Cardiac Flashcards
EKG of stable angina would show
ST depression (subendocardial ischemia)
EKG of stable angina would show
ST depression (subendocardial ischemia)
EKG of Prinzmetal Angina would show
ST elevation (transmural ischemia)
Most common artery causing an MI
Left anterior descending (LAD)
LAD supplies
Apex, anterior left ventricle, one third of the anterior right ventricle, anterior 2/3 of the intraventricular septum
Right coronary a. supplies
remaining 2/3 of anterior right ventricle, posterior right ventricle, posterior half of left ventricle, posterior 1/3 of interventricular septum
Left circumflex a. supplies
lateral wall of the LV
Cardiac enzymes elevated in MI
Troponin I, CK-MB
After an MI, Troponin I peaks at
24 hours
After an MI, Troponin I begins to rise at
2-4 hours
After an MI, Troponin I returns to baseline by
7-10 days
After an MI, CK-MB peaks at
24 hours
After an MI, CK-MB begins to rise at
4-6 hours
After an MI, CK-MB returns to baseline by
72 hours
CK-MB help detect
re-infarction that occurs days after an initial MI
Contraction band necrosis is seen after
returned blood/Ca2+ entry into dead myocytes after MI followed by angioplasty, causes contraction
Reperfusion injury results from
returning of O2 to irreversibly damaged myocytes resulting in the generation of free radicals
Key events seen 4-24 hours after MI
Coagulative necrosis –> arrhythmia
Key events seen 1-3 days after MI
Neutrophil infiltration of acute inflammation –> fibrinous pericarditis
Key events seen 4-7 days after MI
Macrophage infiltration of acute inflammation –> rupture of ventricle wall
Key events seen 1-3 weeks after MI
Granulation tissue (emerging red border)
Key events seen Months after MI
Fibrosis –> aneurysm, mural thrombus, Dressler Syndrome
Scarring after MI contains primarily
Type I collagen
Sudden cardiac death is typically due to
severe atherosclerosis
LSHF causes edema in the _________ causing
lungs, PND, orthopnea, crackles
Heart failure cells are
hemosiderin-laden macrophages
Heart failure cells are seen with what condition/s
LSHF
Nutmeg Liver is seen with what condition/s
RSHF
Nutmeg Liver is due to congestion of
central veins of the liver
What congenital heart defect results typically from fetal EtOH syndrome?
Ventricular Septal Defects
Eisenmenger Syndrome
late-stage VSD; R->L Shunt; RV hypertrophy, cyanosis, polycythemia, clubbing
What congenital heart defect may be associated w/ Down’s Syndrome?
Atrial Septal Defect
What PE finding is associated w/ Atrial Septal Defect?
Split S2 (due to high BV in RA and delayed closure of pulmonic valve)
Significant risk involved w/ Atrial Septal Defect?
paradoxical embolus
What congenital heart defect may be associated w/ Congenital Rubella?
Patent Ductus Arteriosus (PDA)
What PE finding is associated w/ Patent Ductus Arteriosus (PDA)?
holosystolic machine-like murmur
Patent Ductus Arteriosus (PDA) + pHTN resulting in Eisenmenger Syndrome would have what PE finding?
Cyanosis of the LE
Treatment for Patent Ductus Arteriosus (PDA)?
Indomethacin (decreases PGE)
4 Key findings w/ Tetralogy of Fallot
P: Pulmonary stenosis R: RV hypertrophy O: Overriding aorta V: VSD
Clinical presentation of Tetralogy of Fallot
cyanotic baby, relieved by squatting
Key X-ray finding of Tetralogy of Fallot
boot-shaped heart
What congenital heart defect may be associated w/ maternal diabetes?
Transposition of great vessels
Treatment for Transposition of great vessels
PGE
Tricuspid Atresia is almost always seen in association w/
ASD and an aplastic RV
Location of an infantile Coarctation of the Aorta
distal to arch, proximal to PDA
Key PE finding of infantile Coarctation of the Aorta
LE cyanosis
What congenital heart defect may be associated w/ Turner’s Syndrome?
infantile Coarctation of the Aorta
Key PE finding of adult Coarctation of the Aorta
UE HTN and LE hypotension
Key X-ray finding of adult Coarctation of the Aorta
Notching of the ribs due to collateral circulation
Diagnosis of Acute Rheumatic Fever first involves establishing
evidence of a previous GAS infection w/ high ASO or DNase B titers
Acute Rheumatic Fever results from
molecular mimicry from M proteins produced by a previous GAS infection (pharyngitis) 2-3 weeks prior
JONES criteria for Acute Rheumatic Fever findings
Migratory polyarthritis, pancarditis, nodules, erythema marginatum, Syndenham chorea
Pancarditis due to Acute Rheumatic Fever
Endocarditis: vegetations on mitral valve -> mitral regurgitation Myocarditis: Aschoff bodies w/ Anitschkow cells Pericarditis: friction rub
Chronic Rheumatic Valvular Disease affects which valves
Mitral stenosis (thickening of chord tendineae) and occasionally Aortic valve stenosis (fusion of commissures)
Bicuspid aortic valve increases risk of ________?
Aortic stenosis
Aortic stenosis may arise as a complication of
Chronic Rheumatic Valvular Disease (fusion + mitral stenosis)
Key finding of Aortic Stenosis on PE exam?
systolic ejection click followed by a crescendo-decrescendo murmur
Typical presentation of pts w/ Aortic Stenosis?
angina, syncope w/ exercise
Lab findings w/ Aortic Stenosis?
Schistocytes due to Microangiopathic hemolytic anemia
What heart condition may result from Syphilitic aneurysm?
Aortic Regurgitation
Aortic Regurgitation most commonly arises as a result of
aortic root dilatation
Key finding of Aortic Regurgitation on PE exam?
Early, blowing diastolic murmur + Hyperdynamic circulation
Describe the Early, blowing diastolic murmur + Hyperdynamic circulation Sx w/ aortic regurg.
Bounding pulses, pulsatile nail bed, head bobbing
What heart condition may result from Marfan’s or Ehler-Danlos?
Mitral Valve Prolapse
Key finding of Mitral Valve Prolapse on PE exam?
Mid-systolic click ( +/- regurgitation murmur)
Key finding of Mitral Regurgitation on PE exam?
holosystolic “blowing” murmur
Key finding of Mitral Stenosis on PE exam?
opening snap, followed by a diastolic rumble
What heart condition may result from Acute Rheumatic Fever?
Mitral Regurgitation
What heart condition may result from Chronic Rheumatic Valvular Disease?
Mitral Stenosis
Most likely etiologic agent causing endocarditis in a previously injured heart (acute rheumatic fever)?
Strep viridans
Most likely etiologic agent causing endocarditis in a IV drug user?
S. aureus
Most likely etiologic agent causing endocarditis in a pt w/ a prosthetic valve?
Staph epidermidis
Strep bovis is associated w/
Endocarditis w/ underlying colorectal carcinoma
Presentation of pt w/ endocarditis?
Fever, murmur, janeway lesion, osler nodules, anemia of chronic disease (microcytic)
What heart condition is associated w/ SLE?
Libman-Sacks Endocarditis
Biopsy finding of valve in Libman-Sacks Endocarditis would show?
vegetations on BOTH SIDES of valves
Nonbacterial Thrombotic Endocarditis arises due to
hypercoagulable state affecting mitral valve
Dilated Cardiomyopathy leads to
biventricular CHF
Causes of Dilated Cardiomyopathy
Genetic mutation, Coxsackie A or B virus, EtOH use, doxorubicin, cocaine, pregnancy
Genetic mutations in the sarcomere proteins causes?
Hypertrophic Cardiomyopathy
Most common cause of sudden death in young athletes?
Hypertrophic Cardiomyopathy
Key pathology findings w/ Hypertrophic Cardiomyopathy
myofiber hypertrophy w/ disarray
Common causes of Restrictive Cardiomyopathy?
Amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis (children), Loeffler Syndrome
Key finding on EKG of Restrictive Cardiomyopathy?
low-voltage EKG w/ diminished QRS
Myxoma originates from
mesenchymal tissue
Myxoma is most common in what pt population
adults
Myxoma features and location
pedunculated tumor in L. atrium
Presentation of pt w/ myxoma tumor?
Syncope due to tumore blocking mitral valve
Myxoma pathology
ground substance - gelatinous appearance
Rhabdomyoma originates from
cardiac muscle (skeletal)
Rhabdomyoma is most common in what pt population
children
Rhabdomyoma is associated w/ what disease?
Tuberous Sclerosis
Rhabdomyoma arises typically in the
ventricle
Most common metastasis to the heart?
Breast and Lung carcinoma, melanoma, and lymphoma
right ventricle measures
0.3 to 0.5 cm in thickness
left ventricle measures
1.3 to 1.5 cm in thickness
Papillary muscles attached to which valves
tricuspid valve and mitral valve
tricuspid valve and mitral valve close during
Systole
Purkinje fibers are located in which layer
myocardium
Pathway of conduction pathway in the heart
SA node -> AV -> intraventricular septum -> apex -> bundle of his to ventricular walls
End point of all serious heart disease
CHF
CHF results from
decreased ability to contract OR increased pressure SV load
CHF results in
forward failure (decreased CO) and/or backward failure (congestion of the venous system)
LSHF is due to
ischemic heart disease, HTN, aortic/mitral valvular disease, myocardial disease
What is the key pathological finding of pHTN due to LSHF?
perivascular cuffing, edema and widening of the intraalveolar septa
Clinical presentation of pt w/ pHTN due to LSHF?
dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea, productive cough (blood tinged, frothy)
LSHF effects on the kidney?
decreased perfusion causing tubular necrosis, RAAS activation
LSHF effects on the CNS?
decreased perfusion to the brain, encephalopathic changes
RSHF is due to
LSHF, Cor pulmonale, myocardial disease, or tricuspid/pulmonary valvular disease
RSHF effects on the liver?
congestion of central vein causing central lobular necrosis
Key pathological finding of RSHF effects on the liver?
Nutmeg liver
Chronic liver congestion due to RSHF results in
cardiac sclerosis - fibrosis of hepatic parenchyma
Pitting edema of RSHF is due to
increased hydrostatic pressure and decreased hepatic circulation - decreased removal of Aldo, decreased albumin production
Pleural effusion are seen w/ _____ sided HF?
Right
RSHF causes HSM, what deposits are found in the spleen?
Hemosiderin
leading cause of death in the U.S.?
Ischemic heart disease
Ischemic heart disease is defined as
increased O2 demand or decreased O2 supply
Causes of Ischemic heart disease
Stenosing coronary a. atherosclerosis, Platelet aggregation, vasospasm, vasculitides, hemodynamic derangement
Significant myocardial ischemia begins when the atherosclerotic lesion obstructs approximately
80-90% of lumen
Causes of MI include:
atherosclerosis, emboli, arteritis, cocaine abuse, trauma
Treatment for stable angina
Nitro
leading cause of death in the U.S. and industrialized nations
MI
Risk Factors for MI:
Age (40-65), Male, Smoking, Type A
Factors known to decrease risk of MI
exercise, diet, moderate EtOH consumption
Patient may initially become __________ before an MI
tachycardic
What % of MIs are due to causes other than atherosclerotic lesions + thrombus?
10% due to vasospam, mural thrombi, emboli, valvular vegetations, paradoxical emboli
MI size is dependent on
extent, severity, location, collateral circulation, metabolic demands
Most common type of MI
transmural (> 2.5, 4-10cm typically)
Transmural MI of LAD typically affects ___% of heart
40-50
Transmural MI of RCA typically affects ___% of heart
30-40
Transmural MI of LCA typically affects ___% of heart
15-20
Subendocardial MIs typically occur as a result of
drop in BP or systemic oxygen supply (not usually thrombosis)
Infarctions of what age are most prone to ventricular rupture
3-7 days
Fibrosis and scarring occurs how long after an MI
> 7 weeks
coagulation necrosis with edema, microscopic hemorrhage and the infiltration of segmented neutrophils occurs how long after an MI
4-12 hrs
Contraction band necrosis can be seen how long after an MI
18-24 hrs
At _____ there is florid coagulation necrosis with loss of nuclear structure and a very heavy infiltrate of segmented neutrophils
24-72 hours
At ______, necrotic myofiber begins to disintegrate. Macrophages infiltrate the area and phagocytize debris.
3-7 days
By _____ the infarction is well developed with necrosis in the center and fibrovascular response at the margins
10 days
Symptoms of MI
angina, squeezing, impending doom, radiating to left arm or jaw
Old cardiac markers
serum glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH) and MB isomer of creatine phosphokinase (CKMB).
Current cardiac markers
Troponin T (cTnT) and Troponin I (cTnI)
Course of cTnI after MI
rise 4-6 hrs, peaks 10-14h, drops 7-10d
Course of cTnT after MI
rise 4-6 hrs, peaks 10-14h, drops 10-14d
Course of CKMB after MI
rise 7-24h, peaks 20h, drops in 4d
Course of SGOT after MI
rise 8h, peaks 18-36h, drops 3-4d
Course of LDH after MI
rise 6-12h, peak 3-6d, drops 2weeks
Normally LDH1 is _________ than LDH2, but after an MI
lower than; after an MI LDH1 rises above LDH2
LDH of myocardium
LDH1
Course of myoglobin after MI
rise 0-2h, 100% sensitive, no specificity
25% of MI occur as
sudden death
Complications due to MI
arrhythmias, heart block (transmural), rupture (4-5 d post-MI), ventricular aneurysm, mural thrombi/emboli, fibrohemorrhagic pericarditis (fusion), cardiogenic shock
Treatment of ischemic heart disease
preventative (diet, lifestyle) after: O2, thrombolytic agents, angioplasty/stenting, rest
Chronic ischemic heart disease
angina +/- MI 5-10 yrs prior to CHF
Gross Findings in ischemic heart disease
atherosclerosis, calcification of mitral valve
Microscopic Findings in ischemic heart disease
perivascular interstitial fibrosis and patches of fibrosis, areas of myocytolysis
Sudden cardiac death
death w/in 1 hour of onset of symptoms
Sudden cardiac death is typically due to
lethal arrhythmias due to severe atherosclerosis
Other causes of Sudden cardiac death
valvular stenosis, congenital anomalies, myocarditis, cardiomyopathies and mitral valve prolapse
The main cardiac effect of systemic hypertension is
concentric left ventricular hypertrophy without other cardiovascular pathology
The systemic effects of left ventricular hypertrophy
subendocardial myocardial infarction to CHF or sudden death
Cor pulmonale effects on the heart
right ventricular dilation and hypertrophy
Acute Cor Pulmonale
extreme right ventricular dilation caused by massive PE
Chronic Cor Pulmonale
lung disease -> hypoxemia/acidosis -> vasoconstriction -> pHTN -> RV hypertrophy
Causes of Cor Pulmonale
Lung disease (COPD, CF, etc) Pulmonary vessel disorder (PE, sclerosis) Chest movement disorder (neuro, diaphragm) Pulmonary a. constriction (hypoxia/acidosis)
Maternal rubella during 1st trimester
PDA
Boot-shaped heart
tetralogy of fallot
PDA in tetralogy of fallout is
protective
Maternal diabetes
transposition of great arteries
In utero survival of transposition of great arteries is dependent on
PDA and foramen ovale
postnatal survival of transposition of great arteries is dependent on
PDA 60% VSD 30%
Corrected transposition of greta arteries
great arteries and ventricles transposed. allows oxygenation but causes RV hypertrophy
Taussig-Bing
aorta arises from RV, pulmonary a overrides VSD R-to-L shunt
Lutembacher syndrome
atrial septal defect occurring with rheumatic mitral stenosis
machinery murmur is associated w/
PDA
Cyanosis of LE in infants
infantile coarctation of aorta
HTN in UE and hypotension in LE
adult coarctation of aorta
Pulmonary stenosis/atresia is associated w/
ASD and PDA
Aortic stenosis is associated w/
bicuspid valve and calcification
Ectopia cordis
heart is located outside the body
Dextrocardia
apex pointing to the right
Situs inversus totalis
All abdominal and thoracic viscera are on opposite sides
Isolated dextrocardia
only the heart is malrotated
congenital aortic stenosis
calcification extends from the cusp to the base of the valve
age-related aortic stenosis
calcification extends from the base to the cusp
Marfan syndrome
mitral valve prolapse
Patients w/ MVP are at an increased risk for
infectious endocarditis, progressive mitral insufficiency, atrial or ventricular arrhythmias, and sudden death
Aschoff bodies
myocardial Microscopic inflammatory regions associated w/ acute rheumatic fever
Anitschkow cells
acute rheumatic fever
Fibrinous pericarditis
acute rheumatic fever
acute rheumatic fever - migratory polyarthritis
nonspecific mononuclear infiltrates of joints
acute rheumatic fever - subcutaneous nodules
nodules are characterized by the presence of Aschoff bodies and are usually located over the extensor tendons
acute rheumatic fever - arteritis
hypersensitivity arteritis
Patient population of acute rheumatic fever
5-15 y/o w/in 1-5 weeks of initial pharyngitis
Intravenous drug abusers are particularly prone to _______ valve bacterial endocarditis whose vegetations may release septic thrombi, causing _____________________
tricuspid; pulmonary infection and abscess
Valvular endocarditis of the mitral and aortic valves may cause
embolic glomerulonephritis
Calcification of mitral annulus
Calcium is deposited upon and within the supporting ring of the mitral valve
Dilated (congestive) cardiomyopathy may cause
Intraventricular thrombi
Pericardial effusion
fluid accumulation due to CHF, infection, or neoplasm
Hemopericardium
blood accumulation due to infection , neoplasm, trauma, rupture
Hemopericardium that completely fills the pericardium is called
pericardial tamponade
Serous pericarditis definition
inflammatory exudates and inflammation of pericardium
Serous pericarditis causes
rheumatic fever, SLE, scleroderma, neoplasms, and uremia
Cell types found in serous fluid of Serous pericarditis
segmented neutrophils, lymphocytes, and histiocytes
Fibrinous and serofibrinous pericarditis definition
inflammation with the accumulation of serous fluid and fibrinous exudate; COMMON
Fibrinous and serofibrinous pericarditis causes
MI, autoimmune, uremia, radiation, rheumatic fever, SLE, and trauma
Purulent pericarditis causes
infection
Hemorrhagic pericarditis definition
blood mixed with fibrin or suppurative effusion
Hemorrhagic pericarditis causes
tuberculosis, acute bacterial infections, malignant neoplasm, uremia, hematologic disorder
Caseous pericarditis causes
tuberculosis
Adhesive mediastinal carditis
chronic pericarditis cause by caseous pericarditis, surgery, radiation that caused fibrosis and fusion of the pericardium and epicardium
Adhesive mediastinal carditis may lead to
Increased workload, cardiac hypertrophy and/or dilation, CHF
Constrictive pericarditis
Dense fibrocalcific scars adhere the pericardium and epicardium
Constrictive pericarditis may lead to
limited diastolic expansion and restricting cardiac output, hypertrophy cannot occur due to scarring
Rheumatoid heart disease is associated w/
subcutaneous rheumatoid nodules, vasculitis and Felty syndrome
Rheumatoid heart disease manifests w/
fibrinous pericarditis and thickening of the pericardium, Rheumatoid nodules w/in heart, amyloidosis
Lipoma location
LV, RA, or atrial septum
Primary malignant tumors of the heart
angiosarcomas and rhabdomyosarcomas
Secondary malignant tumors of the heart
lung, breast, leukemia, lymphoma, renal cell carcinoma, hepatocellular carcinoma and malignant melanoma