Flashcards in Cardio Deck (145):
1
LAD supplies
anterior LV wall
atnerior septum
His purkinje
2
Left circumflex supplies
lateral LV wall
3
RCA (PDA) supplies
inferior LV wall
RV
posterior septum
AV, SA node
4
What typically increases isotropy?
catecholamines
5
during cardiac contraction, only ___ stays the same
A (H,I,Z all differ!)
6
4 things that decrease contractility and SV
B blockade
heart failure
acidosis
hypoxia/hypercapnia
7
4 things that increase contractility and SV
catecholamines
increase in intracellular Ca
decrease in extracellular Na
digitalis-->increases intracel Na and therefore increases intracellular Ca
8
LV diastolic function determinants (5)
Lusitrophy
LA pressure (aka LV filling pressure)
LV compliance
Heart rate (diastolic filling time) (dec in HR= increase in diastolic fx)
atrial kick
9
S3 represents
early diastole- dilated LV
10
S4 represents
late diastole-atrial kick to stiffened LV
11
paradoxical split
normally A2, P2 (because pressure greater in aorta), but in aortic stenosis P2 actually goes before A2 (breathing will make this go away)
12
4 things that happen when you turn in symp NS
1 increase Hr
2- increase iontropy
3- increase arteriole constriction
4- increase venous constriction
13
three types of shock
hypovolemic
distributive
cardiogenic
14
hypovolemic shock
too little blood
due to endothelial damage, excessive secretion, dehydration
15
distributive shock
enough blood but in wrong place (veins not arteries)
due to sepsis (vasodilator actions), reflex (vaso-vagal syncope)
16
cardiogenic shock
inadequate filling of arteries caused by failure of cardiac pump
due to acute MI, pericardial tamponade, valve rupture PE, myocarditis
17
3 consequences of shock
multi-organ failure
neurohormonal response
death
18
2 differences between physiological and pathological hypertrophy
physiological- high ATPase myosin heavy chains and more SR
path- less ATPase myosin heavy chains and less SR
19
helpful and harmful of intropes
helpful- increase BP and SV
harmful- increase work (so worsen energy expenditure)
20
helpful and harmful of diuretics
helpful- decrease preload, EDV/P
harmful- decrease stroke volume
21
helpful and harmful vasodilators
helpful- decrease after load, so increase SV
harmful- decrease BP and tissue perfusion
22
helps systolic heart failure
inhibit neurohormonal signaling
modify mehcanical stress
23
eccentric hypertrophy compensates for
decreased shortening ability
24
treatment for eccentric hypetrophy
positive inotropic agents
diuretics
vasodilators
beta-blockers
aldosterone inhibitors
anticoagulants
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