Cardiology Flashcards

0
Q

Ostium secundum

A

Formed as tissue degenerates in superior septum primum

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1
Q

Septum secundum

A

Contains F ovale

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2
Q

Truncus arteriosus

A

Becomes ascending aorta and pulmonary trunk

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3
Q

Bulbus cordis

A

Becomes smooth parts ventricles

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4
Q

Left horn of sinus venosus

A

Becomes coronary sinus

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5
Q

Right horn of sinus venosus

A

Becomes smooth part RA

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6
Q

Right common and Right anterior cardinal veins

A

Becomes SVC

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7
Q

ASD

A

Most common type=ostium secundum type. Usu asymptomatic until adulthood.

Signs: wide fixed splitting S2, ESM in aortic area.

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8
Q

VSD

A

Most comm congenital heart malformation. Most commonly from incomplete fusion AV cushions. Most small and resolve spontaneously.

Sxs: easy fatiguability, harsh holosystolic murmur best heard at tricuspid area

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9
Q

Aorticopulmonary septum

A

Separates truncus arteriosus into aorta and pulmonary trunks.

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10
Q

Left to right shunts

A

VSD, ASD, PDA.

Late cyanosis.

If do not close and continued high flow in pulm circulation, can cause hypertrophy of pulm arterial system and even fibrosis.

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11
Q

Right to left shunts

A
TOF
TGA
TAPVR
Tricuspid atresia
Truncus arteriosus

Early cyanosis and squatting

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12
Q

Eisenmenger syndrome

A

Initial L to R shunt but then continued high flow in pulm vasculature causes hypertrophy, RVH until shunt reverses. Late cyanosis.

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13
Q

Squatting-mechanism to alleviate sxs

A

Occurs in R-L shunts. Squatting increases systemic vascular resistance (L sided P) by compressing femorals. Decreases pressure gradient between R and L sides of heart so may alleviate sxs.

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14
Q

1st aortic arch

A

Becomes part of maxillary artery

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15
Q

2nd aortic arch

A

Becomes stapedial artery and hyoid artery

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16
Q

3rd aortic arch

A

Becomes common carotid and proximal internal carotid artery

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17
Q

4th aortic arch

A

Becomes aortic arch and proximal R subclavian artery

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18
Q

5th aortic arch

A

Regresses in humans

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19
Q

6th aortic arch

A

Becomes proximal pulmonary arteries and ductus arteriosus

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20
Q

Pre-ductal coarctation of aorta

A

Proximal to DA. DA typically remains patent

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21
Q

Post-ductal coarctation of aorta

A

Distal to DA. Increased BP in arms, decreased BP in legs, weak/absent femoral pulses, collateral circulation.
*Rib notching due to increased flow through intercostal arteries.

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22
Q

PDA

A

L-R shunt. Most common in premies. Does not result in early cyanosis. Give prostaglandin inhibitors-indomethacin, NSAIDs.

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23
Q

22q11 deletion

A

Assoc with truncus arteriosus, TOF

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24
Down's syndrome
Associated with ASD (especially), VSD, AV septal defect
25
Child of diabetic mother
Association with TGA
26
Congential rubella-cardiac defects
Septal defects, PDA, pulmonary artery stenosis
27
Marfans
Aortic insufficiency=late complication
28
Signs of tamponade
Decreased MAP, distended neck veins (inability SVC to drain), pulsus paradoxus, electrical alternans on ECG
29
Subendocardial infarct
Repeated episodes of temporary occlusion of coronary artery (unstable angina) or severe anemia/hypotension. ST depression. *If flow through coronary artery compromised, subendocardial tissue most vulnerable to ischemic injury sicne farthest from either blood supply.
30
Causes pericarditis
SLE, RA, MI, TB, malignancy
31
Fastest conduction velocity in heart's electrical system
His-Purkinje
32
Slowest conduction velocity in heart's electrical system
AV node
33
Decreased contractility
Beta blockers, CCBs, HF, parasymp stimulation, acidosis, hypoxia, hypercapnia
34
Venous O2
Can be measured at pulmonary artery
35
Ficks CO equation
CO=O2 consumption/(arterial O2-venous O2)
36
S2 splitting
Inspiration increases. Wide-RV emptying delayed, e.g. RBBB, pulmonic stenosis Fixed-ASD. Paradoxical-delayed LV emptying (AS, LBBB). P2A2...when inspire, split eliminated since P2 delayed.
37
Carotid baroreceptors
Tonically active Increased activity indicates increase in BP. Trasmitted by CN IX
38
Aortic arch baroreceptors
Transmitted by CN X
39
Arterioles
Largest resistance in CV system
40
Serum
plasma-clotting factors
41
Fastest to Slowest conduction velovity
His-Purkinje, Atrial, Ventricular, AVN
42
Absolute refractory period
Phases 0-2
43
Effective refractory period
Conducted AP cannot be generated.
44
How cardiac muscle differs from skeletal
Has: plateau, spontaneous depolarization, gap junctions, more mitochindria, increased contractile force through changes in fiber contractility (vs #fibers recruited in skel muscle)
45
Measure of contractility
EF
46
Bowditch effect
Myocardial contractility increases with higher heart rates. Possibly due to inability of Na+/K+-ATPase to keep up with influx od Na so increased Ca within myocyte. Aka Treppe phenomenon or staircase effect
47
Frank Starling law
Force of systolic contraction proportional to initial length of cardiac muscle in diastole. (i.e. increased stretch or preload will increase FOC).
48
S2-effect of inspiration
Increases splitting
49
Wide splitting S2
Where RV emptying delayed, e.g. pulmonic stenosis, RBBB
50
Carotid stretch receptors
Tonically active. Transmitted by CNIX
51
Aortic arch stretch receptors
Transmitted by CNX
52
Mediation of arteriolar dilation and venous constriction
Histamine and bradykinin
53
TXA2
Vasoconstrictor
54
Prostacyclin
vasodilator
55
Capacitance
=V/P. Ability to store charge, i.e. how distensible a BV is. Inversely related to elastance
56
Hypertension
>140 and/or >90 on 3+ readings or single reading >170/110
57
Prehypertension
120-139/80-89
58
Stage 1 HTN
140-159/90-99
59
Stage 2 HTN
>160/>100
60
Initial medication for primary HTN
Thiazides
61
Secondary HTN-causes
Renal artery stenosis, renal parenchymal disease, OCP, glucocorticoids, phenylephrine, NSAIDS, pheo, Conns, hyperthyroidism, Cushings, coarctation, fibromuscular dysplasia
62
Hypertensive retinopathy
AV nicking, pappiledema, loss venous pulsation, flame hemorrhages
63
Malignant hypertension
Severe, rapid increase in BO, usu >240/120. Assoc with end organ damage ("flea bitten kidneys). Young African-Americans, LVH, papilledema, retinal hemorrhage
64
Munckeberg arteriosclerosis
Benign medical calcification of medium sized muscular arteries. Elderly, those with DM, metabolic syndrome, HTN.
65
Arteriolosclerosis
Affects INTIMA of small arterioles and arteries. most often in those with DM, metabolic syndrome, HTN
66
Hyaline arteriolosclerosis
Protein deposits in essential HTN-pink arterial wall thickening with luminal narrowing. DM-due to advanced glycosylation end products being deposited in BM. HTN-increased pressure forces proteins into wall causing hardening of arteries.
67
Hyperplastic arteriolosclerosis
In malignant HTN. Increase in smooth muscle cell proliferation and BM duplication-"onion skinning". Esp prevalent in renal arterioles.
68
Myocarditis-causes
Most common cause in developed world is viral--coxsackie B, rubella, CMV. Worldwide-Chagas disease. Bacterial in immunocompromised (S aureus, C diphtheriae, H influenzae). Others: toxoplasmosis, Kaposis, Lyme, ARF, RhF, lupus, doxorubicin
69
Subacute Bacterial Endocarditis
Usually affects previously damaged valves. VIRIDANS. May see ring enhancing lesions in brain due to septic emboli. Staph epidermidis on prosthetic valves.
70
Duke criteria for endocarditis
Positive serial cultures, prior endocardial involvement, IV drug use, fever, vasc/immune phenomenon, valvular lesions on echo
71
Marantic Endocarditis
Non-Bacterial Thrombotic Endocarditis. Small sterile fibrin vegetations on heart valves of those with devastating disease. Paraneoplastic syndrome-mucin secreting tumors (usu colon or pancreatic)
72
Libman-Sacks Endocarditis
Ab damage to valves from SLE/ Sterile vegetations on BOTH SIDES of heart valves. Oft asymptomatic but may have a heart murmur.
73
DCM-causes
Idiopathic (most common), EtOH abuse, thiamine deficinecy, coxsackie B, Chagas, HIV, cocaine doxorubicin, Lyme, sarcoidois, hypothyroidism, Wegener granulomatosis, acromegaly, peripartum CM
74
DCM-presentation
4 chamber enlargement. R or L HF. Decreased EF, JVD, edema, orthopnea, hepatomegaly, cardiomegaly.
75
HCM-presentation
Syncope, dyspnea, S4, cardiomegaly, MR, pain releived by squatting and exacerbated by strenuous exercise
76
Diastolic HF-causes
Impaired filling: MS, tamponade, pericardial contstriction. Impaired relaxation: hypertrophy, CM, ischemia Impaired compliance
77
"Heart failure cells"
Intra-alveolar hemosiderin-laden macrophages