Term
| age when HF is most common? |
|
Definition
| elderly (>65yo) = HF until proven otherwise |
|
|
Term
| who's more at risk for HF? m or w? |
|
Definition
| men, women (premenopausal) = estrogen cardioprotective unless she SMOKES, then NO protection |
|
|
Term
| 4 big demographic risk factors for HF |
|
Definition
| age, male, smoking (esp women), african american |
|
|
Term
| describe the 4 classes in the NY heart assoc functional classification of HF |
|
Definition
| I: no sx w/ordinary activity; II: slight limitation of phys activity (ordinary phys activity --> sx); III: marked limitation of phys activity (less than ordinary activity --> sx); IV: unable to carry out any phys activity w/o discomfort, sx at rest even |
|
|
Term
| what are the four stages of HF |
|
Definition
| (A) no struc disorder, but pt at high risk for HF (smoking, diabetes, CAD, elderly, HTN); (B) structural disorder w/o sx of HF (C) past or current HF sx assoc with underlying struc heart disease (D) end stage disease, req specialized tx strategies (these are progressive stages, once youre at one stage, cannot move backwards) |
|
|
Term
| three major causes of HF? |
|
Definition
|
|
Term
| what is the mortality at 5 years for HF? |
|
Definition
|
|
Term
| ratio of systolic HF to diastolic HF? which is more serious? |
|
Definition
| 70% systolic; 30% diastolic; both just as symptomatic and prognosis just as bad in both cases |
|
|
Term
| what are the 3 major determinants of SV? |
|
Definition
|
|
Term
|
Definition
| end diastolic volume - end systolic volume |
|
|
Term
|
Definition
|
|
Term
| describe what happens in diastole (first 2/3 vs last 1/3) |
|
Definition
| LV fills quickly with blood when mitral valve opens bc of ventricular compliance --> 2/3 way into diastole LVp=LAp (diastasis) --> atrium contracts (increase in LAp) and overcomes LVp --> more blood rushes in (last 1/3) |
|
|
Term
| what effect does preload have on SV? |
|
Definition
| preload= ventricular wall tension at the end of diastole. if we increase preload we are increasing end diastolic volume --> pressure at the end of diastole will be higher --> SV increases! |
|
|
Term
| what effect does increasing afterload have on SV? |
|
Definition
| afterload=ventricular wall tension during contraction (LV has to overcome systolic BP to open aortic valve); when you increase afterload, you make it so the LV has to generate a higher pressure to overcome systolic BP and therefore cannot sustain that high pressure for very long--> aortic valve closes earlier --> stroke volume DECREASES |
|
|
Term
| how does increasing FOC affect SV? |
|
Definition
| contractility=intrinsic property of the heart that accounts for changes in FOC not dependent on pre or afterload (changes occur in response to CA or hormone levels). if we give pt NE --> increase inotropic activity w/o change in volume or BP --> when aortic valve opens --> further emptying of the LV than usual such that end systolic volume decreases and SV INCREASES |
|
|
Term
|
Definition
| stroke volume divided by end-diastolic volume |
|
|
Term
| whats the normal range for ejection fraction and what EF = systolic dysfunctioN? |
|
Definition
| normal 55-75%. systolic dysfunction= <45% |
|
|
Term
| what 4 things lead to LV HF (dysfunc)? |
|
Definition
| volume overload (secondary to valvular disease); pressure overload (secondary to HTN); loss of myocardium (secondary to MI); impaired contractility (cardiomyopathy) |
|
|
Term
| with LV dysfunction (HF) what are the 2 major consequences? |
|
Definition
| decrease in CO (hypoperfusion --> sx of lethargy, confusion, decrease in kidney func, decrease voiding, anorexic fatigue); increase in end systolic volume (--> increase in end diastolic vol --> pulm congestion) |
|
|
Term
| when we go into HF, what are the 3 compensatory mechanisms we utilize? |
|
Definition
| frank-starling, neurohormonal activation, ventricular remodeling |
|
|
Term
| how does frank-starling work to help us compensate during hF? |
|
Definition
| body tries to increase CO by increasing preload, but in person with HF, the compensatory increase in preload can cause pt to have very minimal increases in CO/SV --> pulmonary congestion (works a little to help us at first, but then can push us into pulm congestion) |
|
|
Term
| describe how neurohormonal activation helps us compensate |
|
Definition
| (many hormones involved in maintaining CV homeostasis: sympathetic NS, renin-angiotensin-aldosterone system, vasopressin) during normal trauma like bleeding, they help keep us stable then when we're stable they go back to normal. during HF, they DONT go back to normal, they keep revving up and the heart can only take so much |
|
|
Term
| vasopressin is released in resopnse to what? and released from where? |
|
Definition
| in response to decreased systemic BP, released by pituitary gland. normally this system is under negative fb. once the SV decreases, there is less negative inhibition to the hypothalamus --> increase vasopressin secretion by pituitary --> free water absorbed from kidneys --> decrease in Na (one of worst prognostic factors) |
|
|
Term
| what causes an increase in renin and where does it come from? |
|
Definition
| decreased CO and sympathetic activation cause increase in release of renin from kidneys (ACE from lungs, angiotensin from liver) |
|
|
Term
| describe, ANP, BNP, and CNP, where you find them and what they do |
|
Definition
| ANP - in atria; BNP - in ventricles, produced in response to ventricular stress or pressure; CNP - in CNS; they all are diuretics and have vasodilatory properties |
|
|
Term
| what does a high level of BNP indicate? |
|
Definition
| the heart is working really hard to overcome the other compensatory actions, means we're at a higher functional class of HF and at a higher mortality rate, means the congestion is worse |
|
|
Term
|
Definition
| <100 = very unlikely that the SOB is secondary to congestion; >100, much more likely to be secondary to volume overload |
|
|
Term
| in HF, the endothelium-derived vasoactive substances are in what sort of balance? |
|
Definition
| vasoconstrictors>vasodilators! (lots of endothelin) |
|
|
Term
| describe the viscious cycle of heart failure |
|
Definition
| LV dysfunction --> decreased CO and BP --> frank starling, remodeling, neurohormonal activation --> increased CO (increased FOC and HR) and increased BP (vasoconstriction and increased blood vol) --> increased cardiac workload --> more LV dysfunc |
|
|
Term
| how does increase in LVp lead to pulm edema? |
|
Definition
| pressure gets transferred to LA --> increase in pulm vein pressure --> increase in lung capillary pressure --> pulm edema |
|
|
Term
| how do we reverse or prevent the process of ventricular remodeling? |
|
Definition
| put patient on ACE inhibitor after first small infarct or even if pt has mild sx of HF (even if EF is wnl) ace inhibitors help prevent ventricular remodeling |
|
|
Term
| what is cheyne stokes respiration? |
|
Definition
| pt stops breathing at night, snorts, restarts. takes longer for blood to transit to brain and for blood CO2 to be detected by the brain --> breathing could lead to sudden death |
|
|
Term
| why is RV much more likely to fail more quickly than LV? |
|
Definition
| bc RV is thin walled and not used to increases in pressure |
|
|
Term
| how do sx of RV failure differ from those of LV failure? |
|
Definition
| LV failure: dyspnea on exertion, paroxysmal nocturnal dyspnea, tachy, cough, hemoptysis; RV failure: abdominal pain, anorexia, nausea, bloating, swelling |
|
|
Term
| physical signs of LV failure vs RV failure |
|
Definition
| LV failure: basilar rales, pulm edema, S3 gallop, pleural effusion, cheyne-stokes respiration; RV failure: peripheral edema, jugular venous distension, abdominal-jugular reflux, hepatomegaly |
|
|
Term
| what is the gold standard for diagnosis of HF? |
|
Definition
|
|
Term
| why do we do a chest xray in HF workup? |
|
Definition
| check for fluid in the lungs |
|
|
Term
| what bloodwork do we check in pt suspected of having HF? |
|
Definition
| BNP, electrolytes (K, Mg) want to assess risk for arrhythmias, anemia |
|
|
Term
| what is digoxin and how do we use it? |
|
Definition
|
|
Term
| what is a frequent complication of diuretic use? |
|
Definition
| electrolyte depletion --> lower threshold for development of malignant arrhythmias |
|
|
Term
| higher doses of diuretics associated with what? |
|
Definition
| increased mortality. pts who lose kidney func die fast, so only use diuretics when necessary |
|
|
Term
| who is recommended to get ACE inhibitors |
|
Definition
| all HF patients. relieves sx, improves exercise tolerance, reduces mortality and decreases disease progression, prevents functional heart deterioration. blocks conversion of angiotensinI to II, but over time our bodies find other pathways to increase II. also increases KININ levels (vasodilator) |
|
|
Term
| what is the gold standard of pharmacological therapy for pts with HF? |
|
Definition
| beta blockers - block excessive SNS stim, decrease myocardial contractility, increase EF after 3 months, symptomatic improvement, reduce risk of morbid and mortal, reduce disease progression. reduce risk of malig arrhythmias and sudden cardiac death |
|
|
Term
| why is aldosterone bad for us? and consequently what do aldosterone antagonists help with in HF? |
|
Definition
| aldosterone causes fibrosis and collagen deposition and electrolyte imbalance (arrhythmias!). use of antagonists reduces HF-related morbid and mortal, reserved for pts with stage III-IV hf |
|
|
Term
| what are the AE of aldosterone antagonists? |
|
Definition
| hyperkalemia (must monitor pt within first 48 hrs cuz can cause hyperkalemia until death), gynecomastia (9%), increases in creatinine and K+ levels (monitor) |
|
|
Term
| compare angiotensin receptor blockers to ACE inhibitors |
|
Definition
| block AT1 receptors, which bind circulating antiotensin II. equal to but not superior to ACE inhibitors, use for people who cannot use ace inhibitors d/t intractable cough or can be used instead of ace inhibitors, but pt is missing out on the positive vasodilatory effect of KININS! if we block AT1 receptors, we leave OPEN AT2 receptors and these are beneficial (vasodilation, growth inhibition) |
|
|
Term
| if you've had an MI, what are your chances of sudden cardiac death compared to rest of pop? |
|
Definition
|
|
Term
| what is the most important risk factor for sudden cardiac death? |
|
Definition
| reduced left ventricular ejection fraction |
|
|
Term
| for sudden cardiac death, why are the first 10 minutes so important? |
|
Definition
| survival falls 10% per minute over the first 10 mins, therefore NEED to defibrillate close to time zero |
|
|
Term
| what are 2 major things that cause diastolic dysfunction and can lead to left sided heart failure? |
|
Definition
| impaired ventricular relaxation (LV hypertrophy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, transient MI); also obstruction of left ventricular filling (mitral stenosis, pericardial constriction or tamponade) |
|
|
Term
| how does the pressure volume loop change in patients who have diastolic dysfunction? |
|
Definition
| the LV has impaired relaxation and high pressure, so the mitral valve will open when the pressure is still elevated (point a will be higher); also bc the ventricle is not compliant, every change in volume is going to have a much more exaggerated change in pressure than normal, so the whole slope b/w a and b will be more steep. mitral valve also closes earlier (bc doesnt take as much to make LVp>LAp) --> less volume/preload and decreased stroke vol. |
|
|
Term
| why are people in diastolic dysfunction dependent on atrial kick for diastolic filling? |
|
Definition
| usually 2/3 filling is moving down concentration gradient, then diastasis, then atrial kick. if the pressure is already high in the LV, diastasis occurs much earlier (first 1/3 or 1/2) and we become really dependent on atrial kick |
|
|
Term
| why do we have an increased risk for atrial fibrillation with diastolic dysfunction? |
|
Definition
| pressure in the LA has to become a lot higher in order to fill the LV (high pressure) --> LA dilates --> increased risk of afib |
|
|
Term
| what are some common causes of dilated cardiomyopathies? |
|
Definition
| idiopathic, familial, kaksaki virus, peripartum cardiomyopathy, hypothyroidism, alcohol, connective tissue disease |
|
|
Term
| how do dilated cardiomyopathies come about? |
|
Definition
| some insult to myocytes (alcohol, viral etc) --> myocyte injury --> decreased contractility --> decrease in stroke volume --> LV dilatation |
|
|
Term
| what are 4 kinds of hypertrophic cardiomyopathy? |
|
Definition
| concentric, septum (subvalvular apparatus, like papillary muscles can also be hypertrophied), apical (asians), lateral (rare) |
|
|
Term
| what is the danger in familial hypertrophic cardiomyopathy? |
|
Definition
| 1/500, most common cause of sudden cardiac death in the young males (physical activity --> increased risk of arrhythmias and syncope, angina, death) **remember for young females, sudden cardiac death commonly from long QT syndrome and EAD--> torsades |
|
|
Term
| what is the danger in cellular disarray (in hypertrophic cardiomyopathies)? |
|
Definition
| cells cannot communicate electrically and chemically --> pts at HIGH risk for arrhythmias. they get multiple infarcts bc the myocardial oxygen demand is so high (thick walls). also, arteries are squeezed by fibrosis or wall stres and this causes infarcts. patient experiences dizziness, syncope dt decreased flow or arrhythmias |
|
|
Term
| what is the danger in a hypertrophied septum? |
|
Definition
| thick septum impinges on the aortic outflow tract (makes it more narrow) --> blood flows thru faster --> anterior mitral valve leaflet gets pulled towards the septum and cuts off outflow --> syncope, dizziness (pt squats to open outflow tract) --> missing forward flow --> often get backwards flow into the atrium (mitral regurg) |
|
|
Term
| describe what restrictive cardiomyopathy is? what causes it? |
|
Definition
| its a rigid LV caused by: idiopathic, scleroderma, amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease, endomyocardial fibrosis, metastatic tumors, radiation rx |
|
|
Term
| compare pathophysiology in dilated, hypertrophic and restrictive cardiomyopathies. |
|
Definition
| dilated (impaired systolic contraction); hypertrophic (imparied diastolic relaxation; LV systolic func vigorous); restrictive (stiff LV with imparied diastolic relaxation, normal systolic func) |
|
|
Term
| what determines the pattern of force transmission in myocardum? |
|
Definition
| series of proteins produced by the cardiac fibroblast that physically connect the sarcomere with the ECM (i.e. dystrophins, among others). sarcomere linked to dystrophin by actin cytoskeleton of cardiomyocyte. dystrophins linked to ECM (fibronectin) via glycoprotein complex (at sarcolemma)and anchored by integrins |
|
|
Term
| what is the force generator in cardiac muscle? |
|
Definition
|
|
Term
| how do valvular diseases cause problems with force transmission? |
|
Definition
| abnormal mechanical stresses and strains (valvular stenosis or regurg) --> transmission of these mechanical influences to the nucleus --> triggers variations in gene and protein expression --> alterations in cellular synthetic and degradative processes of ECM elements --> variations in ECM affect ventricular diastolic characteristics that influence the clinical response to valve diseases |
|
|
Term
| what modulates/determines the passive diastolic properties of the heart? |
|
Definition
| characteristics of the ECM, esp myocardial COLLAGEN. isoform type I collagen = predominant in normal heart, lacks crosslinks, allows normal compliance. isoform type III collagen - cross-linked, reduces compliance. if any condition increases amt of type III collagen ---> increase ventricular diastolic pressure per volume during filling --> pulm vascular congestion and alterations in chamber filling which can lead to hemodynamic disturbances |
|
|
Term
| myocardial fibrosis is net result of synthesis and degradation of various ECM elements. what cells are responsible for synthesis? degradation? |
|
Definition
| synthesis: cardiac fibroblast (dedifferentiated myofibroblast?); degradation: MMPs/TIMP (can also remodel ECM by altering proportions of the specific components) |
|
|
Term
|
Definition
| central collagenous core that all valve leaflets have. it's continuous with the collagen of the cardiac fibrous skeleton. it's covered in loose mucopolysaccharide containing fibroelastic tissue. |
|
|
Term
|
Definition
| semilunar valves are avascular (aortic, pulmonic). distal 2/3 of the AV valves are avascular. |
|
|
Term
| describe the morphology of the semilunar valves |
|
Definition
| 3 cusps (aortic thicker than pulmonary). commissure = space between attachments of cusps. behind each cup = sinus of valsalva. 3 aortic cusps and sinus of valsalva = left, right, and noncoronary/posterior cusp. the left and right coronary arteries originate from the respective sinus of valsalva. |
|
|
Term
| describe the morphology of AV valves |
|
Definition
| mitral has 2 leaflets, tricuspid has 3. also have chordae tendinae, papillary muscles, and valve annulus. anterior leaflet in both valves is largest |
|
|
Term
| loudness of heart sound reflects what? |
|
Definition
| maximum separation of the valve leaflets when systole begins, rate of change of pressure in the ventricle, structure of the leaflets |
|
|
Term
| where should there be no pressure gradient between LV and LA? if there is, what does it mean? |
|
Definition
| during diastole; pressure gradient --> mitral stenosis |
|
|
Term
| when should there be no pressure gradient between aorta and left ventricle? if there is what does it mean? |
|
Definition
| systole; pressure gradient --> aortic stenosis |
|
|
Term
| what are the 3 states of volume overload? |
|
Definition
| acute (ie. sudden valve rupture from infective endocarditis. if severe, ventricle cannot compensate --> HF); chronic compensated (near normal func, no HF); chronic decompensated (prob initially compensated --> ventricular failure --> clinical HF) |
|
|
Term
| what does the pressure volume curve look like for acute regurgitation? |
|
Definition
| continuation of the normal curve, with increases in volume leading to large increases in pressure |
|
|
Term
| what does the pressure volume curve look like for chronic compensated volume overload (regurgitation)? |
|
Definition
| flattened out bc LV dilates to compensate and develops eccentric hypertrophy (mild compensatory hypertrophy with ventricular enlargement) |
|
|
Term
| how would pressure volume loop change for chronic decompensated regurgitation? |
|
Definition
| loop would shift up and to the right (increased volmes and pressures) and would be steeper indicating that for any degree of increased vol there is higher pressure (decreased compliance) |
|
|
Term
| a large c-v wave indicates? |
|
Definition
| mitral regurgitation (increased left atrial pressure) or tricuspid regurgitation |
|
|
Term
|
Definition
| volume of MR/total LV stroke volume |
|
|
Term
|
Definition
| degenerative (mitral valve prolapse, mitral annual calcification), rheumatic heart disease, endocarditis, papillary muscle rupture, dilatation of mitral valve annulus, congenital |
|
|
Term
| what is mitral valve prolapse |
|
Definition
| congenital degeneration of valve leaflets (deposition of mucopolysaccharides in a thickened spongiosa layer replaces dense collagen/elastin. so valves are loose and floopy)--> bending backwards of the mitral leaflets past the mitral annulus into the left atrium during systole when the valve is closed. can be benign with mild MR or severe MR leading to HF and valve surgery. |
|
|
Term
| what physical findings would we find in a pt with MR? |
|
Definition
| enlarged ventricle, displaced apex beat, APICAL PAN-SYSTOLIC MURMUR, 3rd heart sound, reduced intensity of first heart sound |
|
|
Term
|
Definition
| asymptomatic, normal sized ventricle and normal ejection fraction = no tx. BUT if patient (1) has sx (2) has enlarged ventricle (>45mm) or (3) has reduced systolic funcion (EF below normal) --> SURGERY to replace or repair valve. try to do surgery asap, if we wait too long, the pt will have permanently impaired systolic function |
|
|
Term
| what are the complications of a mitral valve prolapse? |
|
Definition
| thrombus formation and peripheral emboli; supraventricular arrhythmias; aortic or tricuspid valve prolapse with AR or TR; rupture of leaflet chordae --> sudden severe MR d/t flail leaflet with acute severe HF |
|
|
Term
| mitral valve prolapse is associated with what condition? |
|
Definition
| marfan syndrome (connective tissue disease) |
|
|
Term
| what is the diagnostic hallmark of mitral valve prolapse? |
|
Definition
| SYSTOLIC CLICK! from sudden prolapsing back of the valve in systole. best diagnostic test is echo. |
|
|
Term
| when does AR typically occur? |
|
Definition
| early diastole (pressure diff is the greatest) |
|
|
Term
|
Definition
| rheumatic disease, endocarditis, congenital (bicuspid or unicuspid valve), senile calcific degenerative disease (elderly), dilatation of the aortic root (aneurysms, syphillis, marfans), marfans, aortic valve prolapse, FEN-PHEN |
|
|
Term
|
Definition
| throbbing in the neck d/t hyperdynamic pulse |
|
|
Term
| physical exam findings for AR? |
|
Definition
| collapsing pulse, wide pulse pressure in chronic AR, displaced apex beat, early decrescendo diastolic murmur high pitched and soft, capillary pulsations in anil beds (quinckes sign), austin flint murmur (diastolic mitral stenosis-like murmur |
|
|
Term
| what 3 things need to be evaluated to determine if surgery is needed in AR and MR? |
|
Definition
| sx, LV systolic function (EF), and LV size |
|
|
Term
| why is TR not as clinically important as MR or AR? |
|
Definition
| RV can better withstand volume overload vs LV |
|
|
Term
| what are some common etiologies of TR? |
|
Definition
| pulmonary HTN (--> dilatation of the RV, for example with COPD or pulmonary embolism), endocarditis, tricuspid valve prolapse |
|
|
Term
|
Definition
| usually does not need tx unless it is severe and pt experiences sx of RHF. then we give diuretics and repair the valve. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| not treated medically or surgically, bc RV can handle volume loads well |
|
|
Term
| how does the pressure volume curve change when the ventricle is compensating for pressure overload? |
|
Definition
| shifts up and to the left (increased contractility and decreased compliance) |
|
|
Term
| what kind of hypertrophy develops with pressure overload? |
|
Definition
| concentric (formation of sarcomeres in parallel) |
|
|
Term
| what type of dysfunction results from pressure overload? |
|
Definition
| pressure overload from stenosis --> increased contractility and decreased compliance --> LV hypertrophy --> severe diastolic dysfunction --> HF sx --> fibrosis --> reduced systolic func (reduced EF) --> systolic HF |
|
|
Term
| what kind of hypertrophy results from volume overload? |
|
Definition
| eccentric (sarcomeres replicating in series) |
|
|
Term
| how does hypertrophy result in heart failure? |
|
Definition
| hypertrophy is initially compensatory to reduce wall stress --> reduced compliance, elevated diastolic pressures --> diastolic dysfunction--> myocyte necrosis, apoptosis, decreased capillary density, ischemia, fibrosis -->systolic dysfunction--> systolic HF |
|
|
Term
| common etiologies of aortic stenosis? |
|
Definition
| senile degenerative calcific stenosis, congenital (bicuspid aortic valve), rheumatic heart disease |
|
|
Term
| what are the 3 classic sx of aortic stenosis? |
|
Definition
| heart failure sx (fatigue, stenosis), angina, syncope (once these sx develop life span is shortened to 2 years and surgery is needed quickly) |
|
|
Term
| how do we diagnose aortic stenosis? |
|
Definition
| echo or measure pressure gradient across valve |
|
|
Term
| mitral stenosis is almost always due to? |
|
Definition
|
|
Term
| what is the diagnostic hallmark of rheumatic heart disease |
|
Definition
| aschoff body: focal fibrinoid necrosis |
|
|
Term
| how do we diagnose rheumatic heart disease? aka mitral stenosis |
|
Definition
|
|
Term
| what is the normal diameter of the mitral valve and what is considered mild or severe stenosis? |
|
Definition
| normal 4-6 cm squared. mild 2 cm squared. severe/critical stenosis 1 cm squared |
|
|
Term
| what usually causes heart failure in pts with mitral stenosis? |
|
Definition
| atrial fibrillation. left atrium becomes severely enlarged --> loss of atrial contraction and tachycardia --> increase left atrial pressure --> afib --> HF |
|
|
Term
| what do we expect to find in the physical exam for mitral stenosis? |
|
Definition
| opening snap (hallmark) diastolic opening sound of abnormally thickened leaflets d/t high left atrial-left ventricular pressure gradient. mid-diastolic low pitched rumbling murmur d/t turbulent flow. left parasternal heave d/t right ventricular hypertrophy |
|
|
Term
| what is the preferred tx for mitral stenosis? |
|
Definition
| percutaneous mitral valvuloplasty. (surgical tx like this necessary once sx develop. if pt is young, give long term antibiotic prophylaxis). replacement with prosthetic valve may be necessary. left atrial thrombus is contraindication for the valvuloplasty bc it can dislodge it. |
|
|
Term
| what is usually the cause of tricuspid stenosis? |
|
Definition
| rheumatic heart disease, but is very rare |
|
|
Term
| what finding is typical for tricuspid stenosis? |
|
Definition
| increase in the a wave in jugular venous pulse d/t atrial hypertrophy and increased atrial contraction |
|
|
Term
| what usually causes pulmonary stenosis? |
|
Definition
| congenital valve abnormality, bicuspid or unicuspid pulmonic valve, rarely seen. |
|
|
Term
| how do we treat pulmonary stenosis? |
|
Definition
| if severely stenotic (gradient of pressure >40mmHg with sx) -->percutaneous valvuloplasty or valve replacement |
|
|
Term
| how long do bioprosthetic valves last for? |
|
Definition
|
|
Term
| what's the biggest danger in having a patent foramen ovale? |
|
Definition
| paradoxical embolism (esp with high RA pressure) --> stroke. clot comes from venous circ --> goes into systemic circ --> stroke |
|
|
Term
| how are mitral and tricuspid valves developed? what abnormality is associated with incorrect development? |
|
Definition
| atrioventricular canal (in the primitive heart tube is between primitive ventricle and primitive atrium bulges) --> later and super and inferior endocardial cushions pinch in and form a left and right AV canal. AV canal defects aka endocardial cushion defects --> abn tricuspid and mitral valves and ventricular septal defects that are close to the AV valves |
|
|
Term
| what does the ductus arteriosis do? ductus venosus? |
|
Definition
| arteriosus: connects pulmonary artery with aorta; venosus: shunts blood past the liver |
|
|
Term
| when youre cyanotic, your deoxygenated Hb and oxygen saturation are at what levels? |
|
Definition
| deoxy hb >4g/dL; oxygen saturation 80-85% |
|
|
Term
| atrial septal defect: sinus venous defect, where would we find that in the heart? |
|
Definition
| near SVC and pulmonary veins (10%) |
|
|
Term
| where is a secundum atrial defect located? |
|
Definition
| middle of atria where foramen ovale would be (75%) |
|
|
Term
| primum atrial defect, where is this? |
|
Definition
|
|
Term
| describe the 2 types of AV canal defects |
|
Definition
| (1) partial: ASD + cleft valve (mitral regurgitation) (2) complete: common AV valve and VSD (down's syndrome) |
|
|
Term
| what is the sinus venous ASD associated with? |
|
Definition
| located on posterior aspect of LA, where pulmonary venous system, IVC and SVC enter, associated with partial abn pulmonary venous drainage into RA instead of LA |
|
|
Term
| describe the pathology of ASD (what happens when the hole is there)? |
|
Definition
| LA to RA blood flow with vol overload of right heart --> pulmonary vascular disease with RHF (esp with defect >0.5cm) --> if RV compliance decreases or severe pulm vascular resistance develops --> R to L flow (eisenmenger syndrome) --> poor prognosis |
|
|
Term
|
Definition
| vol overload of RH (dyspnea, fatigue, respiratory infections); atrial dilatation --> atrial arrhythmias |
|
|
Term
| physical exam findings for ASD? |
|
Definition
| RV (left parasternal) heave. systolic murmur d/t increased pulmonary flow, fixed split S2 |
|
|
Term
|
Definition
| echo for right heart enlargement |
|
|
Term
|
Definition
| SURGERY: patch (large asd), umbrealla device (large asd), leave the small ones alone? controversial |
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Term
| what are the 4 different types of VSD? |
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Definition
| membranous (70%), muscular (20%), near aortic valve (5%) --> valve is normal but abn blood flow near it causes aortic valve to become deformed, near AV valves (5%) assoc with down syndrome |
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Term
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Definition
| same as ASD, L to R blood shunt, volume overload of left heart and RV, if large pulmonary vascular disease may occur. shunt can reverse --> eisenmenger syndrome --> hypoxia and cyanosis. |
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Term
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Definition
| sx of CHF, cyanosis (if eisenmengers), endocarditis at site of jet lesion, harsh systolic murmur, loud P2, small defect may be sx free |
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Term
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Definition
| echo for chamber enlargement (R side) and vol overload, hypertrophy. |
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Term
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Definition
| if theyre small, leave them. if theyre large in adults, close them. up to 50% close by age 2 and 90% by age 10 so if in kids, leave it might close. endocarditis prophylaxis just inc ase |
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Term
| what are the risk factors for a patent ductus arteriosus? |
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Definition
| rubella, prematurity, high altitude births |
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Term
| what causes the ductus arteriosus to close at birth? |
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Definition
| increase in oxygen and decrease in PGE1 |
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Term
| what direction is the shunt in patent ductus arteriosus? |
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Definition
| L to R (aka, blood goes from the aorta into the left pulmonary artery) --> RV dilatation and CHF, pulmonary vascular disease, possibly afib, eisenmengers |
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Term
| what is the murmur like in patent ductus arteriosus |
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Definition
| continuous (systolic AND diastolic) machine-like murmur, lessens as pulm vascular disease develops |
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Term
| how do we treat patent ductus arteriosus in neonates and adults? |
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Definition
| neonates give indomethacin (PG synthesis inhibitor); adults surgical closure (simple but open heart), umbrella device |
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Term
| describe what congenital aortic stenosis is and who's at risk and when they present |
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Definition
| bicuspid aortic valve; males > females, 20% have other conditions (esp, coarctation of aorta), presents MIDlife with stenosis d/t calcified valve (from trauma of only having 2 valves) |
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Term
| what do we find on physical exam in a patient with congenital aortic stenosis? |
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Definition
| harsh crescendo-decrescendo (diamond) murmur that radiates to carotids, systolic click, reversed split A2 if severe stenosis, concentric LV hypertrophy |
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Term
| what are the 2 rarer types of congenital aortic stenosis? |
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Definition
| discrete subaortic stenosis and supravalvular aortic stenosis |
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Term
| what is the severity gradient for congenital pulmonary stenosis? |
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Definition
| <50mmHg mild, 50-80mmHg moderate, >80mmHg severe |
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Term
| physical exam findings for congenital pulmonary stenosis |
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Definition
| ejection click, wide split S2 with soft P2, RV heave, harsh cresc-desc murmur at left sternal border |
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Term
| physical exam findings for congenital pulmonary stenosis |
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Definition
| ejection click, wide split S2 with soft P2, RV heave, harsh cresc-desc murmur at left sternal border |
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Term
| majority of coarctation of the aorta happens where? |
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Definition
| post-ductus-arteriosus (98%) |
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Term
| coarctation of aorta is associated with what? |
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Definition
| turners syndrome, bicuspid aortic valve, brain aneurysm |
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Term
| what are the findings that are unique to coarctation of the aorta? |
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Definition
| (most are asymptomatic or with leg fatigue) HTN pressure in arms> legs; systolic murmur best heard in the back; continuous murmur d/t collaterals; chest xray notching of inferior rib surface; in neonates preductal presents with lower half body cyanotic, postductal can present as HTN in childhood and adults |
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Term
| what is the tetralogy of fallot |
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Definition
| VSD, subpulmonic pulmonic stenosis, overriding aorta, RV hypertrophy d/t pulm stenosis |
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Term
| what is an example of a cyanotic congenital heart defect? |
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Definition
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Term
| what are the sx for tetralogy of fallot? |
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Definition
| dyspnea, "spells" (cyanosis, syncope, seizures), squat for relief, cyanosis, clubbing, RVH heave, systolic murmur |
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Term
| how do we diagnose tetralogy of fallot? |
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Definition
| CXR boot shaped heart (RV hypertrophy and small pulmonary artery), decreased pulmonary vascular markings. echo, catheterization |
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Term
| how do we treat tetralogy of fallot? |
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Definition
| surgical repair by age 1; correct pulm stenosis and patch VSD |
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Term
| what is the most common cause of cyanosis in the neonatal period? |
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Definition
| transposition of the great vessels |
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Term
| is transposition of great vessels compatible with life? if not how do we treat it? |
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Definition
| no, you get a very cyanotic and hypoxic baby and this is lethal without intervention. it progresses rapidly, and the foramen ovale and ductus arteriosus provide some help so to tx we can give PG infusion to maintain the ductus arteriosus patency. OR we can do the RASHKIND procedure (pull balloon across atrial septum to make communication), JANTENE procedure (arterial switch above semilunar valves) |
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Term
| what are the sx of eisenmengers syndrome? |
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Definition
| hypoxemia, dyspnea, fatigue, erythrocytosis/hyperviscosity, cyanosis, clubbing, pulmonary arteriolar media hypertrophy/fibrosis, thrombosis in pulmonary arteries (GOOD TO TAKE ANTICOAGS) |
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Term
| what do we see on CXR in eisenmengers syndrome? |
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Definition
| pulmonary artery is dilated and there is peripheral tapering |
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Term
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Definition
| really need heart-lung transplant. can do palliative tx (avoid strenuous activity, peripheral vasodilators and pregnancy; phlebotomy) |
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Term
| what congenital heart defects go with down syndrome? |
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Definition
| ASD, VSD, PFO, av canal defect |
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|
Term
| what congenital heart defects assoc with turners? |
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Definition
| bicuspid aortic valve, aortic coarctation, hypoplastic left heart |
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Term
| what congenital heart defects are assoc with williams syndrome? |
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Definition
| supravalvular aortic stenosis, pulmonary artery stenosis |
|
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Term
| what congenital heart defects go with holt-oram syndrome |
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Definition
|
|
Term
| what congenital heart defects go with noonan syndrome? |
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Definition
|
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Term
| what are 3 things that contribute to formation of non bacterial thrombotic endocarditis? |
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Definition
| turbulent blood flow, predisposing conditions (malig, chronic disease, underlying disorders), extrinsic factors (mechanical damage from mechanical catheters and IVDU) |
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Term
| what is libmann sachs endocarditis? |
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Definition
| from SLE, indistinguishable from NBTE, present with clinical syndrome identical to infective endocarditis |
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|
Term
| what group of bacteria do we worry about in endocarditis (good at adherence)? |
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Definition
| gram positive cocci (enterococci, s. viridans, s. aureus) |
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|
Term
| early vs late prosthetic valve endocarditis |
|
Definition
| sx onset less than or greater than 60 days post-op (accts for 20% all cases of endocarditis) |
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|
Term
| native valve endocarditis, what is the definition for community-acquired? |
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Definition
| diagnosed within 48 hrs of admission, and sx developed without extensive out of hospital contact with health care interventions or systems |
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Term
| endocarditis is considered nosocomial health care associated when? |
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Definition
| sx occur in a pt hospitalized for more than 48 hrs before onset of sx |
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Term
| native valve endocarditis is non-nosocomial health care if? |
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Definition
| diagnosed within 48 hrs of admission and of sx developed before hospitalization in pt with extensive out of hospital contact with healthcare interventions or systems |
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Term
| top 2 predisposing valvular lesions in pts less tahn 50 yo leading to endocarditis |
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Definition
| congenital heart disease, mitral valve prolapse |
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|
Term
| top 4 predisposing valvular lesions in pt more than 50 yo leading to endocarditis |
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Definition
| mitral valve prolapse, degenerative heart disease, prosthetic valves, no known heart disease |
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Term
| top 6 bacteria causing native valve endocarditis |
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Definition
| strep viridans, enterococci, other strep (s.bovis), s. aureus, coag- staph, HACEK (normal oral flora) |
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Term
| who are the high risk pts that the new guidelines would suggest we give antibiotic prophylaxis before dental procedures |
|
Definition
| prosthetic cardiac valves, previous episode of endocarditis, congenital heart disease, cardiac transplant patients |
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|
Term
| what is a mycotic aneurysm? |
|
Definition
| results from embolism to vasavasorum of larger vessels, can form in any vascular bed and lead to hemorrhage |
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|
Term
| what are 5 peripheral stigmata of infective endocarditis? |
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Definition
| (result of microemboli, seen in <10% pts) oslers nodes, subconjunctival petechiae, roth spots, janeway lesions, splinter hemorrhages |
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Term
| to diagnose infective endocarditis, what do we need? |
|
Definition
| duke criteria for DEFINITE: 2 major, 1 major 3 minor, 5 minor; duke criteria for POSSIBLE: 1 major 1 minor, 3 minor |
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|
Term
| what are the 2 EKG findings that are characteristic of pericarditis? |
|
Definition
| diffuse, concave UP ST elevation; PR depression |
|
|
Term
| in what condition would we find pulsus paradoxus? |
|
Definition
|
|
Term
|
Definition
| dullness over posterior left lung base d/t effusion/atelectesis |
|
|
Term
| what would we see on an EKG in someone with pericardial effusion? |
|
Definition
| electrical alternans (change in height every other QRS complex d/t heart movement) |
|
|
Term
| what do we see on the echo for person with cardiac tamponade? |
|
Definition
| compression of right heart (bc theyre normally at lower pressure. so effusion will compress these first) |
|
|
Term
| when we examine pericardial fluid, what do we check to see if its TB related? |
|
Definition
|
|
Term
| what is most diagnostic sign of constrictive pericarditis? |
|
Definition
| dip and plateau curve seen during cardiac catheterization |
|
|
Term
| what are important physical exam findings for constrictive pericarditis? |
|
Definition
| JVD (cirrhosis-like signs: hepatomegaly, ascites, edema), pericardial knock after S2 (sudden cessation in ventricular diastolic filling), +kussamaul's sign (increased JVD with inspiration) |
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|
Term
| how big does an aortic aneurysm need to be to require surgical intervention? |
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Definition
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