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98 Cards in this Set
- Front
- Back
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total cholesterol levels |
optimal: <150 desirable: <200 borderline: 200-239 high: >240 |
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LDL levels |
optimal: <100 borderline: 130-159 high: 160-189 very high: >190 |
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HDL levels |
desired range: 40-60 in men, 50-60 in women |
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triglyceride levels |
optimal: <100 normal: <150 borderline: 150-199 high: 200-499 Very high: >500 |
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LDL goals by risk category |
high risk (>20% 10yr risk or CHD): <100 moderately high risk (10-20% 10 yr risk): <130 Moderate risk (<10% 10 yr risk): <160 lower risk (0-1 risk factors): <160, initiate therapy w/ LDL>190 |
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Framingham risk score factors |
-Age, LDL/total cholesterol, HDL, SBP, diabetes, smoking, HTN Rx |
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Chylomicrons |
-composed of mainly exogenous triglycerides absorbed in the intestine -degraded by lipoprotein lipase into FFAs and remnant particles |
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VLDL |
-contain mostly triglyceride and phospholipid -made in the liver -degraded by lipoprotein lipase into FFAs and IDLs |
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IDL |
-contain cholesterol esters and phospholipids -formed from VLDLs in circulation -taken up by hepatic LDL receptors or are degraded into LDLs |
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LDL |
-contain high cholesterol esters, some triglycerides -taken up by hepatic and extrahepatic LDL receptors -'bad cholesterol' - target of most therapies |
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HDL |
-contains cholesterol esters, phospholipids, and apoA-1 -picks up cholesterol from cells and returns it mostly to the liver -'good cholesterol' |
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hyperlipoproteinemia phenotype I (hyperchylomicronemia) |
deficiency in lipoprotein lipase-->high chylomicron levels--> high triglycerides but normal cholesterol |
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hyperlipoproteinemia phenotype IIa (Familial hypercholesterolemia) |
defect in LDL receptor--> high blood levels of LDL/cholesterol but normal triglycerides--> premature CAD |
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hyperlipoproteinemia phenotype III (Familial Dysbetalipoproteinemia) |
incomplete catabolism of chylomicrons/VLDLs--> high cholesterol and triglyceride levels--> peripheral vascular disease and CAD |
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hyperlipoproteinemia phenotype IV (familial endogenous hypertriglyceridemia) |
accumulation of VLDLs--> high triglycerides and 'milky' plasma--> premature CAD |
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hyperlipoproteinemia phenotype V (Familial hypertriglyceridemia) |
accumulation of VLDLs and chylomicrons--> extremely high triglycerides and 'milky' plasma |
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Lipoprotein(a) |
associated with LDLs and is a marker for CVD |
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guidelines for initiating statins |
-high risk patients (CHD, CVD, PVD, DM, FH, high LDL) -other pt's 40-75 y/o w/ >7.5% 10 yr risk |
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Obesity criteria |
BMI>30 Waist/hip ratio>9 in men or 8.5 in women (apple shape worse than pear) Waist>40 in in men or 35 in women |
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metabolic products of adipocytes |
-angiotensinogen -FFAs -CRP -Plasminogen activator inhibitor -IL-1/TNF-a -resistin -adiponectin |
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metabolic syndrome |
3 out of 5: abdominal obesity, triglycerides>150, reduced HDL, high BP, fasting glucose>100
-abdominal obesity and insulin resistance are most important -associated w/ a 2x risk of atherosclerotic heart disease and a 5x risk of diabetes |
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treatment of metabolic syndrome |
-first line is weight loss w/ diet and exercise which shows the greatest reduction in risk out of proportion to weight lost -drugs are available eg. orlistat, phentermine, lorcaserin, topiramate -in extreme cases surgery: roux-en Y is highly effective and only intervention shown to reduce MI risk |
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incidence |
number of new cases of disease in a population during a specific time period |
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prevalence |
proportion of population who have the disease at a given point in time |
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relative risk |
association of risk factor and disease using relative likelihood of disease in exposed vs unexposed (Ie/Io): 1=no association, <1=protective, >1=risk factor |
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attributable risk |
measure of association that describes the absolute effect of exposure (Ie-Io) |
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factors in establishing causality |
-strength of RR, consistency, temporality, dose-response, plausibility, coherence w/ current knowledge, experiments, analogies |
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observational studies vs RCTs |
-observational studies good for establishing risk factors in a population but are not as good as RCTs for estimating the impact of modification/treatment of risk factors ('healthy cohort effect') |
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modifiable CRFs |
most beneficial: quit smoking, control HTN, and high cholesterol, increase physical activity
suggestive evidence for benefit in modifying: obesity, DM, hormones (replacement), LVH, stress |
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A's of smoking cessation |
ask, (assess), advise, assist, arrange follow up |
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fatty streak |
-accumulation of foam cells in the intima -does not disturb flow -precursor to atheroma -present by teens in most ppl |
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pathogenesis of atheroma |
-chronic endothelial injury-->lipid insudation -lipids w/in the media get oxidized -inflammation--> production of IL-1, TNF, MCP-1, ICAM/VCAM -activated macrophages accumulate oxidized lipid in cytoplasm -smooth muscle cells migrate into the intima |
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acute plaque changes |
-erosion, rupture-->thrombosis, hemorrhage, eombolism |
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complicated atheromas |
-characterized by: calcification, rupture or erosion, hemorrhage, thrombosis, medial atrophy-->aneurysm |
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significant atheromatous lesion |
>50% reduction in diameter or 75% of cross sectional area -symptoms develop only w/ exertion |
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critical atheromatous lesion |
> 75% reduction in diameter or 90% of cross sectional area -chronic ischemic heart disease w/ symptoms at rest |
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gross changes w/ MI |
0-4 hours= invisible 4-24 hrs= dark mottling 1-14 days= yellowing surround by hyperemia 14+ days= graying scar |
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histopathology changes w/ MI |
1-3 hrs= wavy fibers 4-12 hrs= coagulation necrosis 12 hrs= pyknosis 24-48 hrs= karyolysis 48 hrs= peak of PMN infiltrate (begins at 6-8 hrs) 3 days= vessel proliferation 4 days= macrophage infiltration/fibroblast 9 days= collagen deposition 2-4 wks= granulation tissue 6+ wks= scar |
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complication of transmural infarcts |
-acute fibrinous pericarditis w/in 2-3 days -myocardial rupture->tamponade in 3-6 days -mural thrombi -papillary muscle rupture in 3-6 days -delayed sequelae: ventricular aneurysm, chronic IHD--> cardiomyopathy w/ dilation, pulm edema, hepatic congestion |
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contraction band necrosis |
-often a sign of reperfusion injury -influx of calcium causes hypercontraction w/ overlapping z-lines |
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factors suggesting the presence of CAD |
-classic history of anginal pain: pressure/tightness in the chest on exertion, radiation, goes away with nitro or sufficient rest -patient population: age, gender -physical exam- HTN, body habitus, bruits, heart size, skin, eye grounds etc
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classes of angina |
I- occurs w/ high exertion II- w/ moderate exertion III- w/ activities of daily living IV- at rest other terms: unstable angina- changes in class/gets worse prinzmetal angina- coronary vasospasm at rest |
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stress test |
- can be EKG or imaging w/ exercise or dobutamine, or perfusion w/ adenosine - goal is to achieve 85% of predicted maximal HR (PMHR=220-age) -imaging is more sensitive and specific |
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cardiac cath |
-invasive procedure w/ serious risks -non-functional -current gold standard -can quantify lesions and give anatomical info -helpful for planning revasculization |
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intermittent peripheral vascular claudication presentation |
-exertional lower extremity pain, cramping, aches, tightness, or tiredness -occurs distal to obstruction -resolves w/ rest -differentiated from pseudoclaudication which has symptoms on standing, paresthesia, and is relieved by sitting |
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intermittent peripheral vascular claudication physical exam findings |
-diminished or absent distal pulse -bruits may be heard -atherosclerosis in other vessels -hair loss, color changes and ulceration of skin -ankle brachial pressure index <0.9 |
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prevention of ischemic events in peripheral vascular disease |
-modify risk factors: smoking, LDL, BP, A1C -antiplatelet therapy: aspirin or clopidogrel |
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symptomatic relief in peripheral vascular disease |
-exercise therapy is the best -cilostazol, pentoxifylline may improve exercise tolerance -revascularize in severe cases |
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critical limb ischemia presentation |
-rest pain -gangrene -ulceration |
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treatment of critical limb ischemia |
-goal is to save the limb -high risk of amputation and mortality -wound care, and revascularization |
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presentation of acute limb ischemia |
-6P P's -pain, pallor, paresthesia, paralysis, pulselessness, poikilothermia |
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treatment of acute limb ischemia |
-immediate IV heparin -determine limb viability -embolectomy or thrombectomy -amputate if necessary |
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atheromatous embolism |
-"blue toe syndrome" -plaque emoblization--> showering and occlusion of many systemic vessels that can lead to end organ damage of the CNS, GI, Kidneys, Skin -eventually causes a large immune response |
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abdominal aortic aneurysm definition and risks |
-focal dilation of >1.5x or >3cm -risks include: white MALE >55 y/o, smoking, HTN, CAD, PAD, COPD, FHx |
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AAA presentation |
-may be asymptomatic finding -pulsatile abdominal mass -abdominal or back pain -rupture -embolization -infection -compression of surrounding structures |
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diagnosis/treatment for AAA |
-felt on physical exam + bruit -imaging (MR, CT, US etc.) -indication for surgery: large (>6cm), branch occlusion, source of embolus, compression of other structures
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aortic dissection presentation and diagnosis |
-tear in the intima-->blood separating intima and media -ripping/searing pain along segment effected -may present w/ shock, MI, or pulmonary edema -diagnosis best w/ TEE, MR, CT |
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aortic dissection treatment |
medical: beta-blocker, nitro, ACEi, CCB, narcotic -surgery if acute proximal dissection or complicated distal dissection occurs -endovascular repair possible
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Primary PCI
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-preferred tx for acute stemi
-best within 90 min -pts also get aspirin, heparin, and GP IIb/IIIa inhibitor plus clopidogrel post-op |
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Indications for coronary revascularization
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1. Persistent angina w/ meds
2. Contraindications to angina meds 3. High risk w/ known benefit of revascularization |
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Revascularization procedures
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-PCI: can be PTCA, stent, drug eluding stent
-CABG: esp in multivessel disease |
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Normal cardiac pressures
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RA: 2-8
RV: 15-30/2-8 PA: 15-30/4-12 PCWP: 2-10 LA: 2-10 LV: 100-140/3-12 Aorta: 100-140/60-90 |
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Causes of high right atrial pressure
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-cardiac tamponade
-RV failure -a wave rise: RVH, tricuspid stenosis, atrioventricular dissociation -v wave rise: tricuspid regurg |
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Causes of high RV pressure
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- Systolic: RV failure, pulm hypertension, pulm stenosis
- diastolic: RV hypertrophy, RV failure, cardiac tamponade |
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Causes of high pulm artery pressure
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Systolic and diastolic: pulm vascular disease, chronic lung disease, left heart failure
Systolic only: left->right shunt |
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Causes of increased pulmonary capillary wedge pressure
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-left heart failure
- mitral stenosis or regurg (v wave only) -cardiac tamponade - LV hypertrophy (a wave) - Ventricular septal defect (v wave) |
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Measurement of cardiac output
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- thermodilution method
- ficks method: CO= O2 consumption/ AV O2 difference - cardiac index= CO/ body surface area |
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Measuring vascular resistance |
PVR= (MPAP-LAP) x 80/CO |
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systolic vs diastolic heart failure |
systolic: reduced ejection fraction caused by MI, dilated CMP, Myocarditis -PV loop: End systolic P and V are low
diastolic: preserved ejection fraction caused by hypertension, aging, hypertrophic or restrictive CMP -PV loop: End diastolic P is high, V is low |
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Heart failure compensation |
-RAAS and Sympathetic activation--> Volume expansion Increase preload, contractility/HR/CO, vasoconstriction
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maladaptive heart failure compensation |
-too much demand on the myocardium (eg high wall stress, metabolic needs) -tissue congestion -pathological remodeling |
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Right vs left heart failure symptoms |
left: shortness of breath, orthopnea, pulm. congestion
right: fatigue, cyanosis, venous back-up (ie. JVD, liver congestion, ascites, edmea) |
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acute medical management of heart failure |
-IV diuretics- reduce venous congestion, preload -IV Nitro/nesiritide (BNP analog)- sequester blood in systemic veins -IV inotropes (dobutamine or milrinone)
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Dobutamine vs Milrinone |
-inotropes for heart failure -dobutamine: beta agonist w/ minor vasodilatory effects -Milrinone: PDEi that has more potent vasodilation and increased risk for hypotension |
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standard therapy for systolic heart failure |
Diuretics: as needed ACE i Beta blocker Hydralazine/nitrates +/- spironolactone +/- digoxin |
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3 major goals of therapy for diastolic heart failure |
-control BP below 130/80 -control HR w/ a-fib or tachycardia -reduce blood volume w/ diuretics |
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5 major criteria for acute rheumatic fever |
carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules |
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hemodynamic consequences of valve disease |
stenosis= high pressure= diastolic dysfunction
regurg= high volume= systolic dysfunction |
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mitral stenosis clinical features |
-most commonly result of rheumatic fever -primary issue is high left atrial pressure but that cause left and right sided heart failure -Right ventricular hypertrophy -palpable P2 -atrial fibrillation and tachycardia |
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auscultatory features of mitral stenosis |
-loud S1: mitral closes late and loudly -Opening Snap: mitral opens early and halts abruptly, S2-OS time indicates severity -Mid-diastolic murmur: changes w/ LA-V gradient -pre-systolic murmur: |
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treatment for mitral stenosis |
-diuretics, HR control, control a-fib -surgical repair -percutaneous valvuloplasty |
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etiology of mitral regurgitation |
acute: ichemia/infarction, myxomatous degeneration, endocarditis
chronic: rheumatic, mitral prolapse, endocarditis, degenerative, LV remodeling |
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mitral regurgitation clinical features |
-primary issue is LV volume overload -dilated LV -possible RV hypertrophy and palpable P2 |
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auscultation of mitral regurgitation |
acute: 'explosive' early systolic murmur, 'rumbling' S3
Chronic: 'blowing' holosystolic murmur, diastolic rumble |
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treatment of chronic mitral regurgitation |
-diuretics, after-load reduction -surgery for valve repair or replacement |
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etiology of aortic stenosis |
-congenital: bicuspid valve, monocuspid, supra- or sub-valvular
-rheumatic, degenerative |
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aortic stenosis clinical presentation |
-angina -CHF -syncope -rough mid-systolic murmur |
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clinical features of aortic regurgitation |
-primary issue is volume overload -chronically tolerated -LV dilation -no or late RV failure -wide pulse pressure |
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auscultation of aortic regurgitation |
-mid-systolic murmur -abbreviated, decrescendo early diastolic murmur |
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dilated cardiomyopathy clinical features |
can be asymptomatic but often: shortness of breath, fatigue, edema, rales, JVD, hepatomegaly, S3, S4, mitral regurgitation, impaired systolic fxn |
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dilated cardiomyopathy clinical studies |
-cardiomegaly on CXR -dilated LV w/ reduced ejection fraction on echo -A-fib, Left bundle on EKG |
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causes of dilated cardiomyopathy |
-50% idiopathic/genetic other more common causes: -myocarditis -ischemic heart disease -chemotherapy |
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hypertrophic cardiomyopathy clinical features |
-dyspnea, angina, syncope -impaired diastolic fxn -S4 -holosystolic murmur -dynamic outflow obstruction that increases w/ contractility and decreases w/ LV volume |
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hypertrophic cardiomyopathy diagnostic studies |
-LV hypertrophy, LA enlargement, pseudo-Q's on EKG -asymmetric thickening of the septal wall on echo -LV outflow track pressure gradient |
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treatment of hypertrophic CMP |
-prevent obstruction: keep volume high and give beta-blockers/CCBs -antiarrhythmics for any a-fib possible defib -fix bad obstructions surgically -genetic counseling |
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restrictive cardiomyopathy causes |
endomyocardial disease, amyloidosis, sarcoidosis, hemochromatosis, genetic...etc |
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clinical features of restrictive cardiomyopathy |
-R>L heart failure -impaired diastolic fxn -palpitations -other symptoms of underlying condition -JVD, S3, regurgitation |
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restrictive cardiomyopathy diagnostic studies |
-a-fib on ekg -severe bi-atrial enlargement and possible speckled pattern on echo -infiltrates from underlying disease on biopsy |
