SM Flashcards
1
Q
what is a left dominant heart?
A
LCA gives rise to posterior interventricular artery in addition to its lateral branches
2
Q
characteristics of purkinje fibers on histology
A
larger diameter, lipid loaded, light staining
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
4
Q
where is the greatest pressure drop in systemic circulation?
A
arterioles (resistance vessels)
5
Q
which types of vessels don’t have tunica media or adventitia?
A
capillaries!
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
7
Q
what are the derivatives of the subcardinal veins?
A
middle IVC, renal and gonadal veins
8
Q
what are the derivatives of the supracardinal veins?
A
azygous vein and lower IVC
9
Q
what is the fate of the truncus arteriosus
A
ascending aorta
10
Q
what is the fate of the bulbus cordis
A
conus arteriosus, aortic vestibule
ie the smooth outflow portions of both ventricles
11
Q
what is the fate of the primitive ventricle
A
trabecular ventricles
12
Q
what is the fate of the primitive atria
A
pectinate muscle in left and right atria
13
Q
what is the fate of the sinus venosus
A
coronary sinus, smooth wall of right atrium
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
15
Q
what part of R lung does heart touch
A
middle lobe
16
Q
what part of L lung does heart touch?
A
lingula of L upper lobe
17
Q
what conditions would give you a large A wave for venous filling
A
tricuspid stenosis, RHF (pulmonary HTN)
18
Q
what conditions give you a giant v wave
A
tricuspid regurg
19
Q
when do you get absent a wave?
A
afib
20
Q
what does Glycoprotein Ia-IIa bind to?
A
collagen
21
Q
what does troponin T bind?
A
tropomyosin
22
Q
what does troponin C bind?
A
binds Ca+ when floods cell
23
Q
what does troponin I bind?
A
actin to INHIBIT contraction by covering myosin binding site
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
25
anterior/septal wall best seen in which leads
V1-V4 --> LAD
26
lateral wall of LV best seen in which leads
I, aVL, V4-V6 (mutharsan said V5, V6. not V4) -->LCx (V5-V6 could be LAD)
27
inferior wall of LV best seen in which leads
II, III, aVF --> RCA or sometimes LCx
28
what is normal PR interval
120-200 ms
29
what is normal QRS interval
80-110 ms
30
what is normal QTc
male < 450, female <470 ms
31
how do we quantify ST depression
at least 1mm decrease
32
how do we quantify ST elevation
at least 1 mm increase OR 0.5 mm increase if in leads V2-V3)
33
criteria for abnormal Q wave
lasts at least 0.03 sec (about 1 small box) AND amplitude of one small box. and present in at least 2 contiguous leads
34
ECG changes for NSTEMI
ST depression, T wave changes, or nothing
35
criteria for atrial enlargement
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
36
RVH criteria
V1: R wave > S wave and/or
V6: S wave > R wave
37
what is cushing reflex
ischemic brain senses high CO2, causes increase in PVR to increase MAP
38
which coagulation factors are vit K dependent
II, VII,IX, and X
39
what do alpha granules secrete
fibrinogen, factor V, vWF, wound healing stuff
40
what do dense granules secrete
ADP, ATP, ionized calcium, serotonin, epi
41
what does ADAMST13 do?
cleaves VWF into range of sizes in serum
42
what is bernard-soulier syndrome
GPIb deficiency
43
what is glanzmann thrombasthenia
deficiency in GPIIb/IIIa
44
what is major lipoprotein on HDL
APOa1
45
what is the major lipoprotein on chylomicron
ApoB48
46
what is the major lipoprotein on LDL
ApoB100
47
role of PDGF in atherosclerosis
secreted by endothelial cells to recruit smooth muscle cells
48
role of VEGF in atherosclerosis
recruit endothelial cells and stimulate angiogenesis in mature lesions
49
what layer is fatty streak found in
subintima
50
what is the diff between stable and unstable plaques
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
what are the criteria for hypertensive emergency
>180/120
52
what is the difference between slow and fast pathways in reentry?
slow pathway has short refractory period, fast has longer refractory period
53
what is orthodromic tachycardia
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
what are signs of critical lung ischemia
RUG
| rest pain, ulcer, gangrene
55
what layers are involved in aortic dissection
blood enters between intima and media via focal tear in intima
56
what is staging for HF
```
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
what is NYHA class system for HF
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
what are two main physiologic mechanisms underlying HF sx?
reduced CO, elevated filling pressures (impaired relaxation, reduced compliance, fluid overload)
59
what is BNP and how is it related to HF?
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
what is the difference between eccentric and concentric remodeling in HF?
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
what do we mean by rate control and rhythm control for afib?
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
what drugs used to disrupt AVNRT, AVRT
```
acute- adenosine
chronic- beta blockers, CCB. (class II, IV)
```
63
what drugs used to tx afib/aflutter for RATE CONTROL
need to slow conduction through AV node
beta blockers
CCB
digoxin
64
what drugs used to tx afib/aflutter for RHYTHM CONTROL
```
class Ic
class III (K+ channel blockers)
```
65
what drugs are used to suppress VT and symptomatic PVCs for MI
```
beta blockers
class III: amiodarone
class Ib
```
66
what drugs used to suppress VT and sympomatic PVCs in Torsades?
```
magnesium
phenytoin
isoproterenol
overdrive pacing
shock
```
67
why is mitral stenosis bad
restriction to LV inflow causes pulm venous congestion, low CO, LA dilatation that can lead to afib and systemic arterial emboli
68
mitral stenosis murmur
loud S1, opening snap in diastole followed by diastolic rumble. as gets worse, opening snap happens earlier
69
why is aortic stenosis bad
obstruction to LV outflow, increases afterload, LV hypertrophy, low CO
70
aortic stenosis murmur
systolic thrill, soft S2 (paradoxical spliting), midsystolic outflow murmur, crescendo decrescendo murmur
71
why is aortic regurg bad
increased LV preload and increased LV afterload. LV hypertrophy causes LV systolic dysfunction
72
what is timing for the 4 common murmurs
MS- diastolic
MR- systolic
AS- systolic
AR- both diastolic and systolic
73
aortic regurg murmur
S3, decrescendo diastolic blowing murmur, midsystolic outflow murmur, apical diastolic rumble
74
why is mitral regurg bad
volume overload of both LV and LA. increased preload --> pulm venous congestion, LV systolic dysfunction, afib and systemic emboli
75
mitral regurg murmur
holosystolic apical murmur, apical S3, midsystolic click (pts with MV prolapse), apical diastolic rumble. can radiate a lot
76
what does PCWP reflect
reflects pressure in LA and therefore LVEDP (compliance of LV)
77
what are normal hemodynamic parameters for RA, RV, PA, LA, LV, aorta
```
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
normal SV
50-100 ml/beat
79
normal CO
4-8 L/min or CI 2.5-4 L/min/m^2
80
what does CVP represent
RV filling pressure
81
what does PCWP represent
LV filling pressure
82
normal SVR
800-1200 dynes*sec/cm^5
83
letters on RV tracing
D- beginning diastole, E- end diastole. pressures go all the way to 0
84
PA pressure tracing
contains dicrotic notch when pulmonic valve closes. pressures don't go all the way to 0
85
PCWP wave
no c wave bc greater volume than R side of heart. measure at end expiration when intrathoracic pressure closest to 0
86
normal and abnormal Sv02
SvO2 reflects balance between O2 delivery and utilization. <60% abnormal and suggests low CO
>80% also abnormal and suggests high CO
87
equation to calculate SVR
(MAP-CVP)/CO *80
| normal 800-1200
88
equation to calculate PVR
```
(MPA-W)/CO * 80
normal 120 (>240 bad)
```
89
hypovolemic shock
insufficient blood volume to maintain BP
pt cool, JVP not distended/low CVP
low CVP, low CO, high SVR
90
cardiogenic shock
low CO
pt cool, JVP distented/CVP elevated
high CVP, low CO, high SVR
91
distributive/vasodilatory (septic) shock
profound vasodilation, drop in BP in spite of compensatory increase in CO
pt warm --> vasodilated --> septic likely
low CVP, high CO, low SVR
92
tx for acute pulmonary edema
LMNOP
loop diuretics, morphine, nitrates, oxygen, pos pressure ventilation (BiPaP)
93
tx for ADHF: warm and wet
congested but well perfused
diurese, uptitrate HF meds
94
tx for ADHF: cold and wet
congested with poor perfusion
vasodilators if increased SVR (afterload support), inotropes, diuresis
95
tx for ADHF: cold and dry
not congested but poor perfusion
inotropes, vasodilators, LVAD, transplant
96
tx for HFrEF
- 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
tx for HFpEF
- volume control
- BP control
- spironolactone
- weight management (inflammatory adipokines)
- exercise
- inotropes ONLY indicated for NYHA class IV pts (beta1 agonist or milrinone)
98
what is hematocrit
volume of rbcs in 100 mls blood
99
what is role of HIF-1alpha
activates EPO gene expression
100
kidneys regulate EPO by measuring what...
arterial blood hemoglobin concentration
101
what are reticulocytes and what do they indicate
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
what chromosomes contain globin genes
chromosomes 16 and 11
103
how does pO2 affect hemoglobin saturation?
as pO2 falls, Hb releases oxygen to tissues more easily
104
what factors shift hemoglobin curve right?
increased p50: decreased affinity for O2. release of more oxygen at tissue level
low pH, high 2,3BPG, high T, high pCO2, anemia
105
what factors shift hemoglobin curve left?
```
reduced oxygen available at tissue level
high pH (alkalosis), low 2,3BPG, low T, low pCO2, high affinity Hb (like Hb-F)
```
106
what is the Bohr effect
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
clotting factor testing for hemophilia
prolonged aPTT, normal PT
108
clotting factor testing for liver disease
at first prolonged PT, normal aPTT. Later both prolonged
109
clotting factor testing for anticoagulant use
both PTT and PT variably abnormal
110
deficiencies of factors XII, prekallikrein, HMWK
prolonged aPTT, normal PT, but no bleeding
111
what does antithrombin do
physiologic anticoagulant, targets thrombin and Xa, IXa, XIa, XIIa and VIIa/TF complex
112
what do protein C and protein S do
protein C activated by thrombin-thrombomodulin --> then inactivates Va and VIIIa
protein S is cofactor
113
how to reverse heparin?
protamine
114
what does warfarin inhibit
VII, IX, X, PT, protein C, protein S
115
which factors activated by thrombin (IIa)
V, VIII, XI
116
what does protein C inactivate
Va, VIIIa
117
how do you calculate Qp:Qs
Qp/Qs = (SAsat - SVsat)/(PVsat - PAsat)
if > 1.5 repair is justified
118
how does step up assessment for R heart saturations work
PA sat 75% = small shunt
| PA sat 90% = large shunt
