Pathoma 8- Cardiac zhester
Terms in this set (99)
Angina represents reversible or irreversible injury?
Describe how O2 is delivered to the layers of the heart via coronary aa. What is most susceptible?
Coronary arteries start at epicardium, dive down to myocardium and endocardium. Area just into endocardium is most susceptible to ischemia (subendocardial ischemia)
Transmural ischemia vs subendochardial ischemia
transmural: ST elevation
Acute occlusive thrombosis, full thickness, over cracked JUICY PLAQUE
subendocardial: ST depression
1C artery, aborted MI (by reperfusion). or >1C artery in shock
2) presents how (4)
arises with exertion/emotional stress
1) athlerosclerosis of coronary arteries with > 70% stenosis
2) Chest pain < 20 mins, radiating to left arm or jaw, diaphoresis, shortness of breath
3) ST DEPRESSION (subendocardial ischemia) upon exercise test
4) Rest, Nitroglycerin
Acute Coronary Syndrome (Unstable Angina)
1) due to
2) presents how
5) risk of progressing to
1) rupture of athlerosclerotic plaque -> thrombosis -> INCOMPLETE** occlusion of coronary artery
2) chest pain at rest
3) ST DEPRESSION (subendocardial ischemia) - NSTEMI
risk of MI progression
1) due to
2) presents how
1) coronary artery VASOSPASM - cuts blood supply in episodic pattern
2) Episodic chest pain unrelated to exertion
3) ST ELEVATION (transmural ischemia)
4) nitroglycerin or calcium channel blockers.
MOA of nitroglycerin
dilation of veins -> decreased preload and stress
usual causes (4)
necrosis of cardiac myocytes
rupture and thrombosis of atherosclerotic plaque
vasospasm (prinzmetal, cocaine)
vasculitis (esp. Kawasaki's)
--> and COMPLETE** occlusion of coronary artery.
Myocardial Infarction: clinical features
how does nitroglycerin affect S/S?
severe, crushing chest pain > 20 MINUTES, radiates to left arm or jaw, diaphoresis, dyspnea.
NOT relieved by nitroglycerin
Initially shows ST depression (subendocardial), then ST elevation (transmural)
Infarction in MI usually involves which chambers?
(both atria and RV spared)
Most commonly involved artery in MI? Other aa commonly involved?
what pathology is found early on?
LAD- Ant wall of LV, Ant. portion of IV septum.
subendocardial necrosis involving <50% of myocardial thickness (ST depression)
Other aa: RCA (Post. LV wall and post septum and papillary mm of LV), LCX (lateral wall of LV)
Occlusion of LAD leads to
infarction of ANTERIOR WALL & anterior portion of LV SEPTUM
Occlusion of RCA leads to
infarction of POSTERIOR WALL & posterior SEPTUM, Papillary muscles of LV
Occlusion of LCX leads to
infarction of LATERAL WALL of LV
Irreversible damage indicated by which cardiac enzymes? (3)
when are they apparent?
Troponin I & II ( GOLD STANDARD)
-Rise 2-4 hrs after, peak at 24-48 h, normal by 7-10d
CK-MB (detecting reinfarction)
-rise 4-6 h after, peak at 24, normal by 72 h
myoglobin: earliest to rise after MI; most useful for ruling out MI
Tx of MI (5)
-Aspirin/heparin: limit thrombosis
-Supplemental O2: minimize ischemia
-Nitrates: vasodilate coronary arteries and veins
-Beta-blockers: slow HR, reduce risk of arrhythmia
-ACE inhibitors: blocks AT2- decrease PVR, blocks aldo-> blocks Na reuptake. decrease risk of LV dilatation
-Fibrinolysis or angioplasty (return O2 to ischemic sites)
Complications that can result from fibrinolysis or angioplasty after MI (2)
opens blocked vessel:
-HYPERCONTRACTION of myofibrils as Ca enters with blood (image) -> contraction bands- pink bands in myocytes with no nuclei
-Reperfusion injury: Return of O2 and inflammatory cells can lead to free radical generation --> cardiac enzymes continue to rise
Morphological changes & complications (3) in MI <4 hours:
tissue damage is marked by hypoxia
No gross or microscopic changes
cardiogenic shock, CHF (decreased EF), and arrythmia (no ATP, no Na/K ATP-ase; damage to conducting system within first 24hrs)
Morphological changes & complication (1) in MI
COAGULATIVE NECROSIS (loss of nuclei - karyorhexis, karyolysis, piknosis)
Arrhythmia (damage to conducting system within first 24hrs)
Coagulative necrosis = PMNs, edema, neecrosis, red = dead, ↑ MMPs
Morphological changes & complication (1) in MI
NEUTROPHILS (inflammation after necrosis)
Fibrinous pericarditis may occur (chest pain and friction rub) bc neutrophils can leak into pericardium - shaggy, rough appearance to outside of heart; only occurs in TRANSMURAL infarction only!
may occur in 1-3 days post MI. chest pain and friction rub bc neutrophils can leak into pericardium and inflame - shaggy, rough appearance to outside of heart; only occurs in TRANSMURAL infarction only!
Morphological changes & complications (3) in MI
MACROPHAGES (inflammation after necrosis)
macrophage eating tissue weakens walls
Can cause rupture of: (before scar form)
1) ventricular free wall (can cause cardiac tamponade)
2) IV septum (shunt)
3) papillary muscle (can cause mitral insufficiency; assoc. with occlusion of RCA)
Morphological changes & complications in MI
Red border emerges as granulation tissue enters from edge of infarct. (healing begins)
(Plump fibroblasts, collagen, BVs)
Morphological changes & complications (3) in MI
FIBROSIS (scar is formed)
White scar of type I collagen
wall is now weaker than original:
Can have aneurysm, mural thrombus (thrombus along wall of scar d/t stasis), or dressler syndrome
pericardial antigens exposed during inflammation in pericardium in transmural infarction -> cause autoimmune pericarditis 6-8 weeks after an MI
1 day/1 week/1 month (MI mnemonic)
Coag Nec. [1day] Neutro inflamm -> Macro inflamm [1week] Gran. Tissue [1month] SCAR
clinical complications post-MI (6)
Pericarditis (not a new MI!)
Arrhythmias & heart blocks
Mural thrombus (endocardial damage -> free wall or IV septum rupture)
LV Dysfunction (CHF, Shock)
Infarction extension -> LV aneurysm
Papillary muscle dysfxn -> mitral regurg w/ murmur and pulmonary congestion
Sudden cardiac death
- preexisting risk factor
- followings what heart activity
- causes (4)
unexpected death due to cardiac disease, without sx or <1 hr after sx arise.
90% have preexisting athlerosclerosis
Usually due to fatal ventricular arrhythmia.
less common causes: mitral valve prolapse, cardiomyopathy, cocaine abuse (vasospasm)
poor myocardial fxn due to chronic ischemic damage (with or without infarction) progresses to CHF
Left sided heart failure
1) causes are? (5)
2) clinical features? (4)
HTN (hypertrophy -> inc need for O2 to walls -> ischemic damage)
dilated cardiomyopathy (all chambers dilated, mm stretch-expanded chambers can't contract)
restrictive cardiomyopathy (not enough blood enters)
2) clinical features due to DECREASED FORWARD PERFUSION & PULMONARY CONGESTION
-Decreased flow to kidneys leads to + RAAS -> fluid retention exacerbates CHF (tx is ACEi)
*dyspnea, paroxysmal nocturnal dyspnea (increase venous return when lying flat), ORTHOPNEA, crackles (fluid in interstitial lung space).
Hemosiderin laden macrophages (aka. heart failure cells) - capillaries leak blood cells into alveoli and macrophages consume them
Tx of left sided heart failure
ACE inhibitors (to stop ATII/RAAS from increasing fluid retention)
Right sided CHF
1) caused by? (3)
2) clinical features? (3)
1) MCcause: LEFT SIDED HEART FAILURE (can back up to right side).
- Left-to-right shunt
- chronic lung disease --> hypoxia --> BVs in lung constrict --> increase pressure against RV pumping --> cor pulmonale (right heart failure)
2) Due to congestion:
-Jugular venous distension (JVD)
-painful HepatoSplenoM, NUTMEG (blotchy red and white) liver because central veins are congested, may lead to cardiac cirrhosis
-Dependent pitting edema in lower extremities
Congenital defects of the heart
-usu weeks 3-8
-seen in 1% of live births
-most defects are sporadic
1) Originally right-to-left shunting presents how at birth?
2) Originally left-to-right shunting present how at birth?
3) Eisenmenger syndrome
1) cyanosis shortly after birth (can have paradoxic embolism to brain -> abscess)
2) Relatively asymptomatic
3) When you start with left-to-right shunting, blood backs up in pulmonary circuit, then it reverses due to ↑ in pulmonary HTN, resistance ->
RV hypertrophy (pumping against greater pressure)
Polycythemia (deoxygenated blood enters systemic circuit and activates EPO)
most common cardiac congenital defect?
-defect in septum that divides right and left ventricles
- 90% in the membranous septum
-a/w fetal alcohol syndrome**
- holosystolic murmur
-small defect = often asymp
-large defect = Eisenmenger syndrome - late cyanosis, RVH, polycythemia (dec O2 in blood activates EPO), clubbing of nails (L-to-R shunt** - pulmonary HTN - once this gets too high, shunt reverses - cyanosis)
-small defects may close spont
most common congenital heart disease presenting in adults?
most common subtype? Other type a/w?
heart sound and ECG?
important complications (2)
ASD-defect in septum that divides left and right atria
-MC type is ostium secundum
-ostium primum type is a/w down syndrome**
-split S2 (delayed closure of pulmonic v), incomplete RBBB
-paradoxical embolus is an important complication (bypasses lungs and enters systemic circuit)
- irreversible pulmonary HTN (<10%) bc of L-to-R shunting into RA
a/w with what pathogen?
-failure of ductus arteriosus to close (connects pulm artery and aorta)
-a/w congenital rubella*
- more common in females
- holosystolic machine like murmur + systolic thrill + Corrigan's pulse
-asymp at birth
-pulmonary HTN (LtoR shunt)
-Eisenmerger syndrome = shunt reversed = cyanosis in LE later in life**
(DA connects the pulm. artery and aorta after its 3 major branches. initially start with blood shunting from aorta to pulm. but can reverse after pulm HTN so deoxygenated blood enters systemic circuit - but only after major aortic branches so cyanosis in lower extremities only)
-tx = indomethacin
-dec PGE, resulting in PDA closure
Tetralogy of Fallot
characterized by? (4)
what do the 4 features cause?
what determines extent of shunt?
how to deal with cyanotic spell?
-pulmonary artery stenosis, RVH, VSD, overriding aorta -> RtoL shunt ->cyanosis in newborns
-degree of stenosis determines cyanosis
-cyanosis during exercise (hypercyanotic "tet" spells)
- squatting down helps - increases arterial vascular resistance dec shunting and allows more blood to reach lungs
-xray** - boot shaped heart
Transposition of great vessels
2) associated with
3) Presents how?
4) Physical effects on heart?
5) How to treat?
1) pulm art from LV and aorta from RV
2) Maternal diabetes
3) Early cyanosis, pulm and systemic ciruits DO NOT MIX. (aorta from RV sends deoxygenated blood from the system back to RA)
4) Hypertrophy of RV and atrophy of LV
5) Administer PGE to maintain a PDA until surgery can be performed.
SHUNT required for survival.
Surgery results in AV discordance for a functionally correct system.
-tx = PDA - via PGE until surgical repair can occur
1) Caused by
2) Presents how
3) Stay alive how?
1) Truncus doesn't divide into aorta & Pulm art -> single large vessel arises from both ventricles
2) early cyanosis - deoxygenated blood from RV mixes with oxygenated blood from LV before pulmonary and aortic circulations separate
3) VSD (have several dysplastic valve cusps)
-tricuspid valve orifice (RA->RV) fails to develop so the RV is hypoplastic
-Usually has ASD resulting in right to left shunt
-presents with early cyanosis
Coarctation of the aorta
location, associations, and presentations in infantile and adult forms
-narrowing of aorta
-a/w PDA, MC in boys
-coarctation lies just distal to aortic arch, but proximal to PDA - causes distal blood to be lower pressure so blood is R->L shunted from pulm artery to aorta -> LE cyanosis
-a/w Turner syndrome***
-not a/w PDA
-lies distal to aortic arch
-presents at HTN in the upper extremities, hypotension + weak pulses in LE
-a/w bicuspid aortic valve**
-collateral circulation develops across intercostal arteries = engorged arteries cause notching of ribs on xray**
d/t engorged collateral circulation developing in intercostal aa in adult aortic coarctation.
AV Septal Defect
2) assoc w
3) cyanosis pattern
1) failure of superior and inferior endocardial cushions to fuse adequately
2) Trisomy 21
3) late cyanosis
Congenital heart disease correlated with:
1) Trisomy 21
2) Turner syndrome
4) Maternal Rubella
5) Maternal diabetes
1) endocardial cushion defect
2) Coarctation of the aorta
4) VSD, ASD, PDA
5) Transposition of great arteries
Right to Left shunts:
Tetralogy of Fallot
Transposition of great arteries
Total anomalous pulmonary venous cnxn (TAPVR)
Left to right shunts (4):
AV septal defect
Valvular lesions results in either:
-stenosis - tightens orifice
-regurgitation - backflow across valve
Obstructive congenital lesions: name 3
coarctation of aorta
Pulm stenosis vs pulm atresia
stenosis: cusp fusion with RVH
atresia: Hypoplastic RV with ASD & PDA
Aortic stenosis vs aortic atresia
anomalous development (bicuspid)
Acquired (rheumatic HD)
atresia: HYPOPLASTIC left heart syndrome
1) usually due to
2) presents at what age
3) physiologic changes
4) What is heard? where?
1) fibrosis & calcification from "WEAR & TEAR" (picture) in older patients
2) >60yo ("senile").
middle-aged due to RF
young pt. due to congenital bicuspid valve
3)compensation with concentric LVH leads to a prolonged asymptomatic stage; LV diastolic pressure rises
4) SYSTOLIC EJECTION CLICK followed by <> murmur (severe if extends into S2); S4 in LVH
location: aortic area, may radiate to peripheral vessels and apex
how to distinguish aortic stenosis caused by
1) chronic rheumatic HD
2) wear & tear/"senile"
rheumatic disease will also involve MITRAL stenosis and have FUSION of aortic valves.
1)Complications of aortic stenosis include?
2) 3 major symptoms and the comparative survival rate when it is your major symptom
1) concentric LV hypertrophy, angina/syncope with exercise, microangiopathic hemolytic anemia
2) angina > syncope > CHF
(50% 5 yr, 3 yr, 2 yr survival)
3) if symptomatic:
- neg chronotropes/inotropes, NO VASODILATORS;
- valve replacement:
bioprosthetic (in older pts or "bleeders" as valve will deteriorate); mechanical (anticoagulation needed to reduce thromboemboli)
1) causes? (3)
2) what is heard?
3) Clinical features (chronic & acute)
aortic root dilation (**isolated, syphilitic aneurysm, aortic dissection)
valve damage (endocarditis)
CT disease (myxoid degeneration, ankylosing spondylitis, marfan's -> dilation of aortic root)
2) early, blowing mid-diastolic murmur (Austin Flint murmur)
- Hyperdynamic circulation - regurg. ^preload-> ^ SV-> inc PP -> WATER-HAMMER pulses (bounding pulses), pulsating nail bed (quinke pulse), head bobbing
- LV dilation and eccentric hypertrophy (just one area of LV-seen in volume overload)
(If acute -> pulm edema & shock; chronic -> elevated LVEDP, dec CO, heart failure)
4) replace valve when LV fxn <50%
nifedipine to reduce afterload
avoid neg chronotropes (prolong diastole and regurg)
MITRAL VALVE PROLAPSE
2) caused by
3) what is heard?
1) ballooning of mitral valve into LA during systole
2) Myxoid degeneration of valve making it floppy (accumulate ground substance) - etiology not known; some assoc. w/ Marfan's or ED
3) MID SYSTOLIC CLICK followed by REGURG MURMUR, louder with squatting; click is earlier with decreased preload (underfilled)
4) complications Inf. Endocarditis, arrhythmia, severe mitral regurg - are rare
3) what is heard? where?
4) acute/chronic can lead to
1) blood reflux from LV into LA during SYSTOLE
2) mitral valve prolapse, LV DILATION (pulls valve open), endocarditis, acute rheumatic heart disease, papillary rupture after MI.
3) Holosystolic "blowing" murmur louder with squatting (^PVR) & expiration (^ blood entering to LA)
radiates to axilla in anterior leaflet MR; to P2 area in posterior leaflet MR
4) acute -> congestion with high LA pressure
chronic -> LV volume overload -> left sided heart failure
1) usual cause
2) what is heard
narrowing of the mitral valve orifice
1) chronic rheumatic valve disease
2) loud S1 -> S2 -> OPENING SNAP -> diastolic rumble (time btw S2 and opening snap inversely related to severity)
Volume overload -> dilated LA-> disruption of conduction:
- A. Fib (stasis -> thromboemboli, dec CO) - need Rx for rate control (digoxin, B-blockers, Ca-channel blockers) and anticoagulation
- compression (dysphagia, hoarseness)
Rise in LA vol and Pressure:
-pulmonary congestion (edema, dyspnea & hemoptysis, hemosiderin laden macrophages)
-pulmonary HTN (eventual right side failure - JVDs, ascites)
4) obstruction relief in severe MS
balloon valvuloplasty (if not calcified)
2) heart sounds compared to MS
4) tx (3)
2) diastolic murmur closer to sternum and increases with inspiration; TV OS
3) right-sided congestion (JVD, anasarca)
4) diuretics, slow HR, valve replacement
1) causes (2)
2) compare neck veins a/w TR vs. TS
3) heart sound? where? compare effects of breathing in TR vs. MR
1) 20% of patients with rheumatic MS; carcinoid syndrome
2) prominent v-waves in TR; JVD in TS
3) systolic murmur in left parasternal area; murmur worse with inspiration
4) diuretics, valve repair
1) causes (3)
2) heart sound? where?
1) congenital rubella, carcinoid, tetralogy of fallot
2) systolic murmur at left sternal border; worse with inspiration
3) RV failure - anasarca, JVD
4) balloon valvuloplasty or valve replacement
Define endocarditis & pathogenesis
Inflammation of endocardium that lines surface of cardiac valves. (usually due to bacterial infection)
Endothelial injury followed by bacteremia.
Most common cause of bacterial endocarditis?
Low virulence (subacute - leaves only small vegetations that don't destroy valve)
- infects previously damaged valves
- damaged endocardial surface develops thrombotic vegetations of platelets and fibrin which trap bacteria during transient bacteremia (dental procedure)
Endocarditis in IV drug abusers
High virulence: (acute - valves destroyed)
- infects normal valves (tricuspid)
- large vegetation
Most commonly TRICUSPID valve (shoot up -> enter venous system -> right heart)
agent causing endocarditis of prosthetic valves
complications of prosthetic valves (4)
Anticoagulant related hemorrhage
Surgical or structural deterioration due to calcification
endocarditis with S. Bovis is associated with?
associated with underlying colorectal carcinoma
Endocarditis with negative blood cultures?
Clinical features of bacterial endocarditis (4)
-Murmur (due to vegetations)
Embolization of septic vegetations
- Janeway lesions - non-painful lesions onpalms/soles
- splinter hemorrhages in nail bed
- intracranial bleeding, pulmonary emboli
- glomerulonephritis, vasculitis, arthritis
- Osler nodes - painful finger lesion ("Ouch Ouch Osler")
- Roth spots - retinal hemorrhage
- Anemia of chronic disease (due to chronic inflammation- acute phase reactants (hepsidin) hide Fe)
Lab findings in bacterial endocarditis (3)
-positive blood cultures
-anemia of chronic disease (low MCV bc microcytic, acute phase reactants from liver like hepsidin which trap iron in storage sites -> Increased ferritin, decreased TIBC, decreased serum % saturation bc bone starts taking iron from blood)
-Transesophageal echo to detect lesions on valves
Acute rheumatic fever
usually presents in what pts how?
dx? labs (3); minor criteria (3); major criteria (5)
-Group A beta-hemolytic streptococci
-affects children 2-3 weeks after strep throat (pharyngitis). Bacterial M protein resembles human tissues (molecular mimicry)
-evidence of prior strep infection = Antistreptolysin O antibodies (ASO), positive throat culture, or anti-DNase B titer
-minor = fever, elevated ESR, prolonged PR
-Joint - migratory polyarthritis (large joint)
-O - heart problems - pancarditis- only problem that won't self-resolve
-N - nodules (subcutaneous) in skin
-E - erythema marginatum (rash that is more red at margins.
-S - Syndenham chorea (rapid chorea)
Tx w/ ASA and penicillin
Prophylaxis: PCN until adulthood
heart damage in acute rheumatic fever affects each layer how?
which is the most common cause of death in the acute phase?
1) endocarditis- tiny vegetations on endocardium of mitral (and maybe aortic) valve lead to regurg
2) myocarditis- Aschoff bodies - chronic inflamm with giant cells and fibrinoid necrosis with Anitschoff (caterpillar) cells
-> myocarditis is MC COD in RF
3)pericarditis - friction rub/chest pain, tachcardia, MR or AI murmur
Anitschoff bodies pic
myocarditis in acute rheumatic fever
what are they?
chronic inflamm with giant cells and fibrinoid necrosis
pancarditis (myocarditis) in acute rheumatic fever
Chronic rheumatic valvular disease
1) caused how
2) results in
3) usually what valve
-repeat exposure to group A strep results in relapse of acute phase -> inc risk for chronic rheumatic valvular disease -> valve scarring
2) results in stenosis
3) usually involves mitral valve - thickening of chordae tendinae and cusps
sometimes aortic valve - fusion of commissures (fish mouth appearance**)
4) infectious endocarditis
Libman Sacks endocarditis is due to? aka?
Usually which valve? what does it look like?
a form of marantic endocarditis
Sterile vegetations associated with SLE (aka. verrucous non-bacterial endocarditis)
Mitral valve; vegetations on surface and undersurface (both sides!)
review pic of endocarditis vegetations- rf, ie, nbte, libman
RF, IE = top row
NBTE, libman = bottom row
Diagnosis of bacterial endocarditis:
what are the major criteria? (2)
Major: positive blood cultures and evidence of endocardial involvement
minor: predisposing condition, fever, vascular or immunologic phenomena
high risk patients requiring IE prophylaxis (4)
1) prosthetic heart valves
2) prior bacterial endocarditis
3) complex congenital heart disease
procedures requiring IE prophylaxis (5)
1) dental procedures with gingival bleeding
2) rigid bronchoscopy and/or procedures with bleeding
3) GI procedures (optional for endoscopy)
4) GU procedures
5) vaginal deliveries if infection is present
Nonbacterial thrombotic endocarditis is due to? ("Marantic Endocarditis") (2)
Usually which valve?
sterile vegetations arise in association with HYPERCOAGULABLE STATE or ADENOCARCINOMA
Mitral valve along the lines of closure. -> mitral regurg.
Can't tell difference from picture, you would have to know there are neutrophils, etc to distinguish whether it was infectious type.
Dilated cardiomyopathy vs restrictive cardiomyopathy
dilated: can't contract well- dilation of all 4 chambers
restrictive: can't fill properly
Most common form of cardiomyopathy
1) systolic or diastolic dysfunction?
2) complications (3)
3) heart sound
4) causes (6)
dilated cardiomyopathy-dilation in all four chambers of the heart
1) systolic dysfunction
- biventricular CHF
- mitral and tricuspid valve regurg (stretch)
3) S3 present
4) MC idiopathic
genetic mutations (usu AD)
myocarditis (coxsackie- lymphocyte infiltrate- chest pain, arrhythmia, sudden death)
drugs (doxorubicin, cocaine)
2) systolic or diastolic dysfunction?
3) symptoms/complications (2)
4) classical patient
5) biopsy finding
-massive hypertrophy of LV
1) AD mutations in sarcomere proteins -> hypertrophy -> dec compliance -> dec filling -> dec CO
2) diastolic dysfunction
3) syncope with exercise (hypertrophy of IV septum blocks blood entering aorta -> fxnal aortic stenosis)
sudden death due to ventricular arrythmias
4) common cause of sudden death in young athletes
5) biopsy = myofiber hypertrophy with disarray** (muscle fibers aligned in all directions; not parallel)
eosinophilic infiltrate and inflammation in the endocardium and myocardium-> restrictive cardiomyopathy
2) systolic or diastolic dysfunction?
3) causes (5)
4) present with
5) ECG findings (2)
1) dec compliance of ventricular endomyocardium
2) restricts filling during diastole
endocardial fibroelastosis (kids- dense layer of fibrosis in endocardium)
loeffler syndrome (eosinophilic infiltrate and inflammation in the endocardium and myocardium)
4) presents with CHF
5) low voltage EKG, diminished QRS amplitudes
Most common primary cardiac tumor in adults
1) what does it look like? gross/histo
2) location? which layer?
4) benign or malignant?
5) tumor marker
1) pedunculated (grows on stalk) gelatinous mass of proliferated subendocardial mesenchye; abundant ground substance on histo
2) left atrium; exclusively on endocardium
3) can cause syncope due to obstruction of mitral valve (murmurs and "tumor plop" that appears around when S3 would occur)
5) factor VIII
most common primary cardiac tumor in kids
1) what is it composed of?
1) benign hamartoma of cardiac muscle (disorganized, but normal tissue)
2) ventricles (esp R)
3) a/w tuberous sclerosis
4) usually regress spontaneously; surgery if outflow tract is obstructed
two most common primary malignant cardiac tumors?
on which side of the heart?
angiosarcoma > rhabdomyosarcoma
malignant tumors are usu sarcomas on the left side of the heart (benign tumors are usu on the right)
tumor that arises primarily from valvular endocardium
1) most common valve involved?
2) what's it look like?
3) symptoms? (3)
1) aortic valve
2) "sea anemone" composed of papillary fronds similar to chordae tendinae
3) usu asymptomatic
anginal symptoms (block coronary orifices)
ischemic attacks or stroke (embolization )
locations of these tumors:
3) pericardial cysts
4) bronchogenic cysts
1) anywhere in the heart
2) IV septum
3) right costophrenic angle
smallest tumor that can cause sudden death
AV node mesothelioma
pacemaker in children to correct heart block
2) age, gender
3) 2 most common symptoms
4) other CMs (4)
5) benign or malignant?
1) right atrium
2) 20-50; male
3) usu CHF, thromboembolism
4) non-specific symptoms, palpitations, dyspnea, chest pain
5) malignant (metastases are common to pleura, mediastinum, lungs, liver, bone, adrenals, CNS, lymph nodes)
tumor arising post-transplant
2) causative agent?
post-transplant primary lymphoma of the heart
1) anti-rejection drugs
2) EBV infection
3) reduce anti-rejection drugs; anti-lymphoma tx for refractive cases (CHOP-R)
metastatic cancer in the heart
1) more or less common than primary tumors?
2) common origins (6)
3) most common layer of heart involved
1) more common than primary tumors
2) leukemias, melanoma, thyroid cancer, lung carcinoma, lymphoma, and breast cancer
3) m/c in pericardium
4) pericardial effusion
causes of pericarditis
ECG findings in acute pericarditis
outpatient: usu idiopathic; Coxsackie A/B
MI, meds (hydralazine, procainamide)
Other (bacterial, fungal, TB, SLE, RA, HIV)
concave ST elevation, PR depression
(MI has convex ST elevation only)
2) RA pressure and JVP findings
3) heart sound
4) CM (4)
1) inflammation -> thickening and dec compliance -> ventricular interdependence (limitation in RV filling and compression of LV) -> dec CO and right-sided congestion
2) Kussmaul's sign - increased RA pressure on inspiration
augmented Y descent
3) pericardial knock (sudden stopping of filling by non-compliant pericardium)
4) pulsus paradoxus
5) sinus tachy, Afib, ST flattening, T inversion, low QRS, right axis deviation (RVH)
2) clinical features (3)
3) JVP pattern
1) fluid accumulation in pericardial space -> inc intracardiac pressure -> limited filling -> dec CO
2) dec systemic arterial pressure
inc systemic venous pressure (JVD)
small, quiet heart
3) blunted Y descent