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FA note cards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Bulbus cordis becomes

A

Smooth parts (out ow tract) of left and right ventricles

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2
Q

Endocardial cushion becomes

A

Atrial septum, membranous interventricular septum; AV and semilunar valves

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3
Q

Primitive atrium becomes

A

Trabeculated part of left and right atria

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4
Q

Primitive ventricle becomes

A

Trabeculated part of left and right ventricles

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5
Q

Primitive pulmonary vein becomes

A

Smooth part of left atrium

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6
Q

Left horn of sinus venosus becomes

A

Coronary sinus

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7
Q

Right horn of sinus venosus becomes

A

Smooth part of right atrium (sinus venarum)

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8
Q

Right common cardinal vein and right anterior cardinal vein becomes

A

Superior vena cava (SVC)

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9
Q

When does fetal heart begin to beat spontaneously

A

week 4 of development

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10
Q

Blood supply to SA and AV node

A

branches of the RCA

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11
Q

3 layers of the pericardium:

A

from outer to inner:
Fibrous pericardium
Parietal layer of serous pericardium
Visceral layer of serous pericardium

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12
Q

Innervation to the pericardium

A

Phrenic nerve

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13
Q

Cardiac output

A

Stroke volume x HR or

rate of O2 use)/(art O2 - venous O2

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14
Q

Mean arterial pressure

A

CO x TPR or

2/3 diastolic pressure + 1/3 systolic pressure

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15
Q

Variables that effect SV

A

affected by Contractility, Afterload, and Preload (SV CAP)
↑ SV with:
↑ contractility and preload
↓ afterload

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16
Q

Variables effecting contractility

A

Contractility ↑ with:
Catecholamine stimulation B1 (↑ IC Ca)
↓r EC Na
Digitalis

↓ with:
B1 blockade
HF w/sytolic dysfunction
Acidosis
Hypocia/hypercapnia
ND CCB
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17
Q

Variables with ↑ myocardial O2 demand

A

↑ contractility, afterload, HR, diameter of ventricle

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18
Q

Preload

A

approximated by ventricular EDV

↓ w/venous dilation

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19
Q

Afterload

A

Approximated by MAP
↓ w/arterial dilation
↑ afterload leads to LVH

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20
Q

When would fixed splitting of S2 occur?

A

In ASD (L to R shunt ↑ right sided volume)

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21
Q

Causes of paradoxical splitting

A

Anything that delays aortic valve closure: aortic stenosis, LBBB

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22
Q

Inspiration during auscultation

A

↑ intensity of right heart sounds

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23
Q

Hand grip during auscultation

A

↑ after-load
↑ intensity of MR, AR, VSD
↓ AS and MVP

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24
Q

Valsalva during auscultation

A

↓ preload
↓ most murmurs
↑ intensity of hypertrophic cardiomyopathy MVP

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25
Q

Rapid squatting during auscultation

A

↑ venous return, preload and afterload
↓ hypertrophic sounds
↑ AS, MR, VSD

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26
Q

Diastolic heart sounds

A

murmurs of aortic/pulmonic regurgitation, mitral/tricuspid stenosis

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27
Q

Murmur of aortic stenosis

A

Crescendo-decrescendo systolic ejection murmur (ejection click may be present)
Loudest at base; radiates to carotids

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28
Q

Murmur of mitral or tricuspid regurg

A

Holosystolic, high-pitched “blowing murmur.”

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29
Q

Murmur of MVP

A

Late systolic crescendo murmur with midsystolic click; loudest just before S2

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30
Q

Murmur of VSD

A

Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.

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31
Q

Murmur of aortic regurg

A

High-pitched “blowing” early diastolic decrescendo murmur.

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32
Q

Murmur of mitral stenosis

A

Opening snap with delayed rumbling mid-to-late diastolic murmur

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33
Q

Murmur of PDA

A

Holosystolic machine-like murmur

Loudest at S2.

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34
Q

Congenital long QT syndrome

A

Inherited disorder of myocardial repolarization, typically due to ion channel defects

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35
Q

Defects associated with in utero alcohol exposure

A

VSD, PDA, ASD, tetralogy of Fallot

36
Q

Defects associated with Congenital rubella

A

PDA, pulmonary artery stenosis, septal defects

37
Q

Defects associated with Down syndrome

A

AV septal defect (endocardial cushion defect), VSD, ASD

38
Q

Defects associated with Infant of diabetic mother

A

Transposition of great vessels

39
Q

Defects associated with Marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

40
Q

Defects associated with Prenatal lithium exposure

A

Ebstein anomaly: displacement of tricuspid valve leaflets downward into RV, artificially “atrializing” the ventricle
tricuspid regurgitation and right HF

41
Q

Defects associated with Turner syndrome

A

Bicuspid aortic valve, coarctation of aorta

42
Q

Defects associated with Williams syndrome

A

Supravalvular aortic stenosis

43
Q

Defects associated with 22q11 syndromes

A

Truncus arteriosus, tetralogy of Fallot

44
Q

Progression of atherosclerosis

A

endothelial cell dysfunction -> macrophage and LDL accumulation -> foam cell formation -> fatty streaks -> smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition (d/t platelet release of cytokines) -> fibrous plaque -> complex atheromas

45
Q

Most common type of ventricular pre- excitation syndrome

A

Wolf -Parkinson-White syndrome

46
Q

Wol -Parkinson-White syndrome

A

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node
Delta wave with wide QRS, short PR

47
Q

B-type (brain) natriuretic peptide

A

Released from ventricular myocytes in response to ↑ tension
Acts like ANP with longer 1/2 life
Good to diagnose HF

48
Q

Aortic arch receptors

A

Transmit via vagus to solitary nucleus of medulla in response to↑ and ↓ BP

49
Q

Carotid sinus receptors

A

Via glossopharyngeal n (IX) to solitary nucleus of medulla in response to ↑ and ↓ BP

50
Q

Cardiac baroreceptors

A

Respond to hypotension: ↓ arterial pressure decreases stretch and afferent baroreceptor firing: ↑ efferent SNS firing/↓ PSNS: vasoconstriction, ↑ HR and BP

51
Q

MOA of carotid massage

A

↑ pressure on carotid sinus -> ↑ stretch -> ↑ afferent firing -> ↑ AV node refractory period -> ↓ HR

52
Q

Peripheral vs central chemoreceptors

A

Peripheral stimulated by O2, CO2 and pH

Central only stimulated by pH and CO2

53
Q

Total anomalous pulmonary venous return

A

Pulmonary veins drain into right heart circulation

54
Q

Corneal arcus

A

Lipid deposit in cornea

55
Q

Arteriolosclerosis

A

Small arteries and arterioles

Hyaline (HTN or DM) and hyper plastic (onion skinning)

56
Q

Mönckeberg sclerosis (medial calcifc sclerosis)

A

Affects medium-sized arteries

Calcification of internal elastic lamina and media of arteries causes stiffening

57
Q

Location of atherosclerosis frequency

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery

58
Q

Thoracic aortic aneurysm

A

Associated with cystic medial degeneration

59
Q

Traumatic aortic rupture

A

Due to trauma and/or deceleration injury, most commonly at aortic isthmus

60
Q

Postinfarction brinous pericarditis

A

Occurs 1–3 days after MI. Friction rub.

61
Q

Papillary muscle rupture

A

Occurs 2–7 days after MI. Posteromedial papillary muscle rupture; single blood supply for posterior descending artery

62
Q

Interventricular septal rupture

A

Occurs 3–5 days after MI. Macrophage-mediated degradation

63
Q

Ventricular free wall rupture

A

Occurs 5–14 days after MI. Free wall rupture leads to tamponade
LV hypertrophy and previous MI protect against free wall rupture

64
Q

Causes of dilated cardiomyopathy

A

hronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy

65
Q

Findings in dilated cardiomyopathy

A

HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR

66
Q

Treatment of dilated cardiomyopathy

A

Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant.

67
Q

Causes of Hypertrophic cardiomyopathy

A

Most are familial

Sudden death in young athletes

68
Q

Treatment of hypertrophic cardiomyopathy

A

cessation of high-intensity athletics, use of β-blocker or non-dihydropyridine Ca2+ channel blockers (eg, verapamil). ICD if patient is high risk.

69
Q

Findings in hypertrophic cardiomyopathy

A

S4, systolic murmur. May see mitral regurgitation due to impaired mitral valve closure.

70
Q

Causes of restrictive cardiomyopathy

A

Postradiation brosis, Lofffler syndrome, Endocardial broelastosis (thick broelastic tissue in endocardium of young children), Amyloidosis, Sarcoidosis

71
Q

Acute pericarditis presentation and causes

A

presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward; friction rub
Causes include idiopathic (most common; presumed viral), confirmed infection (Coxsackievirus), neoplasia, autoimmune (eg, SLE, RA), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy

72
Q

Cardiac tamponade

A 
Beck triad (hypotension, distended neck veins, distant heart sounds), ↑ HR, pulsus
paradoxus
73
Q

Myxomas

A

Most common 1° cardiac tumor in adults
90% occur in the atria (mostly left atrium)
“ball valve” obstruction in the left atrium leading to syncope

74
Q

Rhabdomyomas

A

Most frequent 1° cardiac tumor in children (associated with tuberous sclerosis). Histology: hamartomatous growths

75
Q

Kussmaul sign

A

↑ in JVP instead of ↓ during inspiration

76
Q

Giant cell (temporal) arteritis

A

Large cell vasculitis

Focal granulomatous inflammation, ↑ ESR

77
Q

Takayasu arteritis

A

Large cell vasculitis
Pulseless disease” (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Granulomatous thickening and narrowing of aortic arch and proximal great vessels

78
Q

Polyarteritis nodosa

A

Medium-vessel vasculitis
Hepatitis B in 30% of patients
Fever, weight loss, malaise, HA; GI: abdominal pain, melena, HTN, neurologic dysfunction, cutaneous eruptions, renal damage
Typically involves renal and visceral vessels, not pulmonary arteries
Inflammation of arterial wall with fibrinoid necrosis
Treat with corticosteroids, cyclophosphamide.

79
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

A

Medium-vessel vasculitis
Asian children < 4 years old
Conjunctival injection, Rash (desquamating), Adenopathy (cervical), Strawberry tongue (oral mucositis), Hand- foot changes (edema, erythema), fever
Treat with IV immunoglobulin and aspirin

80
Q

Granulomatosis with polyangiitis (Wegener)

A

Small-vessel vasculitis
PR3-ANCA/c-ANCA
CXR: large nodular densities.
Treat with cyclophosphamide, corticosteroids

81
Q

Microscopic polyangiitis

A

Small-vessel vasculitis
Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura
No granulomas; MPO-ANCA/p-ANCA
Treat with cyclophosphamide, corticosteroids

82
Q

Eosinophilic granulomatosis with polyangiitis (Churg- Strauss)

A

Small-vessel vasculitis
Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy
Granulomatous, necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA, IgE level

83
Q

Henoch-Schönlein purpura

A

Small-vessel vasculitis
Most common childhood systemic vasculitis
Classic triad:
Skin: palpable purpura on buttocks/legs, Arthralgias, GI: abdominal pain
2° to IgA immune complex
deposition

84
Q

Hereditary hemorrhagic telangiectasia aka Osler-Weber-Rendu syndrome

A

Blanching skin lesions (telangiectasias), recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding, hematuria

85
Q

Tetralogy of Fallot

A

VSD, pulmonary stenosis, RV hypertrophy, overriding aorta

86
Q

Findings in diastolic HF?

A

↑ LV end-diastolic pressure

Normal LV end-diastolic volume and EF

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