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Cardio Flashcards

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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
What are systolic heart sounds?
aortic/pulmonic stenosis mitral/tricuspid regurg ventricular septal defect
26
What are diastolic heart sounds?
aortic/pulmonic regurg mitral/tricupsid stenosis
27
Sound/cause of mitral/tricuspid regurg
Holosystolic, high pitched from MVP, LV dilation, ischemic heart disease for mitral R ventricular dilation for tricuspid Rheumatic fever/endocarditis can cause either
28
Sound/cause of aortic stenosis
Crescendo-decrescendo after ejection click radiates to carotids/heart base bicuspid aortic or calcific aortic stenosis
29
Sound of ventricular septal defect
holosystolic, harsh murmur
30
Sound/cause of mitral valve prolapse
late systolic crescendo murmur with midsystolic click from myoxmatous degen/Rheumatic fever/chordae rupture
31
Sound/cause of aortic regurg
high pitched, blowing diastolic decresecendo from aoritc root dilation/bicupsid aortic/endocarditis/rheumatic fever
32
Sound/cause of mitral stenosis
delayed rumbling in late diastole often from rheumatic fever
33
Sound of a patent ductus arteriosus
continuous machine like murmur
34
Cause of plateau in ventricular AP
balance of K+ and Ca2+ crossing the membrane eventually K+ overtakes and decreases the AP by exiting more quickly than Ca2+ enters
35
Phases/actions of a ventricular AP
**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
36
Phases/actions of SA/AV node action potentials
**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
37
What is the P wave on ECG?
atrial depolarization
38
What is PR interval on ECG?
conduction delay through AV node (less than 200ms)
39
What is the QRS complex on an ECG?
40
What is the QT interval on ECG?
mechanical contraction of ventricles
41
What is the T wave in an ECG?
ventricular repolarization inversed indicates MI
42
What is the ST segment on an ECG?
ventricles depolarized=isoelectric
43
What is torsades de pointes?
ventricular tachycardia shifting sinusoidal waveforms on ECG
44
Atrial fibrillation characteristics on ECG
irregularly irregular no discrete P waves inbetween irregular spaced QRS complexes
45
Atrial flutter characteristics on ECG
back to back atrial depolarizations
46
Ventricular fibrillation characteristics on ECG
erratic rythm with no identifiable waves
47
What is seen on ECG with 1st degree AV block?
prolonged PR interval (over 200ms)
48
What is seen on ECG with type one 2nd degree AV block?
progressive lengthing of PR interval with dropped P wave
49
What is seen on ECG with type two 2nd degree AV block?
dropped P waves with no change in PR interval length
50
Stimulation of/action of atrial natriuretic peptide
increases with increased blood volume and atrial pressure ANP causes vascular dilation and Na+ reabsorption constricts efferent renal arterioles and dilates afferent
51
Nucleus involved in BP control
solitary nucleus in medulla
52
Cushing reaction pathway
increased ICP-\> cerebral ischemia -\> reflex for increased perfusion pressure -\> increased stretch -\> baroreceptor -\> bradycardia
53
Eisenmenger's Syndrome
VSD, ASD or PDA vascular hypertrophy shunt reverses from L/R to R/L late cyanosis
54
Tetralogy of Fallot
PROVe Pulmonary infundibular stenosis RVH overriding aorta VSD
55
Cardiac defect assc with Turner Syndrome
Coarctation of the aorta
56
Cardiac defect assc with diabetic mother
57
What are lipid laden histiocytes in the skin?
xanthomas
58
Moenckeberg arteriosclerosis
calcification of media of arteries "pipestem" arteries
59
Atherosclerosis
plaques forming in intima of arteries
60
Types of arteriolosclerosis
Hyaline from HTN or DM Hyperplastic from malignant HTN (onion skinning)
61
Progression of atherosclerosis formation
MO and LDL accumulation foam cell formation/fatty streaks smooth m. cell migration (PDGF/FGF) extracellular matrix deposition plaque formation
62
Associations of thoracic aortic aneurysm
HTN cystic medial necrosis teriary syphilis
63
What do you see on an ECG with stable angina?
ST depression
64
What do you see with Prinzmetal's variant angina on ECG?
ST elevation
65
ECG of a myocardial infarct
initial ST depression progression to ST elevation
66
Dx of myocardial infarct
ECG within first 6 hours cardiac troponin I rises after 4 hours
67
ECG of transmural infarct
ST elevation,Q waves
68
ECG of subendocardial infarcts
ST depression
69
What is Dressler's syndrome?
autoimmune reaction resulting in fibrinous pericarditis several weeks post MI
70
Pathology of dilated (congestive) cardiomyopathy
sarcomeres added in series eccentric hypertrophy
71
Pathology of hypertrophic cardiomyopathy
sarcomeres added in parallel asymmetric concentric hypertrophy
72
Causes of obliterative cardiomyopathy (6)
sarcoidosis amyloidosis postradiation fibrosis endocardial fibroelastosis Loffer's syndrome hemochromatosis
73
Sx of bacterial endocarditis (4)
Roth's spots (on retina) Osler's nodes (on finger/toe pads) Janeway lesions (on palm/sole) splinter hemorrhages on nail bed
74
Cause/sx of rheumatic fever
Caused by streptococci infection mitral valve regurg/mitral stenosis Aschoff bodies Anitschkow's cells elevated ASO titer
75
ECG of acute pericarditis
widespread ST elevation or PR depression
76
What is Kussmaul's sign?
increased JVP on inspiration rather than a normal decrease
77
Temporal arteritis sx
unilateral headache jaw claudication irreversible blindness
78
Takayasu's arteritis
Pulseless disease thickening of aortic arch in asian females less than 40 y/o
79
Triad of Wegener's granulomatosis
focal necrotizing vasculitis necrotizing granulomas in lung/airway necrotizing glomerulonephritis
80
Triad of Henoch-Schonlein purpura
palpable purpura on buttocks/legs arthralgia abdominal pain, melena, multiple lesions of same age
81
Sturge-Weber syndrome sx
Port wine stain on face ipsilateral leptomeningeal angiomatosis seizures early onset glaucoma
82
Contraindication for beta blockers
cardiogenic shock caution must be used with decompensated CHF
83
Side effect of Ca+2 channel blockers
AV block/cardiac depression
84
MOA of hydralazine
increase cGMP-\> smooth m. relaxation reduces afterload used for HTN
85
Side effect of hydralazine
compensatory tachycardia therefore contraindicated in angina/CAD
86
MOA of nitroprusside
increase cGMP release of NO releases cyanide and can cause toxicity
87
MOA of fenoldopam
D1 receptor agonist decrease BP and increase natriuresis
88
MOA of nitroglycerin/isosorbide dinitrate
release NO increase cGMP smooth m. relaxation decreases preload
89
Contraindication for pindolol/acebutolol
both partial Beta agonists contraindicated in angina
90
Side effects of HMG-CoA reductase inhibitors
hepatotoxicity rhabdomylolysis
91
MOA of fibrates (gemfibrozil,clofibrate,bezafibrate,fenofibrate)
upregulate LPL increasing TG clearance
92
Class 1A antiarrhythmics
quinidine, procainamide, disopyramide increase AP duration increase refractory period increase QT interval
93
Class 1B antiarrhythmics
lidocaine, mexiletine, tocainide decreases AP duration used in ventricular arrhythmias
94
Class 1C antiarrhythmics
flecainide, propafenone used in ventricular tachycardia contraindicated post MI prolongs refractory period in AV node
95
MOA of Beta blockers (class II antiarrhythmics)
derease SA/AV node activity decreasing cAMP/Ca2+ currents increase PR interval
96
Class III antiarrhythmics
amiodarone, ibutilide, dofetilide, sotalol (K+ channel blockers) increase AP duration, ERP, and QT interval
97
Class IV antiarrhythmics
verapamil, diltiazem (Ca2+ channel blockers) decrease conduction velocity increase ERP and PR interval
98

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