inhibitor/ARB and beta blocker (potassium should be maintained less than 5.0mEq/L) a loop diuretic Hydralazine-nitrates |
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patients with creatinine 2.5 mg/dL or estimated glomerular filtration rate >30 mL/min) Pts who are persistently symptomatic and for whom an aldosterone antagonist is not indicated or tolerated. (routine combined use of ACEI, ARB, and aldosterone antagonist is harmful) |
aldosterone antagonists start at a low dose ie eple at 25 mg e other day avoid NsAIDS. Renal function and potassium re-checked within 2-3 days and at 7 days. monitored at least monthly for the first three months then e 3 months Combined use of ARB and ACE inhibitor might consider substituting components of therapy (eg, ACE inhibitor) with a hydralazine-nitrate, especially in an African American patient with reduced kidney function. |
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Association of higher uric acid levels and HTN |
associated with higher risk of HTN but not CKD |
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Systolic click at the apex and soft ejection murmur does not vary with valsalva or breathing No symptoms, physiologic split second sound, peripheral pulses unremarkable |
Bicuspid aortic valve increased risk for aortic stenosis, aortic regurgitation, typically in the fourth to sixth decades of life. also associated with aortopathy, ascending aortic aneurysm, and risk for aortic dissection. |
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midsystolic ejection murmur heard best at the right upper sternal border, mimicking true aortic stenosis |
Aortic-valve thickening or sclerosis |
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Harsh ejection murmur similar to aortic stenosis, but the murmur typically increases in intensity with the Valsalva maneuver. An ejection click is usually absent. |
Hypertrophic cardiomyopathy |
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left ventricular systolic dysfunction in HF reduces cardiac output, triggering compensatory effects intended to improve cardiac function. |
activation of the sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS), and the natriuretic peptide system. |
