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Undeleted > Cardio > Flashcards

Cardio Flashcards

1
Q

What does the trucus arteriosus become?

A

ascending aorta and pulmonary trunk

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2
Q

Timeframe of eryhtropoiesis in fetus/newborn

A

Yolk sac 3-10 wk

Liver 6wk-birth

Spleen 15-30wk

Bone marrow 22wk-adult

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3
Q

Different between fetal and adult hemoglobin

A

fetal=alpha2gamma2 subunits

adult=alpha2beta2 subunits

fetal has much higher affinity for oxygen

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4
Q

What molecules can impact the ductus arteriosus?

A

prostaglandins E1/E2 keep ductus arteriosus open

Indomethacin helps close PDA

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5
Q

What are SA and AV nodes supplied by usually?

A

R coronary artery

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6
Q

When do the coronary arteries fill with new blood?

A

During diastole

When aortic valve closes and blood is pushed backwards into the sinuses in the valves

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7
Q

Sx of L atrial hypertrophy

A

dysphagia/hoarseness

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8
Q

Molecules increasing contractility of the heart (4)

A

catecholamines

increased intracellular Ca2+

decreased extracellular Na+

Digitalis

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9
Q

Causes of decreased contractility of the heart (5)

A

Beta1 blockade (blockers)

heart failure

acidosis

hypoxia/hypercapnea

nondihydropyridine Ca2+ channel blockers

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10
Q

Results of venodilators on the heart

A

decrease preload

i.e. nitroglycerin

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11
Q

Result of vasodilators on the heart

A

decrease afterload

i.e. hydralazine

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12
Q

Biggest determinant of blood viscosity

A

hematocrit

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13
Q

During cardiac cycle, when is most oxygen consumed by the heart?

A

isovolumetric contraction

b/t closure of mitral and opening of aortic

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14
Q

What is the S1 heart sound?

A

mitral/tricuspid valve closure

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15
Q

What is the S2 heart sound?

A

aortic and pulmonic valve closures

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16
Q

What is the S3 heart sound?

A

rapid ventricular filling in early diastole

more common in dilated ventricle

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17
Q

What is the S4 heart sound?

A

atrial kick from high atrial pressure

assc with ventricular hypertrophy

from L atrium pushing against stiff LV wall

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18
Q

What causes wide splitting of heart sounds?

A

delaying of R ventricle emptying

from R bundle block/pulmonic stenosis

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19
Q

What causes fixed splitting of heart sounds?

A

From atrioseptal defects

due to increased flow through pulmonic valve

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20
Q

What causes paradoxical splitting of heart sounds?

A

delaying of L ventricle emptying

i.e. aortic stenosis/L bundle block

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21
Q

What heart sounds does inspiration excentuate?

A

R heart sounds

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22
Q

What heart sounds does expiration excentuate?

A

L heart sounds

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23
Q

What heart sounds does hand grip/increase systemic vascular resistance excentuate?

A

MR, AR, VSD, MVP

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24
Q

What heart sounds does valsalva/decreased venous return excentuate?

A

MVP, hypertrophic cardiomyopathies

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25
Q

What are systolic heart sounds?

A

aortic/pulmonic stenosis

mitral/tricuspid regurg

ventricular septal defect

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26
Q

What are diastolic heart sounds?

A

aortic/pulmonic regurg

mitral/tricupsid stenosis

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27
Q

Sound/cause of mitral/tricuspid regurg

A

Holosystolic, high pitched

from MVP, LV dilation, ischemic heart disease for mitral

R ventricular dilation for tricuspid

Rheumatic fever/endocarditis can cause either

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28
Q

Sound/cause of aortic stenosis

A

Crescendo-decrescendo after ejection click

radiates to carotids/heart base

bicuspid aortic or calcific aortic stenosis

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29
Q

Sound of ventricular septal defect

A

holosystolic, harsh murmur

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30
Q

Sound/cause of mitral valve prolapse

A

late systolic crescendo murmur with midsystolic click

from myoxmatous degen/Rheumatic fever/chordae rupture

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31
Q

Sound/cause of aortic regurg

A

high pitched, blowing diastolic decresecendo

from aoritc root dilation/bicupsid aortic/endocarditis/rheumatic fever

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32
Q

Sound/cause of mitral stenosis

A

delayed rumbling in late diastole

often from rheumatic fever

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33
Q

Sound of a patent ductus arteriosus

A

continuous machine like murmur

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34
Q

Cause of plateau in ventricular AP

A

balance of K+ and Ca2+ crossing the membrane

eventually K+ overtakes and decreases the AP by exiting more quickly than Ca2+ enters

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35
Q

Phases/actions of a ventricular AP

A

Phase 0-upstroke/Na+ channels open

Phase 1-inactivation of Na+ channels/K+ channels open

Phase 2-Ca2+ influx/K+ efflux causes plateau

also Ca2+ causes SR Ca2+ release and myocyte contraction

Phase 3-massive K+ efflux and closure of Ca2+ channels

Phase 4-resting potential/K+ high permeability

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36
Q

Phases/actions of SA/AV node action potentials

A

Phase 0-upstroke/Ca2+ channels open (Na+ fast inactivated due to less negative RMP)

Phase 2-no plateua

Phase 3-inactivation of Ca2+ channels/efflux of K

Phase 4-spontaneous depolarization of membrane due to increased Na+ conductance

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37
Q

What is the P wave on ECG?

A

atrial depolarization

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38
Q

What is PR interval on ECG?

A

conduction delay through AV node (less than 200ms)

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39
Q

What is the QRS complex on an ECG?

A
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40
Q

What is the QT interval on ECG?

A

mechanical contraction of ventricles

41
Q

What is the T wave in an ECG?

A

ventricular repolarization

inversed indicates MI

42
Q

What is the ST segment on an ECG?

A

ventricles depolarized=isoelectric

43
Q

What is torsades de pointes?

A

ventricular tachycardia

shifting sinusoidal waveforms on ECG

44
Q

Atrial fibrillation characteristics on ECG

A

irregularly irregular

no discrete P waves inbetween irregular spaced QRS complexes

45
Q

Atrial flutter characteristics on ECG

A

back to back atrial depolarizations

46
Q

Ventricular fibrillation characteristics on ECG

A

erratic rythm with no identifiable waves

47
Q

What is seen on ECG with 1st degree AV block?

A

prolonged PR interval (over 200ms)

48
Q

What is seen on ECG with type one 2nd degree AV block?

A

progressive lengthing of PR interval with dropped P wave

49
Q

What is seen on ECG with type two 2nd degree AV block?

A

dropped P waves with no change in PR interval length

50
Q

Stimulation of/action of atrial natriuretic peptide

A

increases with increased blood volume and atrial pressure

ANP causes vascular dilation and Na+ reabsorption

constricts efferent renal arterioles and dilates afferent

51
Q

Nucleus involved in BP control

A

solitary nucleus in medulla

52
Q

Cushing reaction pathway

A

increased ICP-> cerebral ischemia -> reflex for increased perfusion pressure -> increased stretch -> baroreceptor -> bradycardia

53
Q

Eisenmenger’s Syndrome

A

VSD, ASD or PDA

vascular hypertrophy

shunt reverses from L/R to R/L

late cyanosis

54
Q

Tetralogy of Fallot

A

PROVe

Pulmonary infundibular stenosis

RVH

overriding aorta

VSD

55
Q

Cardiac defect assc with Turner Syndrome

A

Coarctation of the aorta

56
Q

Cardiac defect assc with diabetic mother

A
57
Q

What are lipid laden histiocytes in the skin?

A

xanthomas

58
Q

Moenckeberg arteriosclerosis

A

calcification of media of arteries

“pipestem” arteries

59
Q

Atherosclerosis

A

plaques forming in intima of arteries

60
Q

Types of arteriolosclerosis

A

Hyaline from HTN or DM

Hyperplastic from malignant HTN (onion skinning)

61
Q

Progression of atherosclerosis formation

A

MO and LDL accumulation

foam cell formation/fatty streaks

smooth m. cell migration (PDGF/FGF)

extracellular matrix deposition

plaque formation

62
Q

Associations of thoracic aortic aneurysm

A

HTN

cystic medial necrosis

teriary syphilis

63
Q

What do you see on an ECG with stable angina?

A

ST depression

64
Q

What do you see with Prinzmetal’s variant angina on ECG?

A

ST elevation

65
Q

ECG of a myocardial infarct

A

initial ST depression

progression to ST elevation

66
Q

Dx of myocardial infarct

A

ECG within first 6 hours

cardiac troponin I rises after 4 hours

67
Q

ECG of transmural infarct

A

ST elevation,Q waves

68
Q

ECG of subendocardial infarcts

A

ST depression

69
Q

What is Dressler’s syndrome?

A

autoimmune reaction resulting in fibrinous pericarditis several weeks post MI

70
Q

Pathology of dilated (congestive) cardiomyopathy

A

sarcomeres added in series

eccentric hypertrophy

71
Q

Pathology of hypertrophic cardiomyopathy

A

sarcomeres added in parallel

asymmetric concentric hypertrophy

72
Q

Causes of obliterative cardiomyopathy (6)

A

sarcoidosis

amyloidosis

postradiation fibrosis

endocardial fibroelastosis

Loffer’s syndrome

hemochromatosis

73
Q

Sx of bacterial endocarditis (4)

A

Roth’s spots (on retina)

Osler’s nodes (on finger/toe pads)

Janeway lesions (on palm/sole)

splinter hemorrhages on nail bed

74
Q

Cause/sx of rheumatic fever

A

Caused by streptococci infection

mitral valve regurg/mitral stenosis

Aschoff bodies

Anitschkow’s cells

elevated ASO titer

75
Q

ECG of acute pericarditis

A

widespread ST elevation or PR depression

76
Q

What is Kussmaul’s sign?

A

increased JVP on inspiration

rather than a normal decrease

77
Q

Temporal arteritis sx

A

unilateral headache

jaw claudication

irreversible blindness

78
Q

Takayasu’s arteritis

A

Pulseless disease

thickening of aortic arch

in asian females less than 40 y/o

79
Q

Triad of Wegener’s granulomatosis

A

focal necrotizing vasculitis

necrotizing granulomas in lung/airway

necrotizing glomerulonephritis

80
Q

Triad of Henoch-Schonlein purpura

A

palpable purpura on buttocks/legs

arthralgia

abdominal pain, melena, multiple lesions of same age

81
Q

Sturge-Weber syndrome sx

A

Port wine stain on face

ipsilateral leptomeningeal angiomatosis

seizures

early onset glaucoma

82
Q

Contraindication for beta blockers

A

cardiogenic shock

caution must be used with decompensated CHF

83
Q

Side effect of Ca+2 channel blockers

A

AV block/cardiac depression

84
Q

MOA of hydralazine

A

increase cGMP-> smooth m. relaxation

reduces afterload

used for HTN

85
Q

Side effect of hydralazine

A

compensatory tachycardia

therefore contraindicated in angina/CAD

86
Q

MOA of nitroprusside

A

increase cGMP

release of NO

releases cyanide and can cause toxicity

87
Q

MOA of fenoldopam

A

D1 receptor agonist

decrease BP and increase natriuresis

88
Q

MOA of nitroglycerin/isosorbide dinitrate

A

release NO

increase cGMP

smooth m. relaxation

decreases preload

89
Q

Contraindication for pindolol/acebutolol

A

both partial Beta agonists

contraindicated in angina

90
Q

Side effects of HMG-CoA reductase inhibitors

A

hepatotoxicity

rhabdomylolysis

91
Q

MOA of fibrates (gemfibrozil,clofibrate,bezafibrate,fenofibrate)

A

upregulate LPL

increasing TG clearance

92
Q

Class 1A antiarrhythmics

A

quinidine, procainamide, disopyramide

increase AP duration

increase refractory period

increase QT interval

93
Q

Class 1B antiarrhythmics

A

lidocaine, mexiletine, tocainide

decreases AP duration

used in ventricular arrhythmias

94
Q

Class 1C antiarrhythmics

A

flecainide, propafenone

used in ventricular tachycardia

contraindicated post MI

prolongs refractory period in AV node

95
Q

MOA of Beta blockers (class II antiarrhythmics)

A

derease SA/AV node activity

decreasing cAMP/Ca2+ currents

increase PR interval

96
Q

Class III antiarrhythmics

A

amiodarone, ibutilide, dofetilide, sotalol (K+ channel blockers)

increase AP duration, ERP, and QT interval

97
Q

Class IV antiarrhythmics

A

verapamil, diltiazem (Ca2+ channel blockers)

decrease conduction velocity

increase ERP and PR interval

98
Q
A

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