SBM > Cardio > Flashcards

Cardio Flashcards

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1
Q

LAD supplies

A

anterior LV wall
atnerior septum
His purkinje

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2
Q

Left circumflex supplies

A

lateral LV wall

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3
Q

RCA (PDA) supplies

A

inferior LV wall
RV
posterior septum
AV, SA node

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4
Q

What typically increases isotropy?

A

catecholamines

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5
Q

during cardiac contraction, only ___ stays the same

A

A (H,I,Z all differ!)

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6
Q

4 things that decrease contractility and SV

A

B blockade
heart failure
acidosis
hypoxia/hypercapnia

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7
Q

4 things that increase contractility and SV

A

catecholamines
increase in intracellular Ca
decrease in extracellular Na
digitalis–>increases intracel Na and therefore increases intracellular Ca

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8
Q

LV diastolic function determinants (5)

A 
Lusitrophy
LA pressure (aka LV filling pressure)
LV compliance
Heart rate (diastolic filling time) (dec in HR= increase in diastolic fx)
atrial kick
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9
Q

S3 represents

A

early diastole- dilated LV

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10
Q

S4 represents

A

late diastole-atrial kick to stiffened LV

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11
Q

paradoxical split

A

normally A2, P2 (because pressure greater in aorta), but in aortic stenosis P2 actually goes before A2 (breathing will make this go away)

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12
Q

4 things that happen when you turn in symp NS

A

1 increase Hr
2- increase iontropy
3- increase arteriole constriction
4- increase venous constriction

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13
Q

three types of shock

A

hypovolemic
distributive
cardiogenic

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14
Q

hypovolemic shock

A

too little blood

due to endothelial damage, excessive secretion, dehydration

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15
Q

distributive shock

A

enough blood but in wrong place (veins not arteries)

due to sepsis (vasodilator actions), reflex (vaso-vagal syncope)

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16
Q

cardiogenic shock

A

inadequate filling of arteries caused by failure of cardiac pump
due to acute MI, pericardial tamponade, valve rupture PE, myocarditis

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17
Q

3 consequences of shock

A

multi-organ failure
neurohormonal response
death

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18
Q

2 differences between physiological and pathological hypertrophy

A

physiological- high ATPase myosin heavy chains and more SR

path- less ATPase myosin heavy chains and less SR

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19
Q

helpful and harmful of intropes

A

helpful- increase BP and SV

harmful- increase work (so worsen energy expenditure)

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20
Q

helpful and harmful of diuretics

A

helpful- decrease preload, EDV/P

harmful- decrease stroke volume

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21
Q

helpful and harmful vasodilators

A

helpful- decrease after load, so increase SV

harmful- decrease BP and tissue perfusion

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22
Q

helps systolic heart failure

A

inhibit neurohormonal signaling

modify mehcanical stress

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23
Q

eccentric hypertrophy compensates for

A

decreased shortening ability

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24
Q

treatment for eccentric hypetrophy

A 
positive inotropic agents
diuretics
vasodilators
beta-blockers
aldosterone inhibitors
anticoagulants
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25
louder subaortic murmur with
interventions that decrease left ventricular size or velocity of contraction valsalva, standing, positive inotropic agents
26
treatment for dilated cardiomyopathy
ACEI, ARBS, Beta-blockers, diuretics, digitalis
27
treatment for hypertrophic cardiomyopathy
diuretics with caution, treat htn, treat Mischemia, decrease HR
28
Beck's Triad of physical signs of pericardial tampnade
decreased arterial pressure increased venous pressure quiet heart
29
low serum K can be indicative of
primary hyperaldosteronism
30
how can you diagnose a phenochromocytoma
metanephirnes | vanillymandelic acid
31
hyper vs hypothyrodiism
hyper: thyroid stimulation of heart hypo: increased TPR
32
2 phases of HTN
hyperkinetic phase | established or late essential HTN
33
polyarteriosis nodusa
medium vessel vasculitis
34
Wegenerg's polyangitis
smal vessel vasculitis
35
polyangiitis with granulomatosis
nose, lung kidney | PR3>>MPO
36
microscopic polyangitis
kidney MPO>PR3 renal limited variant
37
churg straus angiitis
kidney 15% | MPO>>PR3
38
inferior leads
II, III, aVF
39
anterior septal leads
V1 V2 V3
40
anterior lateral leads
V4, V5, V6
41
lateral leads
I, avL
42
P wave
atrial depolarization (SA node-->ventricle)
43
QRS
ventricular depolarization
44
T wave
ventricular depolarization
45
LAE can be (3)
Left ventricular hyptrophy LAFB- left anterior bundle branch block IMI II- 3 or more wide V1- 1x1 box
46
each small block is
40 ms (0.04 s) 1 mm 0.1 mb amplitude
47
axis
postiive in lead I and avF
48
LAD
+ lead I, - avf
49
RAD
- lead I
50
5 reasons for RAD
``` RVH Lateral MI COPD PE L posterior bundle black ``` II- >2.5 V1- >1.5
51
PR interval should be
120-200 ms
52
short PR interval
WPW | **has to have a bypass tract**
53
widlong PR interval
1st 2nd 3rd degree av block
54
1st degree AV block
p for every QRS | Sanode-->purkinje
55
2nd degree AV block
2:1 Av block I- wenkebach- lengthened PR II- Mobitz I
56
3rd AV block- complete block
SA firing but AV doesn't work
57
wide QRS
LBBB (q) RBB (rabbit ears) WPW (short PR) ICVD- when nothing else fits (look at V1)
58
difference between NSTEMI and unstable angina
troponin - in unstable angina
59
4 aspects of myocardial oxygen demand
HR, BP, contractilibilty, preload/afterload
60
Inferiro MI
AV node, mobitz I
61
Anterior MI
His purkinje, Mobitz 2
62
if V1 is positive
RVH
63
respirophasic, positional
pericarditis
64
P waves come and go
V tach
65
lightheadedness
a fib, mobitz 1
66
hypertension
light headedness
67
definite angina in men and women
men > 50: 95, 50 74, <50 59
68
probable angina
men >50, 73 50, 37 <50, 30
69
nonanginal pain
men >50, 20 >50, 8 | women >50 5, <50, 4
70
stagesof exercise ekg
I- 10, 4 mets II- 12, 7 mets III-14, 10 mets IV- 16, 16 mets
71
MHR
220-age
72
2 factors that predispose patients to sudden cardiac death post MI
LV dysfunction | frequent ventricular ectopy (>10 per hr)
73
Amiodarine & Sotalol
most effective for Vt/vf | efect phase 3 in AP by increasing QT (prolonging repel)
74
genetic heterogenity
same phenotype can have multiple different genes | -->differential diagnosis
75
penetrance
effect of gene on population | --whole room has BRCA1, but only 70% get breast cancer
76
expression
same gene, diff phenotype- person to person
77
fibrillin
main component of extracellular microfibrils
78
marfaans gene
15q21 | FBN1
79
platelet inhibitors
ASAK- decreases Thromb A2 Plavix- inhibit P2y12 receptors Eptifibatide- inhibit IIb/IIIa receptors
80
consider thrombolytics in patients
<65 years old presenting within 2 hrs of symptom onset anterior MI
81
1/2-4 hrs after MI
sometimes waviness of boraders
82
4-12 hrs MI
occasional dark mottling early coat necrosis, edema, hemorrhage
83
12-24 hrs
dark mottling ongoing coag necrosis, early PMN infiltrate
84
1-3 days
mottling with yellow-tan infarct center, more PMNs, can get pericarditis
85
3-7 days
central yellow-tan softening dying neutrophils with dead eating by MOs
86
7-10 days
maximally yellow-tan and soft, red depressed margins granulation
87
10-14 days
red-grey well established granulation tissue and collagen
88
2-8 weeks
grey white scar progressive to core increased collage, decreased cellularity
89
>2 months
scarring complete--white fibrous scar dense collagenous scar
90
eisenmenger syndrome
pulmonary arteries constrict and after 5 years this becomes permanent due to VSD
91
R-->L shunts
cyanotic
92
5 R to L shunts
``` metrology of fallout transposition of great arteries tricuspid atresia truncus arteriosus total anomalous PVR ```
93
4 aspects of tet
VSD pulmonary stenosis overriding aorta RVH
94
annular dilation
cardiomyopathy
95
leaflet perforation
endocarditis, trauma
96
prolapse
myomatous degeneration
97
chordial rupture
MVP, calcification
98
pap muscle rupture
ischemic heart disease
99
medication for MV issues
ditizaem (ca blocker affecting AV node) metoprolol (b blocker) to slow heart rate in Afib and lengthen diastolic time
100
LVH on EKG
- in V1 and + in V5 >35
101
critical aortic stenosis associated with
>60 mmHg, flow >4 m/sec
102
Verapamil | Diltizem
Ca channel blockers
103
abnormal automaticity induced by
hypokalemia hypoxia ischemia digitalis toxicity
104
automaticity/conduction is blocked by
quinidine | lidocaine
105
QRS complex
delays in intraventricular myocardium
106
Strain pattern
subendocardial hypoxia in hypertrophied ventricle
107
distolic depolarization
ischemic shifts ST segment because ischemic tissue injury-->increase in extracellular K concentration-->depolarizes cells-->current directed towards
108
Pericarditis
nonprogressive ST elevation
109
when is the earliest you see q wave
hrs-days
110
q wave + t inversion
months
111
q wave + normal T
years
112
ST elevation and T inversion, no q waves
hrs
113
Mobitz 1 is
AV nodal block
114
Mobitz 1 channel
slow- calcium
115
Mobitz infarction
inferior MI
116
mobitz 1 drugs
digitlais beta-blockers Ca channel blockers
117
mobitz 1 therapy
atropine | sympathomimetics
118
Mobitz ii
his purkinje block
119
Mobitz II vs Mobitz I ORS
I- junctional-narrow QRS | II- idioventricular- wide ORS
120
M2 infarct
anterior MI
121
M2 drugs
type I anti-arry
122
M2 therapy
pacemaker
123
atrial rate of 250-350
a flutter
124
atria rate of >250
a fib
125
1st degree heart block
delay from atria-->ventricle
126
2nd degree heart block
intermittent failure of conduction (some atrial beats conducted, some blocked) occurs in settings of increased vagal tone, decreased sympaethtics
127
3rd degree heart block
persistent failure of conduction (all atria beats blocked)
128
failure of conductivity
heart block
129
decreased automaticity
sinus bradycardia
130
AV nodal/junctional tachycardia
AV node goes to a rate that is faster than sinus rate seen with exercise hypotnesion, anxiety,hyperthyroidism, hypoglycemia, congestive heart failure
131
abnormal automaticity of fast fibers is associated with
``` increase sump tone (drugs, anxiety, hyperthyroidism) hypokalemia hypoxia/ischemia digitalis toxicity atrial enlargement ```
132
delta wave represents
pre-excitation of ventricle via abnormal bypass tract between atrium and ventricle called bundle of kent
133
three characteristics of re-entrant pathways
two anatomically or functionally distinct pathways slow conduction dispersion of refractoriness
134
superavent tachycardia vs vent tachy
supravent- narrow QRS | vent tach- wide QRS
135
prolonged QT usually due to
myocardial ion channel abnormalities | polymorphic Vtach-Torasades
136
digoxin and adenosine
av nodal blockers
137
Ca channels, av nodal blockers, b blockers
decrease how many beats can go through AV node so therefore decreasing HR
138
amidorone
blocks K channels | prevents reentrant Vtach
139
lidocaine
inhibits Na- only useful against Vtach
140
VSD causes LV
eccentric hypertrophy
141
O2 content=
O2 sat x [Hgb] x 1.34
142
LA pressure
6-12
143
RA pressure
6
144
Flow=
02 consumption/AV difference
145
SVR=
MAP-CVP/CO
SBM
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