Exam 2 Flashcards
1
Q
what nerve goes anterior and which goes posterior to root of the lung
A
phrenic is anterior, vagus is posterior
2
Q
layers of the pleura of he heart from out to in
A
fibrous pericardium
parietal serous pericardium
visceral serous pericardium = epicardium
3
Q
ligamentum arteriosum
A
in fetal circulation, gets shunted from RV through ligament into aorta (in fetus it’s called ductus arteriosis)
4
Q
what is the nerve that’s close to the ligamentm arteriosum
A
recurrent laryngeal nerve (branch off of the vagus) - loops under, innervates things in the larynx on the left side
5
Q
muscular ridges in atrium
A
pecinate muscles on the wall of the base of the RA - create turbulent flow
6
Q
muscular ridges in ventricle
A
trabeculae carnae - create turbulent flow
7
Q
openings into right atria
A
superior (From head and neck) and inferior vena cava - dump into opening of coronary sinus
8
Q
edge behind right atria
A
sulcus terminalis - internal change between smooth wall and pectinate muscles
9
Q
coronary sinus
A
hole in right atrium where coronary veins dump
10
Q
impression between inferior and superior vena cava in R atrium
A
fossa ovalis - in fetus it’s an opening - shunt from RA to LA to bypass the RV (to avoid the lungs) - patent foramen ovale if it’s still open
11
Q
valve betwen RA and RV
A
Tricuspid valve - anterior, posterior and septal
12
Q
valve between LV and LA
A
mitral/bicuspid - anterior and posterior
13
Q
cordae tendinae
A
valves are anchored to papilary muscles via cordae tendinae (3 muscles in tricuspid, 2 muscles in mitral)
work with papilary muscles to prevent eversion of cusps into atria
14
Q
moderator band
A
AKA septomarginal trabecula - specialized trabecula that forms a bridge between the interventricular septum and the base of the anterior papillary muscle of the right ventricle that carries the right purkinje fibers
15
Q
semilunar valves
A
ventricles to pulmonary trunk or aorta - have left right and posterior leaflets
16
Q
flow into LA
A
4 pulmonary veins
17
Q
what is right behind LA
A
esophagus
18
Q
pectinate muscles in LA
A
there aren’t any - internal surface is smooth
19
Q
first branch of aorta
A
coronary arteries - can see openings for arteries behind the aortic semilunar valve
20
Q
where do you listen to the tricuspid valve
A
over left lower end of sternum
21
Q
where do you listen to the mitrlal valve
A
over the left fifth intercostal space at the midclavicular line
22
Q
where do you listen to the pulmonary valve
A
over the left second intercostal space lateral to the sternum
23
Q
where do you listen to the aortic valve
A
right second intercostal space lateral to sternum
24
Q
right coronary artery and branches
A
travels off of aorta, supplies R atrium and ventricle, gives rise to 4 branches:
1) (60% of people)SA nodal artery
2) right marginal artier (right border of right ventricle)
3) (67% of people) posterior interventricular artery aka PDA (supplies both ventricles)
4) (85% of people) AV nodal artery
25
left coronary artery and branches
short, quicky branches into the following branches:
1) anterior interventricular artery/ Left anterior descending LAD - supplies both ventricles
2) circumflex artery - supplies LV and LA
3) maybe SA or AV nodes if not supplied by right
26
when you say triple bypass, what does that mean
means that 3 coronary arteries were blocked and had to be bypassed
27
what determines R or L dominance?
if the posterior descending artery comes from L or R coronary artery
28
venous drainage of heart
1) coronary sinus -
2) great cardiac vein
3) middle cardiac vein
4) small cardiac,
29
coronary sinus - where does it come from where does it go
main vein of heart, wide channel that runs in coronary sulcus that collect blood from coronary veins, opens into right atrium
30
great cardiac vein, where does it go?
travels with anterior interventricular and circumflex branch
31
middle cardiac vein, where does it go?
travels with posterior intervenricular
32
small cardiac vein, where does it go?
travels with right marginal and then right coronary artery
33
where is SA node located
in the crista terminalis in the junction of the SVC and the right atrium
34
where is AV node located
in the interatrial septum (Between RA and RV) near the opening of the coronary sinus - right above tricuspid valve
35
AV bundle, where do they travel
located within interventricular septum - branch towards apex. right bundle branch is contained in moderator band, then they ramify into purkinje fibers
36
AV bundle, where do they travel
located within interventricular septum - branch towards apex. right bundle branch is contained in moderator band, then they ramify into purkinje fibers
37
prevalance
proportion of people in a population with disease at a given time -- positive and nevative predictive values are dependent on prevlanance
38
positive predictive value
proportion of people with positive test results who have disease -- true positives
39
negative predictive value
proportion or people with negative result who don't have disease -- true negatives
40
precision
are findings consistent with repeated testing
41
accuracy
do they correctly predict diagnosis, compare to gold standard
42
sensitivity
"positive in disease" - proportion of people with disease in whom the test result is positive
-- true positives
43
specificity
"negative in health" - proportion of people without the disease in whom the test result is negative
-- true negatives
44
as sensitivity increases, what happens to specificity?
decreases
45
likelihood ratio
measure of how much more or less likely the patient is to have the disease because of the test result
some result in patient with disease/the same result in patient without disease
more extreme (over 10 or under 0.1) are more useful
46
how to use nomogram
plot pre-test probability and likelihood ratio, and then extrapolate to find post-test probability
47
action threshold
diagnostic tests are most useful when results push disease probability across a threshold (treatment or test) leading to a specific action
48
layers of endocardium
1) inner most layer has endothelium
2) deep to endothelium is subendothelium which is CT and SM
3) beneath subendothelial layer is subendocardial layer which is CT laer that contains Purkinje fibers and
beneath that is myocardium
49
what is at intercalated disc (3)
fascia adherentes
gap junctions
desmosomes
50
what's in epicardium (4)
1) mesothelium (visceral serous pericardium)
2) fat
3) autonomic ganglia (vagus nerve branches)
4) coronary arteries and venules
51
cardiac skeleton componenets (4)
1) membranoues portion of intervertricular septum
2) 4 annuli fibrosi around big vessels around valves
3) trigona fibrosa - 2 parts (left and right)
4) heart valves
52
valve layers (4)
1) endothelium innermost
2) spongiosum (loose CT)
3) fibrosa (dense CT)
4) ventricularis (elastic)
53
modified myocytes in purkinje fibers as compared to regular myocytes (5)
1) 2x bigger
2) few myofibrils
3) more glycogen centrally
4) binucleated
5) conducts 4x faster
54
chondroid
similar to hyalin collagen but different and found in cardiac skeleton
55
accountable care organization (ACO)
ACO = group (of physicians, hospitals, insurers etc.) that assumes responsibility for quality and cost of care for a population of patients with the goal of minimizing cost of high quality care for medicare patients
56
classical conditioning
pavlov's dog
phase 1: neutral stimulus (no response)
phase 2: pair neutral stimulus with unconditoned stimulus
phase 3: eventually neutral stimulus causes conditioned response
57
operant conditioning
1) positive reinforcement: push lever get reward - or push lever and get punishment
2) negative reinforcement: getting shock and when you push lever it stops, so you keep pushing lever
3) punishment: stop behavior because it hurts - behavior stops
58
social learning theory
how personal factors interact reciprocally with environmental factors - modeling what you see (violence, cigarettes etc)
59
transtheoretical model
stages of change:
1) precontemplation (no interest in changing)
2) contemplation (thinking but no action)
3) preparation (planning for change - scared to take the steps)
4) action
5) maintenance
60
schedule of reinforcement (options)
continuous
intermittent
- interval (fixed or variable)
- ratio (fixed or variable)
61
self-efficacy
I know I can do it
62
prazosin does what
selective a1 blocker
| decreases BP get reflex tachycardia
63
is prazosin reversible?
yes
64
what does phenoxybenzamine do
blocks a1 and some a2
| decreases BP lasts 24hours
65
is phenoxybenzamine reversible?
no
66
phentolamine does what
blocks a1 and a2 nonselectively (a1 decreaes BP, a2 prevents feedback inhibition, causing more NE released onto B1 -- MORE tachycardia)
67
therapeutic use of proazosin
HTN
68
therapeutic use of phenoxybenzamine and phentolamine
pheochromocytoma management (block catecholamines)
69
phenoxybenzamine, prazosin and terazosin therapeutic use
benign prostatic hypertrophy - relax smooth muscle in prostate capsule
70
side effect of alpha1 blockade
postural hypotension
reflex tachycardia
nasal stuffiness
inhibition of ejaculation
71
epi-reversal
pure beta2 - just decrease BP, no "pressor" response
72
do you use beta blockers in people iwth breathing problems?
no
73
propranolol
```
non-selective beta blocker
decreases HR due to beta1 block by:
- decreases cardiac output
- decreases plasma renin
- decreases sympathetic tone via effects in CNS
```
74
metabolic effects of non-selective beta blockers
no effect on glucose of normal people, but slows recovery from hypogycermia in diabetics. increased VLDL and decreased HDL
75
atenolol what does it do
selective beta1 blocker
- similar cardiac effects as non-selective
- no resp effects
76
esmolol what does it do
selective beta 1 with really short half life - used for emergency procedures
77
pindolol
partial agonist - partially activate beta receptor but block access of full agonist NE
78
acebutolol
partial agonist - partially activate beta receptor but block access of full agonist NE
79
what do you use for glaucoma
timolol - decrease acqueus humor production - via beta1
80
labetalol
mixed alpha and beta - blocks beta to alpha1 at 4:1 ratio
used for chronic hypertension or acute management of hypertensive crisis secondary to excessive catecholamines
81
carvedilol
mixed alpha and beta - blocks beta to alpha1 at ratio of 10:1
- used for congestive heart failure
- antioxidant
- antihypertensive
82
beta blocker uses (10)
```
1- hypertension
2- cardiac arrhythmia
3- angina pain
4- prophylaxis for migraine
5- may inhibit cancer progression
6- used in MI (early and after)
7- pheochroocytoma
8- glaucoma
9- heart failure
10 - performance anxiety
```
83
side effects of beta blockers (3)
1- B1 block causes decreased cardiac output, heart block and bradycardia
2- B2 block causes bronchoconstriction
3- CNS: depression and lethargy
84
guathenidine
works at presynaptic site
neither agonist or antagonist, but has anti-adrenergic effect
prevents storage of NE, MAO eats up NE
- originally used as antihypertensive, but has a bunch of side effects - diarrhea, postural hypotension etc.
85
risperpiine
doesn't use NET - dissolves through presynaptic, binds to NE transporter and blocks storage of NE - empty vessicle
- used to be used for hypertension
- side effects were depression and orthostatic hypotension
86
alpha2 agnoist actions (2)
in brain alpha2 block sympathetic outflow and thus decrease blood pressure
at presynaptic postganglionic adrenergic neurons, alpha2 inhibit NE release and reduce tone
87
clonidine mechanism and uses (4)
alpha2 agonist that works directly at alpha2 receptors
- for hypertension
- reduce withdrawl symptoms for opioids
- open angle glaucoma (reduce acqueus humor)
- ADHD
88
a-methyl-dopa mechanism and uses (2)
alpha2 agonist that must be metabolized to alpha-methyl-NE
- for hypertension
- safe in pregnancy
89
side effects for alpha2 agonists (4)
- dry mouth
- sedation
- hypertensive crisis if quick withdrawl of clonidine
- alpha-methyldopa produces autoimmune response (positive coombs test)
90
what kind of cardiovascular diseases are associated with pestilence and famine
rheumatic fever - valve damage,
| cardiomyopathy
91
what kind of CV diseases are associated iwth degenerative and man-made diseases
CHD, stroke, HTN (most deaths in this category)
92
what is fibrillation
re-entry
93
what would you do to give best immediate treatment for venricular fibrillation
shock - depolarize all cells, and first to repolarize and depolarize will be SA to re-establish normal rhythm
94
which has higher conduction rate, bundle of his or sa NODE
bundle of HIS
95
which has higher spontaneous discharge, buldne of his or SA node
SA node
96
which electrode is positive A or B
B is positive, A is negative
97
first thing that happens in ventricular AP, and what kind of deflection do you have as depolarization approaches B
calcium and sodium move into the cell (makes A more negative) B-A gives you positive deflection
98
what happens when depolarization recedes from B
sodium move into cell at B, makes B more negatve, makes B-A deflection negative
99
repolarization receding from B, what kind of deflection do you have
get potassium ion out of cell, makes B more positive- causeing B-A positive deflectioon
100
repolarization approaching B gives what kindof deflection
potassium ions leaving cell at A, makes A more positive, so B-A is negative deflection
101
vector of atrial depolarization
atrium - right side to left side and from base to apex - pointing to left leg
102
vectors of ventricular depolarization (3)
1. across septum from L to R and slightly up (becuase of density of purkinje fibers)
2. from endo to epi at apex of heart
3. up from L ventricular wall (and to lesser extent R because of less mass) and along the septum, away from L leg
103
vector of ventricular repolarization
from epicardium to endocardium at apex of heart away from L leg
104
lead 2 position of electodes, and what does it pick up
neg electrode on R arm, pos on L leg, so can pick up depolarization along that axis (along septum more or less)
105
lead 1 position of electrodes, and what does it pick up
neg R arm, pos L arm (
| can pick up horizontal signals
106
lead 3 position of electrodes, and what does it pick up
neg L arm, pos L leg, picks up signals pointing diagnoally to R leg
107
aVF what does it measure
augmented voltage foot, averages R arm and L arm and makes that negative, and makes L leg pos
108
aVR what does it measure
augmented voltage right, averages L arm and L leg and makes that negative, and makes R arm pos
109
aVL what does it measure
augmented voltage left, averages R arm and L leg and makes that negative, and makes L arm pos
110
what is P wave
atrial depoarlization - small positive deflection
111
what is QRS wave
3 phases of ventricular depolarization:
```
Q= small negative deflection (across septum L and upward)
R = large positive deflection (vector towards apex)
S = medium negative deflection (up septum and walls)
```
112
what is T wave
ventricular repolarization - from epi to endo at apex away from L leg (repolarization receding away from L leg = positive deflection)
113
what are the isopotential lines
1) PR segment -
through AV node
2) ST segment as everything is depolarized
114
what does ST elevation indicate
damaged tissue that continues to depolarize
115
einchoven's triangle
lead 1 + lead 3 = lead 2
116
what do you see in first degree heart block on ECG, what causes it
there is a lag between P wave and QRS (elongated PR interval) (usual is 180ms, >200ms is abnormal)
goes too slowly through AV node
117
what is one big box on the time axis for an ECG
0.2 seconds - 5 big boxes is 1 second
118
what is one big box on voltage xis on ECG
0.5 mV
119
difference between interval and segment
segment is straight line, interval is segment plus at least 1 wave
120
what is normal PR interval
0.12 - 0.2 sec
121
normal QRS interval
0.06 - 0.1
122
normal QT interval
0.35 - 0.4
123
what does QT interval represent
from begining of depolarization to end of repolarization - full AP of ventricular cells
124
second degree heart block
not every P wave is followed by QRS
125
type 1 second degree heart block
increasing delay between P and QRS
| until P doesn't evoke a QRS
126
type 2 second degree heart block
no increasing delays between P and QRS, but you still have Ps that aren't followed by QRS
127
3rd degree heart block
complete dissociation between atrial and ventricular depolarization - P and QRS happen independently
128
ventricular fibrillation
"bag of snakes squirming around"
129
ventricular tachycardia
ventricles are contracting at a rate greater than 100 BPM
130
sinus bradycardia
heart rate lower than 60 bpm - generated by SA node
131
atrial fibrillation
- no distinct P waves, but still get QRS
| - atria quiver, but you can live with this - can depolarize and contract ventricles
132
atrial flutter
looks like saw tooth waves or Zs before QRS wave
133
sinus tachycardia
heart rate greater than 100 bpm originating at SA
134
la place's law for pressure in ventricles
P = (tension x thickness) / r
```
Pleft = 120
Pright = 1/6 Pleft = 20
```
pressure in left is about 5x right
135
kinds of cardiac hypertrophy
1. concentric hypertrophy -
pressure overload (thickness increases, volume decreases, pressure increases)
2. eccentric hypertrophy - volume overload (radius increases, thickness decreases, pressure decreases)
136
how many microns are myocytes
150 microns
137
what does phosphorylation do to proteins
faster contraction (DHPR, Ryanodine etc.), SERCA shortens relaxation time by pumping Ca back in -reabsorption
138
treppe
AKA bodwitch effect. more frequent stimulation causes stronger contraction - staircase effect
less time for calcium to get transported out of cytosol
139
isometric
generates only force, no muscle shortening
140
isotonic
produces shorteining at constant load
141
preload
extent to which muscle is stretched before the onset of contraction (for heart, preload is end diastolic volume)
142
afterload
load lifted by the muscle in isotonic contraction (for heart, afterload is aortic pressure - pressure against which you're trying to eject)
143
frank starling
the more you stretch, the more forecul the contraction - like rubberband
144
mechanisms for grading strength of contraction in cardiac muscle
a. CONTRACTILITY increased amplitude or duration of calcium transient (amount of calcium available for contraction)
b. PRELOAD - stretching the myocyte for optimal force
145
ionotropy
influence of agents that alter contractility - positive ionotrope (exercise allowing for more contractility and more calcium available)
146
systole phases
1- isovolumetric ventrical conraction (builds pressure)
2- ventricular ejection (when pressure exceeds aortic pressure)
147
diastole phases
1- isovolumetric ventricle relaxation
2- ventricular filling (AV valve opens)
3- atrial contraction (upon excitation - end of diastole)
148
how long does systole last
250-300msec
149
how long does diastole last
500-550 msec
150
a wave
measures atrial pressure during atrial contraction
151
c wave
measures atrial pressure during closing of AV valve during ventricular contraction, dips down once ventricular ejection occurs
152
v wave
measures atrial pressure during ventricular relaxation during diastole, until you open AV valve
153
x deflection
venous pressure during systole
154
y deflection
venous pressure during diastole
155
dicrotic notch or insicura - caused by what (3)
aortic pressure at the end of systole when the ventricle relaxes:
1) get some reguritation
2) get rebound of the valve
3) and get some back flow into coronaries
156
mean arterial pressure equation
at rest,
| MAP = 1/3 max arterial systolic pressure + 2/3 minimal arterial diastolic pressure
157
pulse pressure
arterial systolic - arterial diastolic pressure
158
stroke volume equation
end diastolic volume - end systolic volume
120-40 = 80mL
159
ejection fraction - equation and values
stroke volume/end diastolic volume
80/120 = 66%
normal is 60-70%
under 30% is grave
160
S1 is closures of what valve
AV
161
S2 is closure of
semilunar
162
are chylomicrons the most dense or the least dense
least dense - on top
163
as you go from HDL to chylomicron, how does your protein content change
lots of protein in HDL, very little protein in chylomicrons
164
as you go from HDL to chylomciron, how does your cholestorl content change?
HDL has 2nd highest, LDL has highest, and then decreasing from there to chylomicron lowest
165
as you go from HDL to chylomicron, how does your phospholipid content change?
highest at HDL, lowest at chylomicron
166
as you go from HDL to chylomicron, how does your triacylglycerol content change?
lowest at HDL, highest at chylomicron
167
LDL does what
delivers membrane building materials peripherally
168
HDL does what
take membrane materials back to the liver
169
chylomicrons do what
deliver dietary fats (triglycerides)
170
relative size of lipoproteins from HDL to chylomicrons
chylomicrons are really big (120nm), VLDL also big (80nm) IDL is around 50nm -
none of these can diffuse through membranes - need to dock to offload
LDL is smaller, HDL is around 8nm, can diffuse into deeper tissues
171
what does apoB48 do
stabilizes the core
172
what does apoC do
helps chylomicron target a lipase so that fatty acid can get into adipose and muscle cells
173
what does apoE do
targets chylomicron remnant back to the liver, so it can be recycled and reused
174
relationship between cholesterol levels and chylomicron remnants
if you have high systemic dietary cholesterol, chylomicron remnant will get back to liver to tell it to down regulate de novo synthesis of cholesterol (at HMG-oA reductase)
175
SREBP-SCAP and cholesterol levels
regulates HMG CoA reductase and LDL receptor
in low cholesterol:
SREBP gets cleaved and migrates to nucleus to upregulate cholesterol synthesis and LDL receptor
in high cholesterol:
cholesterol binds SCAP, inhibiting cleavage of SREBP by binding with high affinity to SREBP - downregulation of cholesterol biosynthesis and LDL receptor
176
apoB structures in chylomicron
apoB48 (with membrane component solubilizing to get it into circualtory, and core stability component)
filled with triglycerides
177
apoB strucures in VLDL and LDL
apoB100 (more cholesterol and cholesterol ester) and antennae with lysines in it (positively charged) to bind to negatively acids (aspartic/glutamic) - bind to LDL receptor with a lot of aspartic acids
178
where is apoB100 made
liver (for LDL/lipid trafficking building materials to cells) - extra antennae = longer
179
where is apoB48 made
intestines (for dietary fat delivery through cholesterol)
180
what is IDL?
it's basically VLDL remnant that eventually gets converted to LDL:
- has apoB100 and apoE to target to the liver, procesessed IDL to LDL
- also gets shuttled to HDL to strip it of its surface apo proteins - A C E so that you just have apoB100 left (which is LDL)
181
lipoprotein lipase (LPL) function
chylomicrons and VLDL will bind to it through apoC, free fatty acids go in (to muscle cell or adipose tissue), glycerol stays in circulation where it goes back to liver
182
how do fatty acids get mobilized within adipose cells
hormone sensitive lipase is activated by glucagon in a G-protein coupled receptor dependent fashion via activation of Protein Kinase A
183
LDL metabolism (receptor binding, delivery etc.)
delivery of membrane building materials to target tissue by LDL-LDL receptor interaction:
apoB100 (LDL or IDL) binds to receptor with clathrin coated pit endocytosed (receptor will either get recycled back to membrane and LDL will fuse with lysosome and apoB100 is degraded and amino acids are recycled, all other components become part of the membrane system)
most receptors are found in liver
184
PCKS9
protein that promotes internalization but blocks recycling - increasing circulating LDL
anti-PCSK9 IgG binds interaction of LDL receptor with PCKS9 - knocks out ability of PCKS9 to degrade receptors, scavenging circulating LDL
185
HDL metabolism (docking, cholesterol uptake)
when HDL docks with membrane raft with apoA1 stimulates ABCA1 transporter to pump cholesterol into HDL. free cholesterol covers surface, but in order to fill core, you need to convert to cholesterol ester, with the help of LCAT enzyme. goes back to liver where apoE endocytosis occurs
186
Fiber (types, mechanisms)
2 types
- insoluble (skins)
- soluble (metamucil - slurry)
mechanisms:
- adsorbs cholesterol (sticks to cholesterol)
- GI motility changes
facilitate excretion
187
Omega 3 fatty acids
- increase clearance of triglyceride levels (triglycerides lead to pancreatitis)
- anti-inflammatory response
- eat fish, improve cardiac health
188
atorvastatin - mechanism
statin - lipitor
metabolized by CYP3A4
longer half life - can take whenever
more lipophilic - crosses BBB
189
pravastatin
statin - prevacor
metabolized by sulfation and IS NOT P450 dependent!! - fewer drug-rug
half life is lower - have to take before bed
more water soluble (more hepatoselective)
190
ezetimibe (mechanism, metabolism)
absorbtion blocker
inhibits Niemann-Pick C1-Like 1 (NPC1L1) transporter which decreases delivery of intestinal cholesterol to the liver which decreases cholesterol in chylomicrons/remnants, leading to increase in LDL receptors and increase clearance in LDL from plasma
not metabolized by p450s, undergoes repeated enterohepatic circulation causing long duration of drug
no adverse effects really
191
cholesteryamine (use, mechanism, adverse)
bile acid sequestrant/resin
used in combo with statins because it can lead to up-regulation of HMG-CoA reductase
charged - not absorbed, but bind to bile acids, metabolites of cholesterol to prevent absorption which leads to increased conversion of cholesterol to bile acids, which up-regulates LDL receptors and LDL clearance from plasma
adverse: GI effects, absorption of other drugs might be impaired
192
niacin (mechanism, metabolism, adverse)
nicotinamide derivative
only drug to elevate HDL- inhibits lipolysis in adipose tissue, decreases free fatty acid transport to liver (decreases VLDL synthesis in liver) and decreases triglyceride synthesis in liver
: overall effect is decreasing TGs and LDL while raising HDL
Hepatic metabolism
adverse: can cause vasodilation - flushing, hepatotoxicity and GI discomfort
193
gemfibrozil (mechanism
fibrate
works to lower TG levels through activating agonist for PPAR alpha receptor (a TF), which lowers TGs through increasing clearance of TG and VLDL
can cross placenta
short half life
GI discomforta, myopathy (risk with statin), many drug interactions
194
evolocumab/repatha (mechanism, adverse)
PSCK9 inhibitor
binds to PSCK9 protein from being able to bind and endocytose LDL receptor
has to be injected, is expensive, only causes about 15% decrease in primary endpoint,
nasopharyngitis
195
statin mechanism
look like HMG-CoA, binds to receptor, to reversibly inhibit cholesterol production
leading to increasing synthesis of LDL receptors in liver, which increases clearance of LDL in the circulation
196
statin adverse effects (3)
hepatic toxicity (more so for atorvastatin)
muscle pain and weakness (rhabdomyalisis) - caused by drug interaction with gemfibrozil which inhibits transport of statins into liver or with other cyp inhibitors (would not affect pravastatin)
small increased risk for diabetes
197
what does rheumatic fever cause/present in cardiac exam
atrial fibrillation - enlarged left atrium
opening snap, diastolic rumble, NO enlarged left ventricle (normal PMI) - mitral stenosis
198
gender differences with CVD
- women present later in life (risk worsens after menaupause) -
- they present with different symptoms (shortness of breath vs. pain)
- more strokes
- higher complications in sx
- more reserved ejection heart failure later in life
- more non-obstructive coronary disease - microvascualr issue
199
estrogen and stroke risk
increases stroke risk
200
risks for cardiovascular disease in hispanic population
varying ancestral mix = varying risk
- hypertension and diabetes are high, but once controlled, no difference among ethnic groups
- disparities in defibrillator use in hispanics
201
hydralizine
overall population not effective for heart failure, but for AA there is positive effect, perhaps because it's addressing the underlying hypertension, which is overwhelming cause of HF in AA patients
202
3 phases of disparities research agenda
1. detecting (define health disparities)
2. understanding (identifying determinants at different levels)
3. reducing (intervention, evaluation, change policy)
203
what causes murmur in man with heart failure due to uncontrolled hypertension
holosystolic murmur - mitral regurgitation due to dilated left ventricle
204
what causes crescendo-decrescendo systolic murmur
aortic stenosis - with degenerative heart disease
205
what is sternal angle vertebral level
T4/T5
206
which is longer, right or left brachiocephalic
left- because superior vena cava is on the right side of the heart, so the left brachiocephalic has to travel further
207
components of brachiocephalic vein
subclavian and internal jugular
208
branches off of the arch of the aorta
- brachiocephalic artery
- left common carotid
- left subclavian
209
brachiocephalic artery branches
right subclavian and right common carotid
210
branches off of the ascending aorta
- right and left coronary arteries
211
branches coming off of thoracic aorta
- posterior intercostal arteries
| - pericardial, esophageal and bronchial arteries
212
where is the left recurrent laryngeal nerve on chest film
in the aortopulmonary window (between arch and L pulmonary artery or trunk)
213
L vagus becomes ___ as it descends
anterior
214
R vagus becomes ___ as it descends
posterior
215
where do veins drain into on the right side?
right intercostal veins, hemizygous, accessory hemi all dump into azygous, azygous dumps into superior vena cava
216
where do veins drain into on the left side?
left hemiazygous (drains 9, 10 and 11) and accessory hemiazygous (Drains 4, 5, 6, 7 and 8 intercostal veins)
get over to the right side through shunts over to azygous at lower or upper level
217
where does thoracic duct start
cisterna chyli in abdomen
218
where does thoracic duct dump into
venous system near the union of the left internal jugular and subclavian veins
219
what structures does the thoracic duct lie between
the duck between two geese (the duct between azygous and esophagus)
220
which closes earlier, aortic or pulmonic?
aortic - delayed when you breathe in so you can hear the split, or during normal breathing when you have L ventricular problems or aortic stenosis (these people will reduce the split when breathing in)
221
aortic stenosis, what do you hear
narrow, more turbulence - murmur during systole
222
aortic incopetence, what do you hear
doesn't completely close, so hear backflow during diastole
223
mitral stenosis, what do you hear
narrow, more durbulence, murmur during diastole
224
mitral incompetence, what do you hear
doesn't close completely, so you hear backflow during systole
225
pressure-volume loop - describe it
in LV, measure pressure and volume:
starts at 120 volume and low pressure, increases pressure until aortic valve opens, then you keep increasing pressure as volume decreases, then the aortic valve closes, volume stays the same as pressure decreases, and then mitral valve opens and pressure stays low as volume increases back to 120
226
what curve on the pressure-volume loop do you look at to assess compliance
bottom curve - as ventricle is filling - low pressure = compliant, high pressure = not compliant
227
how do you measure stroke volume from poressure-volume loop?
stroke volume is the width of the curve - between two isovolumentric lines (end diastolic and systolic volumes)
228
what is the end diastolic volume on the pressure-volume loop?
the isovolumetric line at max ventricular filling
229
what is the end systolic volume on the pressure-volume loop?
the isovolumetric line at min ventricular filling
230
what is the filling preload pressure on the pressure-volume loop
the point at which the ventricle increases pressure without increasing volume
231
what is the aortic pressure/ afterload on pressure-volume loop
point at which the aorta opens and the volume starts to decrease with increasing pressure
232
what is the external work on the pressure-volume loop and what's the equation
area inside the curve
external work = change in volume x change in pressure
OR
stroke volume x aortic pressure
233
how do you measure heart muscle efficiency ratio?
external work/ internal work
234
what is internal work on the pressure-volume curve
area under the curve at lower volume than end systolic volume - proportional to oxygen consumption
235
what do you see on pressure-volume loop with increased contractility
when you eject you reach a lower end systolic volume so you are able to eject more - more efficient pump
236
what do you see on pressure-volume loop with increased aortic pressure?
because you have to have higher ventricular pressure to reach aortic pressure before ejection, you hit the ESPVR curve earlier and thus your end systolic volume is higher, meaning you're not able to pump as much blood out, creating a less efficient pump
237
if you have higher venous pressure, what do you see with pressure-volume curve
increased venous pressure allows a larger end diastolic volume, which in turn increases total stroke volume, making more efficient pump
238
how do left and right cardiac output compare
about the same
239
2 equations for cardiac output
```
CO = SV x HR
CO = MAP / TPR
```
```
MAP = mean arterial pressure
TPR = total peripheral resistance
```
240
what is the average CO?
5-6 L/min, little less in women
| proportional to tissue mass/metabolic rate
241
what are the long-term factors that can affect cardiac output (3)
1) ventricular geometry (Thicker/thinner, wider/narrower)
2) ventricular compliance
3) electrical coordination of contraction
242
what are the short-term factors that affect cardiac output (4)
1) preload
2) afterload
3) contractility
4) heart rate
243
what is the point at which increased HR does NOT increase cardiac output
around 180 - heart doesn't have time to fill back up
244
chronotropic relates to
HR
245
dromotropic relates to
conduction velocity
246
inotropic relates to
contractility
247
pulse pressure relation to stroke volume and compliance
directly related to stroke volume, indirectly related to compliance
248
do we feel pressure wave or blood flow in wrist?
pressure wave
249
what is the systolic pressure in medium sized arteries compared to aorta, and why is there this difference
systolic pressure is higher in the medium arteries than the aorta, because some of the flow gets deflected back (because of branching points etc) and thus the waves get summated.
250
how do you measure contractility with pulse pressure
steeper slope of ventricular pressure as it rises to meet aortic pressure indicates higher contractility
251
why does pulse pressure increase as we age?
because arteries are not as compliant, and thus are not able to store pressure, so the mean pulse pressure has to increase to compensate
252
things that affect venous return (6)
1) auxillary pumps - without skeletal muscle pump activity (standing still) get pooling of blood, no venous return, and fainting, (also have aortic and respiratory pumps)
2) TPR - increased TPR shifts curve down - decreases venous return, while keeping MSFP (x-intercept) the same
3) Mean systemic filling pressure - how full is circulation if your heart stopped working (around 7mmHg) - increasing MSFP increases venous return
4) compliance of veins - decreased compliance increases venous return
5) effect of gravity - hydrostatic pressure - around 90mmHg at foot, -25 at head, 0 at heart. so at feet, arterial gauge pressure is 170, venous is 100. in the head, arterial is 65, venous is -10 (which is why air gets in if you crack skull)
6) vascular permeability - as venous pressure increases, albumin is not as able to reabsorb fluid into capillaries (starling forces) - leading to edema
253
relationship between venous pressure/RA pressure and venous return
negative - less venous return with higher RA pressure
254
how do you get mean systemic filling pressure from vascular function curve (venous return/RA pressure)
it's the X intercept (around 7mmHg) - flow stops
255
what is flat portion at beginning of vascular function curve
at venous pressure less than 0, veins collapses, flow stops.
256
significance of interception of cardiac function curve and vascular curve
equilibrium point between both systems
257
how does this graph change when you increase the volume
the point shifts up because the vascular curve shifts up (cardiac curve stays put) - now new equilibrium point is at higher CO and venous pressure values
258
how does this graph change when you have a hemorrhage
your venous curve shifts down because you lose volume, but there are 2 compensatory actions:
1) you get venous constriction, so the venous curve will shift back up a bit, and
2) your cardiac curve will try to compensate with sympathetic stimulation (slope increases - increasing contractility)
259
which has worse prognosis, cardiac cause or non-cardiac cause of syncope
worse for cardiac
260
neurally mediated syncope causes (3)
- vasovagal
- carotid sinus
- situation (cough or post-micturation)
261
cardiac arrhythmia causes of syncope (3)
- brady (sick sinus, AV block)
- tachy (VT, SVT)
- long QT syndrome
262
top 3 causes of syncope
1. unknown cause
2. neurally mediated
3. cardiac arrhythmia
263
what does POTS stand for
postural orthostatic tachycardia syndrome (young people who can't stand up)
264
structural cardiac reasons for syncope (3)
- aortic stenosis
- HOCM (hypotrophic cardio myopathy)
- pulmonary hypertension
265
top 3 common causes of syncope for young people
- vasovagal
- situation
- psychiatric
266
top 4 common coauses of syncope for older patients
- orthostatic hypotension
- drug-induced
- neurally mediated
- multifactorial
267
how do patients feel with cardiac syncope
feel fine, on the ground, feel fine after
268
how do patients feel with neural syncope
feel bad for a few seconds or minutes, passed out for longer, feel bad for a while after
269
what to check on physical exam for syncope
1- orthostatic changes in BP and pulse
2- cardiac exam (look for CHF or valve disease)
3- neurological exam
4- carotid sinus massage
270
how to do a carotid sinus massage
just below thyroid cartilage, R and then L (pause between) - do for 5-10 seconds, don't occlude
positive outcome is 3 seconds of asystole or 50mmHg fall in systolic blood pressure -- carotid sinus syndrome
271
what are things on an EKG that could explain syncope (7)
- heart block
- v tach
- long QT
- short QT
- WPW (second electrical connection)
- bruagda (genetic - see ST elevation, right bundle branch block)
- Q waves (sign of MI)
272
what happens in tilt table test
upright posture is sympathetic stimulus - makes HR and BP go up and then we correct and things level out. sometimes this causes too much sympathetic curbing and you get significant drop in both HR and BP (in orthostatic you get dropped BP and increased HR)
273
san francisco syncope rule
```
C- CHF (history of)
H- Hct <30%
E- ECG abnormality
S- Shortness of breath
S- Systolic BP <90 mmHg
```
274
SEEDS
for intermediate risk patients to go to syncope clinic - screen for high or low risk
275
midodrine
alpha agonist - works to reduce vasovagal neurally mediated syncope
276
at what week of fetal development does the heart start beating
4 weeks (earliest system)
277
does the CV system come from endoderm, mesoderm or ectoderm?
mesoderm
278
what are angiogenic cell clusters
mesenchymal cells that arrange into epithelial vesicles - precursors of heart, BVs, and nucleated RBVs
279
changes in orientation of atria and ventricles in early fetal development
atria are caudal, ventricles are cephalic - as it grows, it loops, so that atrial end bends dorsally, up and left, and the ventricular end bends ventrally, down and right (but there's no septation between L and R atria, ventricles, or outflow tracks)
280
how do atria get divided
flap that allows for flow from R to L as long as pressure is higher in R than L, but at birth will close off because L atria pressure increases and R atria decreases because detached from placenta
281
what is ductus venosus
shunt through liver that hooks umbilical vein to inferior vena cava
282
septum primum and secundum
- septum primum is a curtain that starts at apex of atria and descends down heart -restricts interatrial orifice.
- the hole at bottom of this curtain is ostium primum.
- once it curtain fuses, a second hole appears above, called ostium secundum.
- septum secundum grows down over ostium secundum and fuses with endocardial cushions, leaving a hole called foramen ovale -- creating one-way valve from high pressure RA to LA
283
pathway of fetal blood from RA to LA
from RA, throuhgh foramen ovale, between septum P and S, through ostium secundum to LA
284
ventricular septation
thick muscular structure with 2 portions - muscular and membranous (part of cardiac skeleton - where you have defects)
downgrowth of membranous from valves, and muscular that grows up from apex and fuse
285
outflow spetation
spiraling septum separates pulm and aortic septum
286
what is the most common congenital heart defect
ventricular septal defects (1.4/1,000 births)
287
major disorders (genetic and environmental) that lead to congenital heart defects (5)
1. DiGeorge syndrome (22q11 deletion)
2. trisomy 21
3. turner syndrome
4. diabetic mother
5. congenital rubella
288
what CHD does digeorge's syndrome present with
(22q11 deletion) = truncus arteriosus, tetralogy of fallot
289
what CHD does trisomy 21 present with
ASD, VSD, Atriventricular septal defect
290
what CHD does turner syndrome present with
coarctation of aorta
291
what CHD does a diabetic mother present with
transposition of great vessels
292
what CHD does congenital rubella present with
PDA, pulmonary artery stenosis
293
what does CHD present with
either:
1- congestive heart failure
or:
2- cyanosis
sometimes:
3- pulmonary hypertension
294
reasons why CHD presents with congestive heart failure (4)
1- volume overload
2- pressure overload
3- cardiomyopathy
4- rhythm disturbances
295
ventricular septal defect prevalance
1/4 of all CHDs
296
how does a large VSD present
large VSD with pulmonary vascular resistance that's lower than systemic resistance, a large amount of overflow of L side of heart to right side to the lungs will occur - causing CHF. sometimes the pulmonary vascular resistance will get so high that it equals the systemic vascular resistance and you'll get some deoxygenated blood crossing over to the LV, causing cyanosis
297
treatment for ventricular septal defect
if defect is in muscular part and small-ish, it can close on itself
can place surgical patch through RA
percutaneous repair - meshwork of metal with thrombin - clots off, and closes hole
298
L to R shunt causes
increased pulmonary blood flow/ O2 content
299
R to L shunt causes
decreased systemic O2 content (hypoxemia)
300
bidirectional shunt
decreased systemic O2 content (hypoxemia)
301
Eisenmenger's syndrome
ireversible changes in pulmonary arterioles caused by pulmonary hypertension secondary to chornic volume overload from large L to R shunt (in beginning). eventually vascular damage causes increased pulmonary resistance which causes reversed shunt later on - R to L shunt
get hypoxemia, clubbing, cyanosis, polycythemia
302
cyanosis - types
blue discoloration of skin
2 types
- peripheral (slow, reynods)
- central (CHD, greater than 5g/dL unoxygenated Hgb in arterial blood) - if you put on oxygen and it improves, it's a pulmonary cause, not cardiac
303
in what conditions do you see decreased pulmonary blood flow (2)
- septal defects with severe pulmonary stenosis
| - tetralogy of fallot
304
in what conditions do you see increased pulmonary blood flow (4)
1. transposition of great arteries
2. mixing lesion w/o pulmonary stenosis- single ventricle
3. mixing lesion w/o pulmonary stenosis-- tricuspid atresia
4. mixing lesion w/o pulmonary stenosis- total anomalous pulmonary venous return
305
tetralogy of fallot mechanism
RV outflow to lung is stenonic (pulm valve stenosis) and malalignment of ventricular septum causes hypertropy of RV - R to L shunt - systemic circulation has deoxygenated blood
"tet spell" - RV outflow goes into spasm and causes crisis where not enough blood goes to lung to get oxygenated - increased R to L shunt, can cause seizure
306
treatment for tetralogy of fallot
little kids:
palliation - BT shunt between subclavian artery to pulmonary artery
older:
can patch close defect and cut out hypertrophic pulmonary stenosis
render pulmonary valve incompetent - has pulmonary valve regurgitation now - right heart failure
307
blood pressure equation
BP = CO x TPR
308
How to decrease TPR (2)
1- relax resistant vessels
| 2- decrease symp activity
309
how to decrease CO (4)
CO = HR x SV
SV is proportional to contractility and preload
you can change either of those things to lower BP
preload is proportional to venous tone and blood volume
you can change these things to alter BP
310
hydrochlorothiazide mechanism
inhibits Na-Cl co-transport in the distal convoluted tubule - gets excreted with water - works to decrease blood volume, preload, stroke volume, cardiac output and thus BP
311
long term effect of thiazide (positive)
reduce vascular resistance, thus reducing afterload
312
adverse effects of thiazide (3)
- sexual impotence
- increased loss of K (increased risk of arrhythmias and fibrillation)
- don't use with renal issues
313
amiloride
blocks Na+ channels in collecting duct, reducing potassium loss. given with hydroclorothiazide to minimize adverse effects of K loss
314
ACE mechanism
ACE (angiotensin converting enzyme)
ang1 is inactive, ACE converts ang1 to ang2 which is active hormome that acts on receptors (AT1) that causes vasoconstriction, aldosterone secretion and sodium retention
ACE also breaks own bradykinin
315
losartan
ARB (ang2 receptor blocker), decreases blood volume
316
captopril effects (5)
ACE inhibitor -
- decreases blood volume
- also inhibits breakdown of bradykinin causing dry cough
- regress LV hypertrophy
- can prevent/delay MI and heart failure
- slow progression of renal disease in diabetics
317
in what patients do you NOT give ACE inhibitors or ARBS
1) pregnant ladies
| 2) people with bilateral renal artery stenosis (may cause decrease in GFR and possibly renal failure)
318
adverse effect of ACE inhibitors
angioedema
319
how to decrease contractility (and drugs)
1) use beta blockers (propranolol)
| 2) use calcium channel antagonists (amlodipine, verapamil)
320
what are beta blockers used for? (7)
```
1- decrease contractility (cause dephosphorylation of calcium channels)
2- decrease HR (block symp)
3- reduce renin secretion
4- reduce levels of ang2
5- treat angina and arrhytmias
6- decrease mortality after MI
```
321
who don't beta blockers work well for
- elderly
- African American
- people with asthma
322
adverse effects of beta blockers
- erectile dysfunction
- depression
- insomnia
323
how do calcium channels work
less influx of calcium, weaker contraction, less contractiltiy
324
nifedipine vs verapamil effects on coronary vasodilation
nifedipine way way up, verpamil up
325
nifedipine vs verapamil effects on peripheral vasodilation
nifedipine way way up, verapamil up
326
nifedipine vs verapamil effects on HR
nifedipine increased reflex (because they have such a pronounced vasodilatory effect)
verapamil decreased HR
327
nifedipine vs verapamil effects on contractility
nifedipine increased reflex (because they have such a pronounced vasodilatory effect)
verapamil decreased contractility
328
nifedipine vs verapamil effects on rate of recovery of calcium channels
nifedipine has no effect on calcium channel recovery rate
verapamil decreases calcium channel recovery rate
329
nifedipine vs verapamil effects on AV conduction
nifedipine has no change on AV conduction
verapamil slows AV conduction
330
what is the risk of too much vasodilation
reflex HR and contractility increase and risk of MI - less risk for long acting dihydropyridine
331
who could take long acting calcium channel blockers
- angina
- arrhymtia
- elderly
- african american
- low renin
FYI, amlodipine is a long acting calcium channel blocker
332
how to decrease total peripheral resistance (and drugs)
1) relaxation of resistance vessels by direct vasodilators (hydralazine, minoxidil, sodum notroprusside)
2) decrease symp activity and vasocontriction (alpha-1 blockers like prazosin)
3) decrease symp activity and vasocontriction (adrenergic inhibitors - guanethidine, reserpine)
4) decrease symp activity and vasocontriction (alpha2-agonists, methyldopa, clonidine)
333
how do hydralazine and minoxidil work?
direct vasodilation of arterial vascular SM
334
what are the adverse effects of hydralazine and minoxidil? (4)
1) increased HR and contractility (b/c of baroreflex)
2) increased plasma renin (b/c of baroreflex)
3) fluid retention because (b/c of baroreflex)
4) cardiac ischemia due to incrased cardiac oxygen demand
335
how does prazosin work
alpha-1 blockers, blocking NE binding to BVs, blocking symp
336
adverse effects of prazosin
"first dose phenomenon" --drop in BP so much that they can faint (can't be used as monotherapy)
337
who should use prazosin
men with prostatic hyperplasia and bladder obstruction symptoms
338
how does guanethidine work?
gets transported in, replaces NE, depletes it, and blocks excitation-secretion coupling
(mostly post-ganglionic)
339
guanethidine adverse effects (3)
1) postural hypotension
2) sexual dysfunction (retrograde ejaculation)
3) diarrhea
340
how does reserpine work?
binds to NE storage vessicles, interferes with transmitter uptake and leaving empty vesicles
works more upstream (on pre-ganglionic) - central (thus CNS side effects) and peripheral
341
adverse effects of reserpine (3)
1) sedation
2) inability to concentrate
3) severe depression
342
what do methyldopa and clonidine do?
alpha 2 agonist that reduce activity of neurons in brainstem responsible for generating and maintaining symp activity
343
adverse effects of methyldopa and clonidine (5)
1) immunological abnormalities (just methyldopa)
2) dizziness
3) reduced libido
4) sedation
5) depression
344
what happens with sudden discontinuation of methyldopa and clonidine?
withdrawl syndrome with BP rising to levels above those present prior to treatment
345
who should use methyldopa
pregnant ladies
346
newer treatments for hypertension (4)
1- aldosterone blockers (spironolactone)
2- vasopressin antagonists
3- renal denervation
4- baroreceptor electrical stimulation devices
347
firstline drug choice for uncomplicated hypertension in someone with systolic hypertension
diuretics
348
firstline drug choice for someone with history of ischemic heart disease
beta blockers
349
firstline drug choice for type1/2 diabetes
ACE inhibitor
350
firstline drug choice for heart failure
ACE inhibitor
351
firstline drug choice for cardiac hypertrophy
ACE inhibitor
352
firstline drug choice for MI
beta blocker (or ACE inhibitor)
353
firstline drug choice for angina
beta blocker (or Ca antagonist)
354
firstline drug choice for fribrillation or arrhythmia
beta blocker (or Ca antagonist - not DHP)
355
what anti-hypertensives should be avoided in asthma
beta blockers
356
what anti-hypertensives should be avoided in depression
beta blockers, alpha2 agnoists
357
what anti-hypertensives should be avoided in pregnancy
ACE and ARB
358
what anti-hypertensives should be avoided in heart failure
Ca antagonists
359
what anti-hypertensives should be avoided in bilateral renal stenosis
ACE and ARB
360
What do you do for someone who is not getting BP reduction or is having side effect on current medication
switch to another drug in a different class
361
what do you do if a drug is well tolerated but is not working to decrease BP
add a second agent from another class (esp diuretic)
362
how many americans have high BP
1:2
363
3 big bad things that happen from uncontrolled hypertension
CVD
Stroke
Kidney disease
364
what does left ventricular hypertrophy evenutally cause
diastolic dysfuction and CHF
365
what does MI eventually cause
systolic dysfunction and CHF
366
pathophysiologic findings on kidney in hypertension leading to kidney disease (2)
1) hyaline atherosclerosis around arterioles
| 2) onion-skin pattern of hyperplastic ateriosclerosis
367
risk for stroke increaes dramatically after what BP
110/75
368
risk for CHD increases dramatically after what BP
130/80
369
what defines stage 1 hypertension
greater than 130/80 less than 140/90
370
what defines stage 2 hypertension
greater than 140/90
371
what defines elevated BP
greater than 120/80, less than 130/80
372
what intervensions do you give for stage 1
assess 10 year ASCVD risk
| if above 10%, start treatment, if below, advise on lifestyle changes and reassess in 3-6mo
373
what is first line for AA with hypertension but WITHOUT chronic kidney disease or heart failure
thiazide diuretic or calcium channel blocker
| even with diabetes
374
how do you assess for end organ damage for HTN in exam (6) and testing (3)
physical exam:
1. check BP in both arms to screen for aortic dissection or coarctation
2. examine jugular veins for JVD
3. auscultate for 3rd or 4th heart sounds or murmurs
4. listen to lungs to listen for pulmonary edema
5. look for swelling in extremities
6. neurologic exam for localizing signs (vision changes etc.)
testing:
1. serum chemistries to look for renal problems
2. CXR for pulm vasc congestion
3. EKG for MI
375
what happens if you bring people down too quickly from really high BPs
hypoperfusion of brain and watershed infarcts
376
what are the only cases where you would do this - bring down super quickly (more than 25% immediately) (3)
1. aortic dissection
2. severe preeclampsia or eclampsia
3. pheochromocytoma crisis
377
most common patients seen by vascular surgeons (3)
1. carotid artery disease
2. aortic aneurysms
3. lower extremity disease
378
what diameter is considered aortic aneurysm
3cm (50% larger than normal)
379
two types of aneurysms
1. fusiform (most common, univorm dilation)
| 2. saccular (focal dilation)
380
where does abdominal aortic aneurysm occur?
below the renal arteries above aortic bifurcation (right above umbilicus)
381
at what diameter do you start to think about intervention for abdominal aorta aneurysm
5-6cm (risk of rupture is from 3-15%) - risk exceeds risk of operation
382
stroke is the ___ leading cause of death in US
3rd
383
examples of symptomatic carotid artery disease
1. TIA (less than 24 hours, reversible)
2. amaurosis fugax (temp blindness - shade coming down)
3. stroke (neurologic deficit - brain injury)
384
example of asymptomatic carotid artery disease
1. bruit
385
what is lower extermity arterial disease mostly due to
atherosclerotic occlusive disease - blood flow does not meet the tissue demands of the lower extremities
386
symptoms of lower extremity arterial disease
75% are asymptomatic
| common symptom is claudication - cramping of calves with walking
387
physical exam for lower extremity arterial disease (7)
1. pulse exam
2. hair loss
3. poor nail growth
4. dry scaly thin skin
5. dependent rubor (red when down)
6. elevation pallor (white when up)
7. ulcers or gangrene
388
ankle-brachial index
measure ankle bp/arm bp (0.9 or higher is normal)
389
3 indications for intervention for lower extremity arterial disease
1. lifestyle limiting claudication
limb-threatening ischemia:
2. rest pain (dangle leg off of bed at night)
3. tissue loss (non-healing ulcer or gangrene)
390
lower extremity arterial disease therapeutic interventions
1. endovascular therapy (angioplasty and stent)
2. surgery (endarterectomy removal of plaque and patch, bypass procedure with great saphenous vein or prosthetic PTFE teflon or dacron graft)
391
what does the ST wave do in MI versus ischemia
ST segment up in MI, down in ischemia
392
T wave in inschemia
deep symmetric T wave inversions
393
what do you see with toursaddes de pointes, what could it be caused by?
elongated QT interval (more than 400ms) -sometimes caused by meds (amiodarone, quinolones, fluconazole, methadone, tamoxifen, grapefruit juice)
394
tachy vs brady
tachy more than 100 (less than 3 boxes), less than 60 is brady (more than 5 boxes)
395
what causes sinus bradycardia (6)
1. hypothyroidism
2. sinus node dysfunction
3. high vagal tone (athletes)
4. Bblockers, non DHP CC blockers
5. amiodarone, sotalol, propafenone
6. digoxin
396
what causes sinus tachycardia (8)
1. fever
2. anemia/blood loss/ orth hypo
3. drugs (NE, Epi, cocaine)
4. exercise
5. pain
6. anxiety/panic
7. hyperthyroidism
8. illness (PE, pneumonia, CHF)
397
what is P mitrale and what does it mean
broad p wave in "m" shape >120msec -- indicates enlarged LA (caused by mitral regurg, for example)
398
what is a delta wave and what does it signify
short PR interval and slurred slope - delta. signifies that there's an accessory pathway between A and V - WPW
399
How do you measure LV hypertrophy
S wave V1 + R wave V5 > OR = 35
400
what is the QT intervial = what to what
beginning of Q to end of T
401
what is too long for QT interval
400ms - tourssades de point
402
what causes low voltage on EKG (3)
1. Fluid (pericardial effusion)
2. air (emphysema)
3. fat (obesity)
403
what causes type 1 second degree heart block (3)
increased vagal tone that can affect AV conduction
- benign, when sleeping
- older
- too much B blocker or CC blocker
404
what causes type 2 second degree heart block (2)
more dangerous, associated with:
- acute MI (look for ST elevation)
- chagas disease (kissing bug)
405
what causes 3rd degree/complete heart block
AV conduction doesn't work - P waves are consistent (SA node ok) but not generating QRS consistently. can lose ventricular escape and can die
need pacemaker
406
what is the R to R interval like in a fib
variable
407
why are a fibs important to diagnose
cause strokes (give anticoag - warfarin, dabigatran etc.)
408
what does supra ventricular tachycardia (SVT) look like? what do you do?
fast, narrow complex tachycardia, no p wave (buried in QRS) - AV node re-entry, get QRS at about the same time
can block AV node (adenosine, push on carotids)
409
Who should get defibrillator implanted?
previous MI, low ejection fraction
410
two types of ventricular tachycardias
1. stable (BP is okay - give amiodorone)
| 2. unstable (BP is low - shock them)
411
what does v tach look like
1. wide QRS tachycaridia
| 2. AV dissociation (p at different rates than QRS)
412
who has v tach
people with dilated cardiomyopathy, past infarct (causing re-entry)
413
1A,B,V, 2, 3, 4 classes of antiarrhythima - what are they used for
1B - just VT
1C&A - mostly VT, some SVT
3 - both VT and SVT
4&2 - SVT
414
examples of class 1B (2)
lidocaine (post MI), mexiletine (long QT)
415
examples of class 1C (1)
flecainide (no ischemia, v fib)
416
examples of class 1A (2)
quinidine, procainamide (a fib)
417
examples of class 3 (2)
amiodarone (low 1st line a fib, high 1st line VT abnormal hearts), sotalol (use with defibs)
418
examples of class 4 (2)
verapamil, diltiazem (rate control, NOT in CHF)
419
examples of class 2 (1)
metoprolol (good post MI, symp arrhythmias)
420
what classes do you worry about for long QT
class 1A and class 3
421
what classes are used for rhythm control
1C, 1A, 3
422
what classes are used for rate control
4, 2, and other
423
examples of "other" class antiarrhythics (2)
digoxin
| adenosine
424
which classes block sodium channels
1A,B, and C
425
which classes are beta blockers
2
426
which class blocks calcium channels
4
427
which class blocks potassium channels
3
428
what are the properties of sodium channels that are voltage dependent
1. # of excitable channels (at -80 all are excitable, at -50 only some are)
2. time to recovery (at -80, recovery is shorter than at -50)
429
effective refractory period
when you cannot activate the channel - time from un-activatable to activatable
430
group 1A drugs that directly increase BP and directly increase contractility (4)
1) dobutatime
2) high dose dopa
3) high dose NE
4) high does Epi
431
group 1B drugs that directly increase BP but do NOT directly affect contractility (4)
1) phenylephrine
2) vasopressin (ADH)
3) angiotensin 1
4) angiotensin 2
432
group 2A drugs that directly decrease BP and directly increase HR (3)
1) low dose dopa
2) isoproterenol
3) theophylline
433
group 2B drugs that directly decrease BP but do NOT directly increase HR (8)
1) Ach
2) charbachol
3) clonidine
4) verapamil
5) nitroglycerin
6) terbutaline
7) histamine
8) bradykinin
434
drugs that cause bronchodilation (5)
1) terbutaline
2) theophylline
3) dopa
4) epi
5) isoproteranol
435
what do you use to block the reflex caused by NE
ATROPINE
436
interaction between physostigmine and Ach
potentiation
437
interaction between atropine and Ach
competitive inhibition
438
what does altering the fast sodium channel control
1) conduction velocity
| 2) effective refractory period
439
what does altering the calcium channel control
1) AP duration
| 2) indirectly ERP
440
what does altering the TEA type K channel control
1) AP duration
| 2) indirectly ERP
441
what ion is phase 0 determined by in SA node and myocardium
SA - calcium
| myocardium - sodium
442
main causes of tachycardias (3)
1) reentry circuits
2) ectopic pacemakers
3) early after depolarizations (fib)
443
is hypoxic tissue more or less depolarized
less depolarized - more positive
444
do hypoxic tissues have a longer or shorter refractory periods
longer (more sodium channels are un-activatable)
445
what do you do for rate control in A fib
anesthetize AV node - 10:1 block "screw the p wave"
| - also consider anticoag
446
what do you do for rhythm control
restore normal sinus rhythm - pharmacological cardioversion - gets rid of a fib
447
drugs for rate control (3)
1) metoprolol
2) verapamil
3) digoxin
448
drugs for rhythm control (2)
1) amiodarone
| 2) flecainide
449
during what "states" of the sodium channel do class 1 drugs bind and what do they do (2)
1) open (makes them less-ecitable, slows phase 0, slows conduction velocity)
2) un-activatable (increases refractory period, takes longer to repolarize)
450
How do class 1 drugs affect rhythm control
effect reentry:
| makes effective refractory period longer than conduction time
451
class 1a (effect on Na+ and K+ channels)
- medium reduction in slope (medium Na+ block)
| - prolonged AP (partially block K+) - long QT
452
class 1B (effect on Na+ and K+ channels)
- mild Na+ block, little reduction in slope
| - shortened AP (paritally activating K+) - short QT
453
class 1C (effect on Na+ and K+ channels)
- marked Na+ block, big reduction in slope (longest effective refractory period)
- no change in repolarization - no interaction with K+
454
what do you use class 1B for
- only for VT
| - best post MI
455
Which is more selective or sick cells, Ib or 1C
1B
456
adverse effects for 1A (3)
- torsades de pointes long QT
- V tach (use calcium channel to slow AV node)
- can cause asystole in incomplete heart block
457
what channels do class 3 block
- blocks potassium efflux during phase 3 (increase AP)
| - blocks Na+ channels (increase ERP)
458
amiodarone adverse effects
1) torsades de pointes
2) pulmonary fibrosis
3) blue man syndrome
459
can you use rate control drugs in WPW?
no! because you have accessory pathway and can cause arrhymthmia
460
major effect of class 4 drugs
- blocking Ca2+ channels in AV node (slow down responsiveness)
461
class 2 drug effects
block symp, decrease AV node conduction and decrease excitability
462
when do you use adenosine
in supraventricular tachycardia that you think is from the AV node (would see narrow QRS), used acutely
463
what drug types cause long QT
1A and 3
464
familial hypercholesterolemia findings
- tendon xanthoma
- defect in LDL receptor
- coronary artery disease
465
what are the polar (2) and non-polar (2) parts to lipoprotein structure
polar:
1- phospholipid
2- free cholesterol
non-polar
1- triglyceride
2- cholesterol ester
466
Friedewald Forumla
(LDL-C) = TC - (HDL-C) - (VLDL-C)
VLDL-C --> TG/5
467
sources of error in friedwald formula (30
1. super high TGs >400
2. non-fasting
3. errors in each individual measuremnt
468
C Reactive Protein
as it increases, it raises risk for cardiac event - used in Reynolds Risk Score
469
coronary calcium score
on cat scan can see calcium. high levels of calcium in coronary arteries predict levels of coronary events - MESA risk score
470
if someone has clinical ASCVD and over 75 vs under 75 management
under 75 - high intensity statin
| over 75- moderate-intensity statin
471
if someone does NOT have clinical ASCVD but has baseline LDL-C >190 management
high intensity statin
472
if someone does NOT have clinical ASCVD but has DM
moderate intensity statin
473
if 10-year ASCVD risk is over 7.5 and age is under 75
moderate intesnsity statin
474
PCSK9 monoclonal antibodies (2)
1) alirocumab
| 2) evolocumab
475
endothelial cell injury theory
the endothelial cell lining undergoes some kind of insult (hypertension, toxins, lipidemia) then infusion in lipids and cells through endothelium accumulation of macrophages, that become foam cells, cytokines trigger inflammation - cytokine cascade increase acute phase reactants (CRP levels reflect atherosclerosis)
476
where do lesions occur (atherosclerotic plaques)
aorta near branch points
lower extremities
in circle of willis
coronary arteries
477
histologic changes of atheroslerosis
thicking of intima, accumulation of lipids under thickened intima, fibroblasts and macrophages between the two layers, fibrous cap on most intimal layer
tunica media then becomes thinned and weakened
478
aortic dissection causes and pathogensis
hypertension, marfans, pregnancy
rip through iintima that dissects along outer 2/3 of media
more in males
presrents with chest/back pain
479
aortic dissection classifications (debakey)
```
type1 = ascending and descending = poor
type2 = just ascending = poor
type3 = desencding only = better
```
480
mycotic aneurysm - syphillis - findings
associated with infection (syphillitic in aortic arch = leutic aortitis)
vaso vasorum (that are BVs to the heart itself) have predelection for syphillis - cause infarction of aortic wall - proximal ascending aorta - see grainly inflammaed appearance, see spirochetes on stain
481
vascular pathology of hypertension that affects small arteries (2)
1) hyaline arteriolosclerosis
| 2) hyperplastic ateriolosclerosis
482
monckeberg medial calcific sclerosis
medium sized muscular arteries
over 50 years old
no narrowing of lumen
483
hyalien aterioloslerosis
pink, smooth, deep proteinaceous infiltration
associated with prolonged hypertension
narrowing of lumen
seen in kidneys often
484
hyperplastic arteriolosclerosis findings
concentric laminated thickening of intima
cellular proliferation making onion skin appearance (consists of SM, BM)
can be associated with characteristic fibrinoid necrosis
associated with malgnant hypertension
485
malignant hypertension
rapid, severe hypertension (200/120)
| patients have headache, renal railure, retinal exudates, organ failure
486
characteristics of hypertensive heart disease (5)
- heart is larger than 500g
- see concentric hypertrophy
- LV wall is greater than 2cm
- reduction of luman size
- microscopically see large mycocytes, large nuclei (box car) and fibrosis
487
characteristics of hypertensive changes in the brain (3)
- lacunar infarcts
- slit hemorrhage (rupture of small vessles with hemorrhage, browinish slit cavity)
- intercerbral hemorrhage (common cause of death in people with chronic hypertension)
488
characteristics of hypertensive change sin kidneys (2)
- benign nephrosclerosis (hyaline arteriolosclerosis (grainy surphace), glomerulosclerosis, tubular atrophy, iinterstitial fibrosis)
- chronic renal failure
489
exercise ECG testing use (5)
- measure exercise capacity and duration
- BP respose
- HR response
- provoked ysmptoms (dizziness, chest pain)
- see changes in EKG that might suggest CAD
490
echocardiography use (5)
ultra sound
- look at valves and chambers
- 1st line test for LV structure and function - ejection fraction assessment
- pericardial effusion
- masses
- aortic diseases
491
normal ejection fraction and how is it calculated
>55%
= (LVEDV - LVESV) / LVEDV
= amount pumped out of ventricle/total amount in ventricle
492
nuclear cardiology indications (3)
- diagnosis and assessment of CAD
- evaluation of ventricular function
- myocardial viability imaging (recoverability of heart)
493
cardiac CT indications (3)
- non-invasive anatomic assessment of CAD
- risk stratification (coronary calcium scoring)
- eval acute chest pain quickly
494
cardiac MRI indications (4)
- tissue charactization (muscle, fat, blood etc)
- whole heart imaging
- cardiomyopathies
- congenital heart diseases
not so great in obese, coaustrophobic, costly, need long breath hold
495
cardiac cath indications (1)
- CAD
- into fem or radial artery into ascending aorta into main coronary artery
risks of death and stroke
496
SA and AV are typically supplied by
RCA
497
when do coronary arteries fill
diastole
498
what supplies posterior papillary muscle
RCA
499
what supplies anterior and anteroseptal heart region
LAD
500
what supplies anteriolateral and lateral heart region
L circumflex
501
what supplies inferior and posterior heart region
RCA
502
what is the first line test for evaluating CAD
EKG stress test
503
what is sensitivity and specificity for exercise treatmill test
60 and 70
504
what is sensitivity and specificity for stress echo
80 and 84
505
what is sensitivity and specificity for nuclear SPECT MPI
90 and 75
506
what is sensitivity and specificity for coronary CTA
95-99 and 83
507
are primary tumors of the heart rare or common
rare
| secondary tumors are 40x more common
508
are primary tumors of the heart malignant or benign
```
mostly benign (58%) usually myxoma
malignant (42%) usually sarcoma
```
509
myxoma treatment
resection
510
carney complex
familial variety (10%) of myxomas
511
where do you find myxomas
most commonly LA, usually arising from interatrial septum, may have peduncle - obstruction in valves
the familial version can be found in multiple locations, ventricular, and recur after resection
512
where do you find cardiac sarcomas
R side of the heart more likely, pericardial space as well
513
where do you usually find metastatic cardiac tumors
pericardium
514
does aortic stenosis cause volume or pressure overload
pressure overload
515
at what area do you start to see symptoms with aortic stenosis
below 0.5-0.8 cm2
516
clinical manifestations of aortic stenosis (3)
angina
CHF
syncope during exercize
517
what do you hear on PE for aortic stenosis
crescendo decrescendo murmur during systole (radiates into neck)
518
treatment for aortic stenosis
valve replaement
519
benefit of mechanical valve
longevity
520
downside of mechanical valve
have to take anticoag
521
transcath aortic valve replacement
take balloon with stent with tissue valve sewn into it (bovine pericardium)
522
is mitral stenosis pressure or volume overload
pressure (increased LA pressure)
523
when do people become symptomatic with mitral stenosis (at what area)
less than 2 cm2
524
4 cuases of mitral regurg
1- mitral valve leaflet disorder (marfans, rheum)
2- annulus disorder
3- chordae disorder
4- papillary muscle
525
what do ou hear on PE for mitral regurg
parasystolic murmur
526
what do you hear on PE for mitral valve prolpase
midsystolic clinck and late systolic murmur
527
is regurg pressure or volume overload
volume (both mitral and aortic)
528
what is classic BP for someone with aortic regurg
120/40 - large pulse pressure
529
alpha1 adrenergic receptor (location and net effect)
vasculature (also some alpha2) = vasoconstriction (Gq)
530
alpha2 adrendergic receptor (location and net effect)
CNS = synaptic transmission
531
beta1
heart = increase HR, contractility, conduction (Gs)
532
beta 2 location and net effect
skeletal muscle = vasodilation
| bronchial SM = bronchodilation
533
beta 1
juxtaglomerular apparatus = renin release
534
leading cause of acute bacterial endocarditis and cause of death
staph aureus
535
is the underlying valve normal or abnormal is subacute and acute bacterial endocarditis
normal in acute, abnormal in subacute (need turbulent flow - high to low pressure sinks)
536
venturi principle
vegetation occurs distal/in the direction of the turbulent flow
537
what are 3 examples of bacteria that are adherent
enterococcus
strep viridans
staph aureus
538
why is treatment difficult for bacterial endocarditis
because they divide so slowly
539
what are the etiologic agents responsible for subacute bacterial endocarditis (4)
strep viridans
group D step (enteroocci, strep bovis)
coag negative staph
540
where do IV drug users get vegetations
tricuspid valve
541
classic triad for clinical presentation of infective endocarditis
1. fever (maybe not in elderly or uremic patients)
2. anemia (maybe not in acute endocarditis)
3. heart murmur (actually a changing/new regurg murmur, not always present)
542
are systolic flow murmurs holosystolic or "diamond shaped"
diamond shaped - crescendo decrescendo
543
are mitral regurg murmurs holosystolic or "diamond shaped"
holosystolic - same throughout
544
peripheral manifestations of endocarditis 5)
1. conjunctival petecchiae
2. splinter hemorrhages
3. osler;s nodes
4. janeway lesions
5. roth spots
545
if you have a patient with endocarditis with PR interval heart block, what is that a clue to
myocardial abcess in septum, needs surgery
546
do you anticoag a patient with endocarditis?
no, could have a mycotic aneurysm that could burst in brain and cause death
547
what should you do for a patient with endocarditis and heart failure
surgery immediatley. don't try to give diuretic and wait and see. go to the OR
548
how much is 1 MET
3.5 ml/min/kg - resting
549
how many mets can you get to with minimal exercise
20 METS
550
What is respiratory quotient equation
CO2 production/ O2 consumption - during anaerobic metabolism, RQ is greater than 1
551
O2 pulse equation
O2 consuption/ HR
approximation of stroke volume
552
breathing reserve equations
max voluntary ventilation (MVV) = 35 x FEV1
breathing reserve = MVV - max exercise ventilation
553
heart rate reserve equations
Predicted HR = 220 - age
HR reserve = (predicted HR - actual HR) x highest exercise HR
554
what hapens in acute coronary syndrome
vasospasms episodically reduces coronary blood flow, AKA variant angina
555
unstable angina is caused by what
rupture of atherosclerotic a plaque - must be treated to prevent MI
556
what are treatments for variant angina
calcium channel blockers - reduce likelihood of vasospasm
557
coronary blood flow equation
(diastolic pressure in aorta - LV pressure during diastole) / coronary vascular resistance
558
nitroglycerin mechanism of action
converts to NO, increases guanylate cyclase, increases cGMP, dephosphorylates MLC kinase, DECREASING contractile state of SM particularly in venules (less so in arterioles) decreasing pressure in preload, increasing coronary blood flow and decreasing tension (decreasing ischemia)
nitroglycerine ALSO dilates the large epicardial arteries increasing coronary blood flow reducing coronary steal, shunting to where you need it
559
what is coronary steal
shunting to places where you don't need it - ubiquitous vasodilation
560
do calcium channel blockers work on arterioles or venules
more so on arterioles
561
in what patient population with angina would you ot to use beta blocker
someone with hypertension or prievious MI
562
when would you want to give someone ranexa for angina
if they have not responded to the other anti-anginal drugs (nitrates, CC blockers or BBs)
563
why would you give nitrate with beta blocker
same reason you give diuretic for antihypertension. you want to reduce preload as well
564
what does Kawasaki disease do to the heart
autoimmune inflammatory disease that involves coronary arteries - aneurysms and ischemic changes in heart
565
which part of the heart dies with occlusion of LAD
anterior 2/3 of septum and anterior left ventricle
566
which part of the heart dies with RCA occlusion
posterior 1/3 of septum, posterior left ventricle
567
which part of the heart dies with LCircumflex occlusion
lateral left ventricle
568
microscopic changes from 4-12 hours
some wavy fibers,
some gross mottling
569
microscopic changes from 12-24 hours
coagulation necrosis, acute inflammatory cells, neutrophils, edema, heomorrhage,
grossly see pallor and mottling
570
microscopic changes from 24-72 hours
coag necrosis, DENSE neutrophil infiltrate, loss of nuclei and cross striations
grossly see pallor
571
microscopic changes from 3-7 days
macrophages replace neutrophils, granuation tissue forms from periphery - at greatest risk for rupture
grossly see pallor
572
changes from 7-10 days
yellow in center grossly
| more macrophage and granulation tissue at edges
573
changes from 10-21 days
gray collor grossly
| fibrosis increasing
574
6wk to 1 year changes
scar reaches full tensile strength at 1 year, fibrosis
575
reperfusion injury
tissue damage breaks down BVs, even though you release obstruction of BV you might have leakage and extend area of infarction and lead to fatality (rare fatality)
see contraction bands - shocked sudden re-oxygenation causes contraction of myocardium
576
what are 2 EKG findings in unstable angina
1) T-wave inversion
| 2) ST segment depression
577
common cause of myocarditis
coxsackie A and B (enterovirus)
578
common cause of pericarditis
rheumatic fever, uremia
| or extension from myocarditis
579
defifnition of cardiomypoathy
non-inflammatory disorder of the myocardium - can be dilated (aka congestive), hypertrophic or restricrtive
580
causes of dilated cardiomyopathies (4)
1. genetic (pheochromocytoma, dystrophin etc.)
2. infectious (sequelae from viral myocarditis)
3. post partum
4. toxins (diabetes, hemochromatosis, alcohol, amiodarone)
581
causes of hypertrophic cadiomyopathy (1)
1. sarcomere protein mutations (B- myosin heavy chain, myosin binding protein C, Troponin T)
582
is hypertrophic cardiomyopathy aymmetric or symmetric?
asymmetric (with or without obstruction)
583
who gets hypertrophic cardiomyopathy
young adults - sudden death in kid playing basketball
584
restrictive vardiomyopathy causes
1. amyloidosis
2. sarcoidosis
3. endomyocardial fibrosis
585
bugs and worms that cause infectious myocarditis (4 categories)
VIRAL
1. cocksacie B enterovirus
2. adenovirus
3. parvovirus B19
4. influenza
5. herpes
6. HIV
BACTERIAL
1. diptheria
2. lyme
PROTOZOA
1. trypanosoma vruzii - chagas
HELMINTH
2. trichinella spiralis (nematode)
586
who gest myocarditis
```
bimodal - young children and teenagers (get acute presentation)
older adults (insidious symptoms of dilated cardiomyopathy and heart fiailure)
```
587
causes of infectious pericarditis (2)
viral: coxsackie
bacterial: TB, staph, h. flu, legionella
588
what are the 4 mechanisms that can lead to heart failure
1. increased blood volume (increased preload)
2. increased resistance to blood flow (increased afterload)
3. decreased contractility
4. decreased filling
589
3 scenarios with increased afterlad
1. CHF
2. HTN
3. aortic stnosis
590
4 scnearios with decreased afterload
1. mitral regurg
2. VSD
3. A-V fistula
4. septic shock
591
what does aldosterone secretion do
1. increases salt and water retention
| 2. myocardial fibrosis
592
neprilysin
does the same thing as angiotensin 2
| blocks natriuretic peptides which are helpful, so you want to inhibit it
593
administration of BNP to patient with heart failure causes
1. natriuresis
2. reduced filing pressures
BNP causes decreased systemic vascular resistance and sodium excretion
594
symptoms with isolated right-sided congetsion (2)
GI discomfort and edema
595
symptoms with left-sided congestion (3)
orthopnea, immediate dyspnea, fatigue
596
what is wedge presssure
back pressure from pulmonary artery wedge, no more forward flow,
should be equal to left atrial pressure (equal to LV diastolic pressure)
597
wet and warm =
dry and cool =
wet and cool =
wet and warm = congestion (over hydrtation)
dry and cool = hypoperfusion (dehydration)
wet and cool = hypoperfuson AND congestion
598
ivabradine mechanism of action
works on funny current i(f) in slow repolarization. no effect on contractility. reduces SA node rate
use for stable, symptomatic CHF with EF less than 35% and tachycardic
quality of life, not curative
599
when do you see narrow pulse pressure
aortic stenosis, severe CHF
600
when do you see wide pulse pressure
aortic insufficiency
601
when do you hear S3 pathologically
floppy dilated heart
602
when do you hear S4
hypertrophy stiff heart
603
when do you hear opening snap
rheumatic mitral stenosis
604
when do you hear ejection click
bicupsid aortic valve
605
when do you hear midsystolic click
mitral valve prolapse
606
when do you hear flow murmur (4)
- normal
- anemia
- AV fistula
- aortic or pulmonic (semilunar) valve stenosis
"diamond shaped"
607
when do you hear holosystolic murmur (2)
- AV valve(mitral.tricuspid) insufficiency
| - VSD
608
when do yo have diastolic murmurs (2)
- semilunar valve insufficiency (aortic or pulmonic)
- AV valve (mitral or tricuspid) valve stenosis
(low pitched murmur)
609
when do you have continuous murmurs
- abnormal connection artery and vein (AV fistula)
| - abnormal connection aorta with R heart (PDA)
610
high reisk statin therapy
atorvastatin 40-80
| rosuvastatin 20-40
611
moderate risk statin therapy
atorvastatin 10-20
rosuvastatin 5-10
simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin (all above 30/40mg)
612
low risk statin therapy
simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin (all below 30/40mg)
613
long erm complications of heart transplants
```
acute cellular and Ab mediated rejection
osteoporosis
hypertension
DM
neuropathy
```
614
mean pulm artery pressre equation
= diastolic pressure + 1/3 (sys - dias)
615
pulm vasc resisyance equation
(mpap-pcwp)/ co
616
dias pulm gradient
iff btw padp and pcwp
617
definition of pulm hyepertension
mean pulm artery pressure greater than 25mmHg
618
pre cap vs. post cap PH
pre Cap has less than 15 wedge pressure, post has more than 15
pre AND post wedge pressure more than 15, DPG more than 7
619
groups for PH classification
1. pulmonary arterial hypertension (plexiform lesions)
2. PH due to left heart disease (most common)
3. PH due to lung diseases or hypoxia
4. chronic thrombo-embolic pulmonary hypertension (only one with cure, do VQ scan)
5. PH with unclear/multifactorial mechanisms
