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Terms**What are the common causes of these valvular lesions: Mitral Stenosis Mitral Insufficiency Aortic Stenosis Aortic Insufficiency What are congenital bicuspid AVs prone to?

DefinitionsMitral stenosis --- rheumatic heart disease (RHD) Mitral insufficiency --- mitral valve prolapse Aortic stenosis (AS) --- calcification of valves (normal or bicuspid) Aortic insufficiency --- dilation of ascending aorta, most commonly due to aging or hypertension calcification, IE, CoA (narrowing), and aortic dissection Myxomatous degeneration refers to a pathological weakening

What is myxomatous degeneration, and which condition is it most commonly associated with?

of connective tissue. The term is most often used in the context of mitral valve prolapse, which is known more technically as "primary form of myxomatous degeneration of the mitral valve."

What condition does this describe: one or both leaflets is (are) enlarged, hooded or tent- mitral valve prolapse like, and floppy? what are common sequelae of Rheumatic heart disease (RHD)? In what disease would you see an Aschoff body? deforming fibrosis of AV and/or MV

RHD (acute only) activated macrophage -- RHD (acute only)

What is an Anitschkow cell? what disease do you see them in? (fyi - nuclear chromatin within cell forms a central irregular ribbon resembling a caterpillar) *what disease (& where) do you see a "fishmouth" valve? What is another term for IE? what can cause it? vegetations (offending agent + thrombotic debris) are common to RHD, IE, NBTE, and LSE (Libman-Sacks Endocarditis)... which one has vegetation that affects both sides of the leaflets? which can affect cordae? what are verrucae? where do they typically form? ** What is carcinoid syndrome? Small wart-like projections (verrucae) appear along the lines of closure Carcinoid syndrome is a group of symptoms associated with both sides: LSE (inflmmatory - Lupus linked) chordae: IE Chronic RHD causing mitral stenosis (looking from LV) bacterial endocarditis, even though can be caused by fungi, rickettsiae, or Chlamydia

carcinoid tumors -- tumors of the small intestine, colon, appendix, and bronchial tubes in the lungs. These tumors release too much of the hormone serotonin, as well as several other chemicals that cause the blood vessels to open (dilate). Does carcinoid syndrome usually affect the L or R heart? why? What is the most common cause of calcific aortic stenosis? *myxomatous valves are common to MV prolapse, what substance is more abundant in these valves? and what color do they stain (Movat)? what is the initial infection that leads to Rheumatic fever? what is the cardiac implication of long term RHD? * which valve disease are verrucae most commonly seen in? Can endocarditis invade the endocardium and lead to the destruction of the underlying tissue? The endocardium is the innermost layer of tissue that lines the chambers of the heart. Its cells are embryologically and biologically similar to the endothelial cells that line blood vessels. FYI* yes, often group A b-hemolytic strep infection, usually pharyngeal (RHD is an immune mediated disease) Deforming fibrosis of AV and/or MV which may not present clinically until years later RHD proteoglycans - blue/green Right - first exposure to bioactive substances released by carcinoid tumors, also serotonin is deactivated when it passes through the lungs before reaching the left heart. aging

The endocardium underlies the much more voluminous myocardium, the muscular tissue responsible for the contraction of the heart. The outer layer of the heart is termed epicardium and the heart is surrounded by a small amount of fluid enclosed by a fibrous sac called the pericardium. - marantic endocarditis

what is another term for nonbacterial thrombic endocarditis (NBTE)? * what type of patients does this most commonly occur in?

- Occurs in debilitated patients (e.g. cancer) Deposition of small noninfected, loosely attached masses of fibrin, platelets, and other blood components on valves Often associated with hypercoagulable state, as in mucinous adenocarcinoma

what type of patients does Libman-Sacks Endocarditis most commonly occur in? * what do carcinoid tumors secrete?

LSE - lupus (predisposed to clotting) serotonin

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Definitionssmall box = 1mm or 40ms, big box = 5mm or 200ms, Pwave = < 100ms wise

Standard EKG

and < 3mm high and upright in I/II/aVF and inverted in aVR, 120 < PR < 200, 60 < QRS < 100?, Q < 3mm, QT < 420?, T wave upright in I/II and inverted in aVR, T wave 120

Hs and Ts of PEA/asystole/vfib/vtach incomplete vs complete BBB RBBB LBBB AV blocks 1st degree AV block

hypovolemia, hypoxia, hypothermia, hypo/hyperkalemia, acidosis, tension pneumo, tamponade, MI/PE, toxin complete = QRS > 120ms, incomplete = QRS 90-110ms QRS > 120, RSR' in V1, wide S waves in I/V5-6 QRS > 120, Wide R in V5-6, LAD 1st degree = PR prolongation, 2nd degree = dropped beats (type 1 vs type 2), 3rd degree (AV dissociation) PR prolongation (> 200ms)

2nd degree type 1 AV block progressive PR prolongation to dropped beat 2nd degree type 2 AV block random dropped beats (no PR prolongation) 3rd degree AV block Wolf-Parkinson-White syndrom Lown-Ganong-Levine syndrome AVNRT treatment complete AV dissociation pre-excitation through bundle of kent (atria to ventricle accessory pathway) resulting in delta wave, PR shortening, wide QRS pre-excitation through James fibers (atria to His bundle accessory pathway) resulting in PR shortening without delta wave/QRS widening "vagal maneuvers then adenosine then synchronized cardioversion if stable (go directly to cardioversion if unstable) first episode, paroxysmal (recurrent), persistent (recurrent, > 7days), permanent (recurrent, > 1yr) risk of stroke in pt with a-fib - CHF, HTN, Age > 75, DM, prior stroke or TIA if unstable - cardioversion, if stable but symptomatic - control rate first (BB/CCB a-fib/a-flutter treatment unless EF < 40 then use dig/amio) then cardiovert (DC or amio), must perform TEE or anticoagulate with heparin x3wks before cardioversion if a-fib > 48hrs how to reveal a-flutter give adenosine "if stable - medical cardioversion (lido, amio, procainamide or Mg), if unstable VT treatment electrical cardioversion then medical maintinance, if pulseless defibrillation/epi/lido Vfib/pulseless VT treatment PEA/asystole treatment first degree AV block treatment second degree mobitz 1 treatment second degree mobitz 2 treatment third degree AV block treatment defibrillation, epi, lido/amio epi, search for Hs/Ts nothing

types of a-fib CHADS2 score

nothing if asymptomatic, if symptomatic use atropine or transcu pacing transcu pacing bridge to transvenous pacing (usually happens in acute anteroseptal MI) treat like mobitz 1 if narrow (usually inferior wall MI), if wide treat like mobitz 2 (usually anteroseptal MI)

if unstable use cardioversion, if stable depends on ortho vs antidromic - if WPW narrow complex (orthodromic) treat as SVT (vagal/adenosine/cardioversion) but if wide complex (antidromic) treat with procainamide (although will look like VT so will probably use lido first) pacemaker letters pts who present with atypical MIs first letter - champer paced, second letter - chamber sensed, third letter response to sensing of electrical activity elderly, DM, women, alcoholics, spinal cord disease myoglobin - rises first (2-3 hrs) but nonspecific to cardiac muscle, CK - rises serum markers in acute MI within ~6hrs but nonspecific, CKMB - rises within ~6hrs and fairly specific, tropinin T/I - rise within ~6hrs and are very specific but remain elevated for weeks acute MI treatment IV/O2/monitor, aspirin/clopidogrel/heparin, morphine(if pain)/NTG(unless inferior MI or sildenafil), abciximab?, lytics/cath, BB/ACE (within first 24hrs) anterior MI associated with mobitz 2 (can decompensate to complete heart block) while inferior MI associated with type 1 or mobitz 1 AV block cephalization of pulmonary vasculature, vascular congestion, Kerly B lines ~10mmHg IV/O2/monitor, NTG/furosemide, consider nitroprusside (if need more ACPE treatment preload/afterload reduction), consider dobutamine/norepinephrine (if low BP or decreased CO), consider CPAP/intubation (if poor ox/vent) Kussmaul's sign increased JVD on inspiration - sign of poor RV filling (constrictive pericarditis, restrictive CMP, cardiac tamponade etc) S3 (ventricular gallop) = diastolic filling of dilated ventricle; S4 (atrial gallop) = atrial kick against stiff ventricle AS murmur increases with squatting; HOCM murmur increases with valsalva (decreased LVEDP) LVH/LAE, septal Q waves assesses PE risk, low risk can be r/o with D-dimer (there is also a Wells score for DVT) heparin or lytics (if limb is in danger) venostasis, hypercoaguability, vessel wall injury dyspnea, pleuritic chest pain, hemoptysis (uncommon); dyspnea/CP/tachypnea (almost always present) heparin or lytics (if hemodynamically unstable) left trapezius muscle ridge STEMIs have convex ST segments while pericarditis has concave ST

MI and AV block association ACPE CXR signs normal PAWP

gallops

AS vs HOCM murmurs HOCM ECG findings Wells criteria DVT treatment Vichows triad PE triad PE treatment where does pericarditis pain radiate to? convex vs concave ST

segments pulsus paradoxus

segments decrease in inspiratory (relative to expiratory) blood pressure > 10mmHg; or the absence of radial pulse during inspiration; sign cardiac tamponade class triad - hypotension, JVD, distant heart sounds (late findings); narrow

cardiac tamponade findings pulse pressure, pulsus paradoxus and kussmaul's sign are earlier; low voltage or electrical alternans on EKG and