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Cardiovascular Exam I > Arrhythmias, SCD, HTN, Cardiac Valve Dz, Cardiomyopathy, Pericardial Dz, Cardiac Tumors, Transplantation > Flashcards

Arrhythmias, SCD, HTN, Cardiac Valve Dz, Cardiomyopathy, Pericardial Dz, Cardiac Tumors, Transplantation Flashcards

1
Q

Ischemic injury is the most common cause of rhythm disorders including sick sinus syndrome, afib, and heart block. What is sick sinus syndrome?

A

Bradycardia d/t SA node damage

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2
Q

Condition in which myocytes depolarize independently and sporadically (atrial dilation) with variable transmission through AV node; auscultated as irregularly irregular rhythm

A

Atrial fibrillation

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3
Q

Heart block occurs as a result of dysfunctional ___ node

What are the 3 degrees of heart block?

A

AV

3 degrees of heart block:

First degree = prolonged PR interval

Second degree = intermittent transmission

Third degree = complete failure

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4
Q

Arrhythmias may result from abnormalities in ____ junction structure or spatial relationship, such as those that occur in IHD, dilated cardiomyopathies, myocyte hypertrophy, inflammation (myocarditis or sarcoid), amyloid, etc

A

Gap

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5
Q

Most hereditary conditions resulting in arrhythmia are _____ inheritance. Primary electrical disorders are dx through genetic testing. ______ are diseases associated with mutations in genes that are required for normal ion channel function, often associated with skeletal m. disorders and diabetes

A

Autosomal dominant; channelopathies

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6
Q

Most common inherited arrhythmogenic disease

A

Long QT syndrome

[associated with gene defects in KCNQ1, KCNH2, SCN5A, CAV3; results in LOF of K+ channel or GOF of Na channel or caveolin]

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7
Q

4 inherited arrhythmogenic diseases

A

Long QT syndrome (most common)

Short QT syndrome (GOF in K+ channel)

Brugada syndrome (LOF in Na or Ca channel)

CPVT syndrome (GOF or LOF in diastolic Ca release)

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8
Q

Sudden cardiac death is due to a fatal _____ most often arising from ischemia-induced myocardial irritability; it may occur without symptoms or within 1-24 hours of symptom onset. 80-90% of successively resuscitated pts show ____ on ECG

A

arrhythmia; Nothing!

80-90% show no lab or ECG changes

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9
Q

_______ precipitates sudden cardiac death in 80-90% of cases

A

CAD — usually with >75% stenosis of one or more of the 3 main coronary arteries

Unfortunately, SCD may be the first manifestation of IHD; healed remote MIs are seen in about 40%

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10
Q

CAD is the most common cause of sudden cardiac death. What are some other possible causes?

A

Cardiomyopathy, myocarditis, congenital abnormalities of conduction system, myocardial hypertrophy

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11
Q

Describe changes in the heart with left-sided hypertensive disease

A

Pressure overload —> left ventricular hypertrophy (concentric thickening)

Diastolic dysfunction can result in left atrial enlargement, which may lead to afib

May lead to CHF

Risk factor for SCD!

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12
Q

Describe right-sided hypertensive disease

A

Isolated right-sided hypertensive heart disease arises in the setting of pulmonary hypertension

Acute cor pulmonale may arise from a large pulmonary embolus —> marked dilation of RV without hypertrophy

[remember most common cause of pulmonary HTN is LEFT-sided heart dz]

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13
Q

Diseases predisposing to cor pulmonale include diseases of pulmonary parenchyma, diseases of pulmonary vessels, disorders affecting chest movement, and disorders inducing pulmonary arterial constriction. What are some associated diseases of the pulmonary parenchyma?

A 
COPD
Diffuse pulmonary interstitial fibrosis
Pneumoconiosis
Cystic fibrosis
Bronchiectasis
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14
Q

Diseases predisposing to cor pulmonale include diseases of pulmonary parenchyma, diseases of pulmonary vessels, disorders affecting chest movement, and disorders inducing pulmonary arterial constriction. What are some associated diseases of the pulmonary vessels?

A 
Recurrent PE
Primary pulm HTN
Extensive pulmonary arteritis
Drug, toxin, radiation-induced obstruction
Extensive pulmonary tumor microembolism
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15
Q

Diseases predisposing to cor pulmonale include diseases of pulmonary parenchyma, diseases of pulmonary vessels, disorders affecting chest movement, and disorders inducing pulmonary arterial constriction. What are some associated disorders affecting chest movement?

A

Kyphoscoliosis
Marked obesity (OSA, pickwickian syndrome)
Neuromuscular dz

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16
Q

Diseases predisposing to cor pulmonale include diseases of pulmonary parenchyma, diseases of pulmonary vessels, disorders affecting chest movement, and disorders inducing pulmonary arterial constriction. What are some associated diseases inducing pulmonary arterial constriction?

A

Metabolic acidosis
Hypoxemia
Chronic altitude sickness
Obstruction of major airways

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17
Q

What is the difference between valvular stenosis and valvular insufficiency?

A

Stenosis = valve doesn’t OPEN completely; occurs chronically, impeding FORWARD flow

Insufficiency = valve doesn’t CLOSE completely; may occur acutely or chronically, allowing REVERSED flow

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18
Q

Chronic stenosis may cause _____ overload hypertrophy —> CHF

Chronic insufficiency may cause ____ overload hypertrophy —> CHF

A

Pressure

Volume

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19
Q

Virtually the ONLY cause of mitral stenosis

A

Postinflammatory scarring d/t rheumatic heart disease

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20
Q

Causes of mitral regurgitation

A

Abnormalities of leaflets and commissures: postinflammatory scarring, infective endocarditis, mitral valve prolapse, drugs (fen-phen)

Abnormalities of tensor apparatus: rupture of papillary muscle, papillary muscle dysfunction/fibrosis, rupture of chordae tendinae

Abnormalities of LV and/or annulus: LV enlargement (myocarditis, dilated cardiomyopathy), calcification of mitral ring

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21
Q

Causes of aortic stenosis

A

Postinflammatory scarring (rheumatic heart disease)

Senile calcific aortic stenosis

Calcification of congenitally deformed valve

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22
Q

Causes of aortic regurgitation

A

Abnormalities of leaflets and commissures: postinflammatory scarring (RHD)

Abnormalities of tensor apparatus: degenerative aortic dilatation, SYPHILITIC AORTITIS, ankylosing spondylitis, rheumatoid arthritis, MARFAN

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23
Q

Most common valve abnormality and commonly associated comorbidities

A

Calcific aortic stenosis — “wear and tear” phenomenon associated with chronic HTN, hyperlipidemia, and inflammation

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24
Q

With calcific aortic stenosis, ____ valves will show an accelerated course. Affected valves contain ____-like cells which deposit substance that creates mounded calcifications in cusps which prevent complete opening of the valve

A

Bicuspid; osteoblast (deposit osteoid like substance that ossifies)

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25
Q

Symptoms and clinical features of calcific aortic stenosis

A

Angina, CHF, or syncope

Increased pressure causes LVH

Most pts with aortic stenosis will die within 5 years of developing angina, within 3 years of developing syncope, and within 2 years of CHF onset

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26
Q

Mitral annular calcification involves calcific deposits in the fibrous annulus. It normally does NOT affect valve function. However, nodules may becomes sites for ______ formation or _____ _____. It is most common in females > males, > 60 yrs, and with pts who have ________

A

Thrombus; infective endocarditis; mitral valve prolapse

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27
Q

Most bicuspid aortic valves are prone to calcification. Patients can remain relatively asymptomatic until stenosis reaches a critical point when _____ rapidly ensues. The dense white nodules of calcification are present on both valve surfaces

A

CHF

[while bicuspid aortic valves are especially susceptible, an aortic valve does not need to be bicuspid to calcify. Sometimes in older adults, a normal aortic valve will undergo calcification = “senile calcific aortic stenosis”]

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28
Q

Mitral valve prolapse often occurs in those with ____ syndrome or as a complication of other cuases of regurgitation like dilated hypertrophy. On auscultation, a _____ may be noted

A

Marfan; mid-systolic click

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29
Q

Mitral valve prolapse occurs when valve leaflets prolapse into the ____ during systole. It affects 2-3% of adults in the US with a female predominance. Leaflets become thickened and rubbery due to disorganized ______ deposits, aka ______ degeneration, and elastic fiber disruption

A

LA; proteoglycan; myxomatous

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30
Q

Symptoms and complications associated with mitral valve prolapse

A

Most are asymptomatic but a minority may experience pain mimicking angina and/or dyspnea

Serious (but rare) complications may include:
Infective endocarditis
Mitral insufficiency
Thromboembolism
Arrhythmias
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31
Q

Rheumatic fever is a multisystem inflammatory disorder occurring 10 days to 6 weeks following pharyngeal infection with _________; acute rheumatic fever may include a carditis component, and over time may evolve into ____________

A

Group A streptococcus

Chronic rheumatic heart disease

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32
Q

Pathogenesis of rheumatic fever

A

Immune response to streptococcal M proteins, which cross react with cardiac (among other) self-Ags

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33
Q

Lab tests used to dx acute rheumatic fever

A

ASO and anti-DNase B

34
Q

General clinical features of rheumatic fever

A 
Pancarditis
Migratory polyarthritis
Subcutaneous nodules
Rash (erythema marginatum)
Syndenham chorea
35
Q

Specific cardiac features of acute rheumatic fever

A

Pancarditis featuring Aschoff bodies

Inflammation and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)

[Repeated strep infections will cause these features to recur!]

36
Q

Cardiac findings with chronic rheumatic heart disease

A

Mitral leaflet thickening, fusion and shortening of commissures, fusion and thickening of tendinous cords, resulting in mitral stenosis, neovascularization

LA enlargement may lead to afib or thromboembolic events

Pulmonary congestion/RHF

Infective endocarditis

Surgical repair/prosthetic valve replacement

37
Q

Where do the verrucae tend to line up in rheumatic fever?

A

Along lines of valve closure

38
Q

Central wavy ribbon of chromatin in macrophages is characteristic of ____ cells in acute RHD

A

Anitschkow

39
Q

Infective endocarditis is an infection of valves and endocardium, characterized by ____ consisting of microbes and debris, associated with underlying tissue destruction.

What is the difference between acute and subacute IE?

A

Vegetations

Acute: rapidly progressing, destructive infection of previously normal valve; requires surgery in addition to abx. Necrotizing, ulcerative destructive lesions, ring abscesses, emboli —> septic infarcts or mycotic aneurysm

Subacute: slower-progressing infection of previously deformed valve (such as chronic RHD); can often be cured with abx alone. Granulation tissue, fibrosis, calcification, chronic inflammatory cells, vague flu-like sxs

40
Q

Predisposing conditions to infective endocarditis

A

Valvular abnormalities — RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV

Bacteremia — another site of infection, dental work, surgery, contaminated needle, compromised epithelium

41
Q

Classic features of infective endocarditis

A

Friable, bulky destructive valvular vegetations; pts present with fever, weight loss, fatigue

Left-sided vavles more commonly affected - usually hear murmur (right-sided valves — think IV drug users)

Friability leads to septic emboli (PE if right sided valve)

Vegetations are mixtures of fibrin, inflammatory cells, and organisms; subacute vegetations may have granulation tissue component

42
Q

Organisms typically involved in infective endocarditis

A

S.viridans —> valve abnormalities

S.aureus —> normal valves, abnormal valves, IV drug abusers

S.epidermidis —> prosthetic valves

HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

43
Q

In summary: vegetative endocarditis manifesting as —

Warty, line of closure = _____

Large, irregular = _______

Small, line of closure = ______

Both sides of valve affected = ____

A

RHD

IE

NBTE

LSE (libman sacks endocarditis — think lupus)

44
Q

Name some of the vascular lesions and immunologic phenomena that constitute minor diagnostic criteria for infective endocarditis

A

Vascular lesons: arterial petechiae, subungual/splinter hemorrhages, Janeway lesions

Immunologic phenomena: osler nodes, roth spots

45
Q

Disease characterized by small, sterile thrombi on cardiac valve leaflets along the line of closure that are loosely attached, non-invasive, and do not elicit an inflammatory reaction but may be a source of emboli; associated with malignancy (especially mucinous adenocarcinomas), sepsis, or catheter-induced endocardial trauma

A

Nonbacterial thrombotic endocarditis (NBTE)

46
Q

Systemic disorder marked by flushing, diarrhea, dermatitis, and bronchoconstriction d/t release of bioactive compounds such as serotonin

A

Carcinoid syndrome

[5-hydroxyindoleacetic acid levels correlate with severity of cardiac lesions]

47
Q

50% of pts with systemic carcinoid syndrome develop cardiac manifestations. Describe carcinoid heart disease

A

Affects right endocardium and valves; the left side is protectd d/t pulmonary vascular bed degradation of mediators

[lesions appear similar to pts taking fen-phen or ergot alkaloids for migraine as they affect systemic serotonin metab]

48
Q

Gross and histologic findings associated with carcinoid heart dz

A

Grossly: glistening white intimal plaque-like thickenings of the endocardial surfaces of the cardiac chambers and valve leaflets

Histo: intimal thickening (acid mucopolysaccharide-rich)

49
Q

Complications of cardiac valve prostheses

A

Thrombosis/thromboembolism

Anticoagulant-related hemorrhage

Prosthetic valve endocarditis

Structural deterioration — wear, fracture, poppet failure in ball valves, cuspal tear, calcification

Inadequate healing (paravalvular leak), exuberant healing (obstruction), hemolysis

50
Q

Most common cardiomyopathy and its associated mechanism of heart failure

A

Dilated cardiomyopathy — causes impairment of contractility (systolic dysfunction) — also has most significant change in EF —> <40%

[indirect myocardial dysfunction includes IHD, valvular heart disease, hypertensive heart disease; congenital heart disease]

51
Q

Causes of dilated cardiomyopathy

A 
Genetic
Alcohol
Peripartum
Myocarditis
Hemochromatosis
Chronic anemia
Doxorubicin toxicity
Sarcoidosis
Idiopathic
52
Q

What 2 types of cardiomyopathy result from impairment of compliance (diastolic dysfunction)?

A

Hypertrophic cardiomyopathy — presents like hypertensive heart disease or aortic stenosis

Restrictive cardiomyopathy — presents like pericardial constriction

53
Q

LV EF and causes of hypertrophic cardiomyopathy

A

LV EF = 50-80%

Causes: genetic, friedrich ataxia, storage diseases, infants of diabetic mothers

54
Q

LV EF and causes associated with restrictive cardiomyopathy

A

LV EF = 45-90%

Causes: amyloidosis; radiation-induced fibrosis; idiopathic

55
Q

Dilated cardiomyopathy = progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

What are the genetic components of dilated cardiomyopathy?

A

Thought to be familial in 30-50% of cases

TTN (titin) mutations may account for 20% of all cases

Usually autosomal dominant

56
Q

Risk factors and associations in the pathogenesis of dilated cardiomyopathy

A

Alcohol is strongly linked to DCM

Myocarditis

Cardiotoxic drugs/substances like doxorubicin and iron overload (may occur with hereditary hemochromatosis (HFE mutation))

57
Q

Morphology of dilated cardiomyopathy

A

Dilation of all chambers

Mural thrombi are common

Functional regurgitation of valves

58
Q

Clinical Presentation of dilated cardiomyopathy

A

Usually manifests between ages 20-50

Progressive CHF —> dyspnea, exertional fatigue, decreased EF (<25% end stage)

Arrhythmias

Embolism

59
Q

Cardiomyopathy associated with excess catecholamines following extreme emotional or psychological stress; occuring in women 90% of the time, typically ages 58-75

A

Takotsubo cardiomyopathy

60
Q

What cardiomyopathy is associated with apical ballooning of the left ventricle with abnormal wall motion and contractile dysfunction?

A

Takotsubo cardiomyopathy

61
Q

Hypertrophic cardiomyopathy is considered 100% genetic. What is the associated phenotype?

A

Marked hypertrophy as well as asymmetrical septal hypertrophy

MYOFIBER DISARRAY

Fibrosis

LV outflow tract plaques

Thickened septal vessels

62
Q

Describe myocardial findings and inheritance pattern associated with arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

Right ventricular failure and arrhythmias — myocardium of the right ventricular wall is replaced by ADIPOSE and FIBROSIS —> ventricular tachycardia or fibrillation —> sudden death

Familial, autosomal dominant (defective cell adhesion proteins in desmosomes that link adjacent cardiac myocytes)

63
Q

Arrhythmogenic right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces

A

Naxos syndrome

64
Q

Naxos syndrome = Arrhythmogenic right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces. This is caused by mutations in the gene encoding the desmosome-associated protein ______

A

Plakoglobin

65
Q

Hypertrophic cardiomyopathy is a genetic disorder leading to myocardial hypertrophy and diastolic dysfunction —> reduced stroke volume and often ventricular outflow obstruction. It is due to numerous mutations involving _____ proteins, most commonly ______

A

Sarcomeric; beta-myosin heavy chain

66
Q

Consequences of hypertrophic cardiomyopathy

A

Foci of myocardial ischemia may occur

Left atrial dilation and mural thrombus

Diminished CO and increased pulmonary congestion —> exertional dyspnea (may be seen in athletes!)

Arrhythmias

Sudden death!

67
Q

In what type of cardiomyopathy are the ventricles usually normal sized but BOTH atria can be enlarged?

A

Restrictive cardiomyopathy

68
Q

Describe restrictive cardiomyopathy

A

Decreased ventricular compliance (increased stiffness) —> diastolic dysfunction (impaired filling), while systolic function of LV remains normal

May be secondary to deposition of material within the wall (amyloid) or increased fibrosis (radiation)

Ventricles are usually of normal size but both atria can be enlarged

69
Q

Describe restricive cardiomyopathy associated with amyloid deposition

A

Extracellular deposition of proteins which form an insoluble beta pleated sheet — stains with congo red stain —> apple green birefringence

May be systemic (myeloma) or restricted to the heart (usually transthyretin)

Note: certain mutated version fo transthyretin are more amyloidogenic; amyloid can involve different parts of the heart, but when deposits are in the interstitium of the myocardium, a restrictive cardiomyopathy results

70
Q

In the US, myocarditis is most commonly due to a virus. What are the most common viruses implicated? What are some other infectious causes?

A

Most common = Coxsackie A and B

Other infectious causes = Trypanosoma cruzi (Chagas disease), various bacteria and fungi

71
Q

Describe myocarditis caused by trypanosoma cruzi

A

10% die during acute attack

May progress to cardiac insufficiency in 10-20 years

Parasitization of scattered myofibers; mixed inflammatory cell infiltrate (PMN, lymphocytes, macrophages, and occasional eosinophils)

72
Q

Noninfectious causes of myocarditis

A

Immune mediated reactions including RF, SLE, drug hypersensitivity (see eosinophils on histology!! Vs. parasites if caused by chagas)

73
Q

Pericardial disease is characterized by > 50 mL of fluid surrounding the heart. What is the difference between slow vs. fast accumulation?

A

Slow accumulation of <500 mL may remain symptomatic as long as it is slow enough — may see globular enlargement of the heart shadow on CXR

An acute, rapid gain of 200-300 mL —> cardiac tamponade

74
Q

Most common types of pericardial disease

A

Fibrinous and serofibrinous — associated with AMI, postinfarction (Dressler’s), uremia, chest irradiation, RF, SLE, trauma, etc.

Fibrinous = dry, finely granular

Serofibrinous = yellow-brown, turbid fluid w/ WBCs, RBCs, and fibrin

75
Q

Symptoms of fibrinous or serofibrinous pericarditis

A

Pain (sharp, pleuritic, and positional)

Fever

+/- CHF

Most striking feature = loud pericardial friction rub!

76
Q

Primary cardiac tumors are rare, what are some examples?

A 
Myxoma
Fibromas
Lipomas
Papillary fibroelastomas
Rhabdomyomas
Angiosarcomas
77
Q

Most common primary, pedunculated or sessile, cardiac tumor; usually located in region of fossa ovalis

A

Myxoma

78
Q

Familial syndromes associated with myxomas have activating mutations in the ____ gene, in association with ______ syndrome; OR null mutations in ______ as part of the _____ complex

A

GNAS1; McCune-Albright

PRKAR1A; Carney

79
Q

Describe appearance of myxoma

A

Globular hard mass, mottled with hemorrhage; may also be soft, translucent, papillary, or villous with a gelatinous appearance

80
Q

Symptoms associated with myxoma

A

“Ball-valve” obstruction — meaning sxs may be positional

The pedunculated form causes intermittent obstruction during systole of AV valve; or “wrecking ball” causing damage to the valve leaflets

Constitutional sx: elaboration of IL-6 by some myxomas

Auscultation may reveal positional “tumor plop”

81
Q

Describe major complications associated with heart transplants

A

Allograft rejection (requires routine endomyocardial bx to monitor)

Allograft arteriopathy = most important long-term compl. —late, progressive, diffusely stenosing intimal proliferation, silent MI (denervated transplanted heart = no angina)

EBV associated B-cell lymphoma — d/t chronic T-cell immunosuppression

Cardiovascular Exam I (8 decks)

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