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CV-B Review > SM > Flashcards

SM Flashcards

1
Q

what is a left dominant heart?

A

LCA gives rise to posterior interventricular artery in addition to its lateral branches

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2
Q

characteristics of purkinje fibers on histology

A

larger diameter, lipid loaded, light staining

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3
Q

why does diastolic pressure drop less significantly in arteries?

A

more blood arrives to PA and aorta before all the blood runs off distally

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4
Q

where is the greatest pressure drop in systemic circulation?

A

arterioles (resistance vessels)

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5
Q

which types of vessels don’t have tunica media or adventitia?

A

capillaries!

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6
Q

what are the derivatives of the cardinal veins?

A

veins above heart:
anterior cardinal: brachiocephalic vein, SVC
posterior cardinal: pelvic and leg veins

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7
Q

what are the derivatives of the subcardinal veins?

A

middle IVC, renal and gonadal veins

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8
Q

what are the derivatives of the supracardinal veins?

A

azygous vein and lower IVC

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9
Q

what is the fate of the truncus arteriosus

A

ascending aorta

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10
Q

what is the fate of the bulbus cordis

A

conus arteriosus, aortic vestibule

ie the smooth outflow portions of both ventricles

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11
Q

what is the fate of the primitive ventricle

A

trabecular ventricles

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12
Q

what is the fate of the primitive atria

A

pectinate muscle in left and right atria

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13
Q

what is the fate of the sinus venosus

A

coronary sinus, smooth wall of right atrium

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14
Q

describe the components of jugular venous pulsation and their physiologic significance

A

v- atrial “Villing” (filling) during ventricular systole while TV closed
y descent- RA emptYing into RV once TV opens
a- atrial systole
x descent- atrial relaXation
c wave- tricuspid valve Closing

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15
Q

what part of R lung does heart touch

A

middle lobe

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16
Q

what part of L lung does heart touch?

A

lingula of L upper lobe

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17
Q

what conditions would give you a large A wave for venous filling

A

tricuspid stenosis, RHF (pulmonary HTN)

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18
Q

what conditions give you a giant v wave

A

tricuspid regurg

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19
Q

when do you get absent a wave?

A

afib

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20
Q

what does Glycoprotein Ia-IIa bind to?

A

collagen

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21
Q

what does troponin T bind?

A

tropomyosin

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22
Q

what does troponin C bind?

A

binds Ca+ when floods cell

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23
Q

what does troponin I bind?

A

actin to INHIBIT contraction by covering myosin binding site

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24
Q

what does the space constant tell us

A

the point at which amplitude of impulse has decreased to about 1/3. for good impulse conduction, we want high membrane resistance and low internal resistance

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25
Q

anterior/septal wall best seen in which leads

A

V1-V4 –> LAD

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26
Q

lateral wall of LV best seen in which leads

A

I, aVL, V4-V6 (mutharsan said V5, V6. not V4) –>LCx (V5-V6 could be LAD)

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27
Q

inferior wall of LV best seen in which leads

A

II, III, aVF –> RCA or sometimes LCx

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28
Q

what is normal PR interval

A

120-200 ms

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29
Q

what is normal QRS interval

A

80-110 ms

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30
Q

what is normal QTc

A

male < 450, female <470 ms

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31
Q

how do we quantify ST depression

A

at least 1mm decrease

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32
Q

how do we quantify ST elevation

A

at least 1 mm increase OR 0.5 mm increase if in leads V2-V3)

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33
Q

criteria for abnormal Q wave

A

lasts at least 0.03 sec (about 1 small box) AND amplitude of one small box. and present in at least 2 contiguous leads

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34
Q

ECG changes for NSTEMI

A

ST depression, T wave changes, or nothing

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35
Q

criteria for atrial enlargement

A

Lead II –> amplitude >2.5 mm (RA) or width >3mm (LA)

Lead V1 –> amplitude >2.5 mm (RA) or area of neg component at least 1 small box area

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36
Q

RVH criteria

A

V1: R wave > S wave and/or
V6: S wave > R wave

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37
Q

what is cushing reflex

A

ischemic brain senses high CO2, causes increase in PVR to increase MAP

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38
Q

which coagulation factors are vit K dependent

A

II, VII,IX, and X

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39
Q

what do alpha granules secrete

A

fibrinogen, factor V, vWF, wound healing stuff

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40
Q

what do dense granules secrete

A

ADP, ATP, ionized calcium, serotonin, epi

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41
Q

what does ADAMST13 do?

A

cleaves VWF into range of sizes in serum

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42
Q

what is bernard-soulier syndrome

A

GPIb deficiency

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43
Q

what is glanzmann thrombasthenia

A

deficiency in GPIIb/IIIa

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44
Q

what is major lipoprotein on HDL

A

APOa1

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45
Q

what is the major lipoprotein on chylomicron

A

ApoB48

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46
Q

what is the major lipoprotein on LDL

A

ApoB100

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47
Q

role of PDGF in atherosclerosis

A

secreted by endothelial cells to recruit smooth muscle cells

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48
Q

role of VEGF in atherosclerosis

A

recruit endothelial cells and stimulate angiogenesis in mature lesions

49
Q

what layer is fatty streak found in

A

subintima

50
Q

what is the diff between stable and unstable plaques

A

unstable- few SMCs, thin fibrous cap, inflamm cells, eroded epithelium, activated macrophages
stable- more SMCs, thick fibrous cap, lack of inflamm cells, foam cells, intact endothelium

51
Q

what are the criteria for hypertensive emergency

A

> 180/120

52
Q

what is the difference between slow and fast pathways in reentry?

A

slow pathway has short refractory period, fast has longer refractory period

53
Q

what is orthodromic tachycardia

A

type of AVRT with narrow QRS, accessory pathway from ventricle to atrium from AV node down to ventricle and then back up via accessory pathway

54
Q

what are signs of critical lung ischemia

A

RUG

rest pain, ulcer, gangrene

55
Q

what layers are involved in aortic dissection

A

blood enters between intima and media via focal tear in intima

56
Q

what is staging for HF

A 
cannot move back once in next stage
stage A- high risk for HF (HTN, CAD, DM)
stage B- asymptomatic HF (LV remodeling, MI, LVH)
stage C- symptomatic HF (HFpEF, HFrEF)
stage D- end stage refractory HF (HFrEF)
57
Q

what is NYHA class system for HF

A

Based on SYMPTOMS. can go back and forth between

class I- no sx
class II- sx with major exertion
class III- sx with minor exertion
class IV- sx at rest
58
Q

what are two main physiologic mechanisms underlying HF sx?

A

reduced CO, elevated filling pressures (impaired relaxation, reduced compliance, fluid overload)

59
Q

what is BNP and how is it related to HF?

A

ventricular stretch and LV dilation trigger BNP release

BNP causes reduced PVR (and BP), inhibits RAAS and endothelin pathwya, and causes increased natriuesis/diuresis

60
Q

what is the difference between eccentric and concentric remodeling in HF?

A

eccentric- no change in thickness, volume overload, myocytes in series, LV dilation

concentric- pressure overload, myocytes in parallel, normal cavity size. increase stiffness, ischemia, diastolic dysfunction

61
Q

what do we mean by rate control and rhythm control for afib?

A

rate control- slow down AV node to control ventricular rate, leave atria infibrillation. AV NODE
rhythm control- modify atrial electrical properties to restore sinus rhythm. SA NODE

62
Q

what drugs used to disrupt AVNRT, AVRT

A 
acute- adenosine
chronic- beta blockers, CCB. (class II, IV)
63
Q

what drugs used to tx afib/aflutter for RATE CONTROL

A

need to slow conduction through AV node

beta blockers
CCB
digoxin

64
Q

what drugs used to tx afib/aflutter for RHYTHM CONTROL

A 
class Ic
class III (K+ channel blockers)
65
Q

what drugs are used to suppress VT and symptomatic PVCs for MI

A 
beta blockers
class III: amiodarone
class Ib
66
Q

what drugs used to suppress VT and sympomatic PVCs in Torsades?

A 
magnesium
phenytoin
isoproterenol
overdrive pacing
shock
67
Q

why is mitral stenosis bad

A

restriction to LV inflow causes pulm venous congestion, low CO, LA dilatation that can lead to afib and systemic arterial emboli

68
Q

mitral stenosis murmur

A

loud S1, opening snap in diastole followed by diastolic rumble. as gets worse, opening snap happens earlier

69
Q

why is aortic stenosis bad

A

obstruction to LV outflow, increases afterload, LV hypertrophy, low CO

70
Q

aortic stenosis murmur

A

systolic thrill, soft S2 (paradoxical spliting), midsystolic outflow murmur, crescendo decrescendo murmur

71
Q

why is aortic regurg bad

A

increased LV preload and increased LV afterload. LV hypertrophy causes LV systolic dysfunction

72
Q

what is timing for the 4 common murmurs

A

MS- diastolic
MR- systolic
AS- systolic
AR- both diastolic and systolic

73
Q

aortic regurg murmur

A

S3, decrescendo diastolic blowing murmur, midsystolic outflow murmur, apical diastolic rumble

74
Q

why is mitral regurg bad

A

volume overload of both LV and LA. increased preload –> pulm venous congestion, LV systolic dysfunction, afib and systemic emboli

75
Q

mitral regurg murmur

A

holosystolic apical murmur, apical S3, midsystolic click (pts with MV prolapse), apical diastolic rumble. can radiate a lot

76
Q

what does PCWP reflect

A

reflects pressure in LA and therefore LVEDP (compliance of LV)

77
Q

what are normal hemodynamic parameters for RA, RV, PA, LA, LV, aorta

A 
RA- 6 mmHg
RV- 24/6 mmHg
PA- 24/12 mmHg
PCWP- 6-12 mmHg
LA- 6-12 mmHg 
LV- 120/6-12 mmHg
aorta- 120/60 mmHg
78
Q

normal SV

A

50-100 ml/beat

79
Q

normal CO

A

4-8 L/min or CI 2.5-4 L/min/m^2

80
Q

what does CVP represent

A

RV filling pressure

81
Q

what does PCWP represent

A

LV filling pressure

82
Q

normal SVR

A

800-1200 dynes*sec/cm^5

83
Q

letters on RV tracing

A

D- beginning diastole, E- end diastole. pressures go all the way to 0

84
Q

PA pressure tracing

A

contains dicrotic notch when pulmonic valve closes. pressures don’t go all the way to 0

85
Q

PCWP wave

A

no c wave bc greater volume than R side of heart. measure at end expiration when intrathoracic pressure closest to 0

86
Q

normal and abnormal Sv02

A

SvO2 reflects balance between O2 delivery and utilization. <60% abnormal and suggests low CO
>80% also abnormal and suggests high CO

87
Q

equation to calculate SVR

A

(MAP-CVP)/CO *80

normal 800-1200

88
Q

equation to calculate PVR

A 
(MPA-W)/CO * 80
normal 120 (>240 bad)
89
Q

hypovolemic shock

A

insufficient blood volume to maintain BP

pt cool, JVP not distended/low CVP

low CVP, low CO, high SVR

90
Q

cardiogenic shock

A

low CO

pt cool, JVP distented/CVP elevated

high CVP, low CO, high SVR

91
Q

distributive/vasodilatory (septic) shock

A

profound vasodilation, drop in BP in spite of compensatory increase in CO

pt warm –> vasodilated –> septic likely

low CVP, high CO, low SVR

92
Q

tx for acute pulmonary edema

A

LMNOP

loop diuretics, morphine, nitrates, oxygen, pos pressure ventilation (BiPaP)

93
Q

tx for ADHF: warm and wet

A

congested but well perfused

diurese, uptitrate HF meds

94
Q

tx for ADHF: cold and wet

A

congested with poor perfusion

vasodilators if increased SVR (afterload support), inotropes, diuresis

95
Q

tx for ADHF: cold and dry

A

not congested but poor perfusion

inotropes, vasodilators, LVAD, transplant

96
Q

tx for HFrEF

A
  • ACE-I/ARB or sacubutril/ARB (everyone) (specifically lisinopril, captopril, ramipril for ACE)
  • beta blocker (everyone) (metoprolol succinate, bisoprolol, carvedilol)
  • MRA (mineralocorticoid receptor antagonist)
  • hydralazine and isosorbide dinitrate combination therapy (veno and arteriolar vasodilation)
  • ivabradine
  • digoxin
  • diuretic (usually loop)
  • ICD or cardiac resychronization therapy
97
Q

tx for HFpEF

A
  • volume control
  • BP control
  • spironolactone
  • weight management (inflammatory adipokines)
  • exercise
  • inotropes ONLY indicated for NYHA class IV pts (beta1 agonist or milrinone)
98
Q

what is hematocrit

A

volume of rbcs in 100 mls blood

99
Q

what is role of HIF-1alpha

A

activates EPO gene expression

100
Q

kidneys regulate EPO by measuring what…

A

arterial blood hemoglobin concentration

101
Q

what are reticulocytes and what do they indicate

A

immature rbcs, no nucleus but have residual mRNA, mitochondria, ribosomes, centriole, golgi. stain with methylene blue. indicate increased production of RBCs (happens in 4-5 days)

102
Q

what chromosomes contain globin genes

A

chromosomes 16 and 11

103
Q

how does pO2 affect hemoglobin saturation?

A

as pO2 falls, Hb releases oxygen to tissues more easily

104
Q

what factors shift hemoglobin curve right?

A

increased p50: decreased affinity for O2. release of more oxygen at tissue level
low pH, high 2,3BPG, high T, high pCO2, anemia

105
Q

what factors shift hemoglobin curve left?

A 
reduced oxygen available at tissue level
high pH (alkalosis), low 2,3BPG, low T, low pCO2, high affinity Hb (like Hb-F)
106
Q

what is the Bohr effect

A

when concentration of CO2 in blood increases, pH decreases. as consequence, oxygen released from Hb in rbc causing reduction in Hb saturation = RIGHT SHIFT

107
Q

clotting factor testing for hemophilia

A

prolonged aPTT, normal PT

108
Q

clotting factor testing for liver disease

A

at first prolonged PT, normal aPTT. Later both prolonged

109
Q

clotting factor testing for anticoagulant use

A

both PTT and PT variably abnormal

110
Q

deficiencies of factors XII, prekallikrein, HMWK

A

prolonged aPTT, normal PT, but no bleeding

111
Q

what does antithrombin do

A

physiologic anticoagulant, targets thrombin and Xa, IXa, XIa, XIIa and VIIa/TF complex

112
Q

what do protein C and protein S do

A

protein C activated by thrombin-thrombomodulin –> then inactivates Va and VIIIa

protein S is cofactor

113
Q

how to reverse heparin?

A

protamine

114
Q

what does warfarin inhibit

A

VII, IX, X, PT, protein C, protein S

115
Q

which factors activated by thrombin (IIa)

A

V, VIII, XI

116
Q

what does protein C inactivate

A

Va, VIIIa

117
Q

how do you calculate Qp:Qs

A

Qp/Qs = (SAsat - SVsat)/(PVsat - PAsat)

if > 1.5 repair is justified

118
Q

how does step up assessment for R heart saturations work

A

PA sat 75% = small shunt

PA sat 90% = large shunt

CV-B Review (2 decks)

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