IM Cardio Flashcards
1
Q
Features of the Chest pain that will not help determine a dx
A
associate with multiple dx and are therefore nonspecific
nausea
fever
sob
sweating
anxiety
2
Q
what is the worst prognostic significance that goes along with chest pain
A
sob, if a fever is also present think pe or pneumonia
3
Q
EKG
A
the best initial test for all forms of pain
in the officebased ambulatory setting you can expect the ekg to be normal most of the time but you cannot go on to other forms of testing until the ekg is performed
4
Q
Enzymes (ck-mb-troponin)
A
these are not the answer in the office or ambulatory setting if you are being asked to evaluate chronic or stable chest pain, best answer in clinic would be to transfer pt to ed if they have acute chest pain
5
Q
office (ambulatory clinic) chest pain for days to weeks
A
no enzymes
6
Q
ed chest pain for minutes to hours
A
ekg then enzymes
7
Q
Stress (exercise tolerance) testing
A
indispensible tool to evaluate chest pain when the etiology is not clear and the ekg is not diagnostic
ett is based on 2 factors:
you can read the ekg
the pts can exercise (get hr up to 85% of max)
8
Q
maximum hr =
A
220 minus the age of the pt
9
Q
stress testing is the answer when the etiology of the pain is..
A
uncertain and the ekg is not diagnostic
10
Q
ischemia is detected by what on the ekg
A
st segment depression
11
Q
what if you cannot read the ekg
A
if you cannot read the ekg bc of a baseline abnormality then the 2 best methods for detecting ischemia are:
nuclear isotope uptake thallium or sestamibi
echo detection of wall motion abnormalities
12
Q
reasons for baseline ekg abnormalities are:
A
left bundle branch block
lvh
pacemaker
digoxin
13
Q
thallium or sestamibi uptake
A
abnormalities are seen when the isotopes are not picked up
14
Q
abnormalities on echo
A
decreased wall movement called
dyskinesis
akinesis
hypokinesis
15
Q
ischemia vs infarction
A
ischemia or decreased perfusion will be detected by seeing a reversal of the decrease in thallium uptake or wall motion what will return to normal after a period of rest
infarction is irreversible or fixed that way
16
Q
dipyridamole may provoke?
A
bronchospasm avoid in asthmatics
17
Q
what if the pt cannot exercise
A
alternate methods of increasing myocardial oxygen consumption:
persantine (dipyridamole) or adenosine in combination with the use of nuclear isotopes such as thallium or sestamibi
dobutamine in combination with the use of echo: dobutamine will increase myocardial oxygen consumption and provoke ischemia detected as wall motion abnormalities on an echocardiogram
18
Q
exercise tolerance testing
A
determpines persence of ischemia
set segment depression if ischemia is present
19
Q
exercise thallium
A
inabelitiy to read the ekg or baseline st segment abnormalities
decreased uptake of nuclear isotope if ischemia is present
20
Q
exercise echo
A
inabelitiy to read the ekg or baseline st segment abnormalities
wall motion abnormalities if ischemia is present
21
Q
dipyridamole thallium
A
inability to exercise to target heart rate
decreased uptake of nuclear isotope if ischemia is present
22
Q
dobutamine echo
A
inability to exercise to target heart rate
wall motion abnormalities if ischemia is present
23
Q
whas is the right thing to do in a pt with reversable ischemia?
A
coronary angiography
isotope uptake will be normal at rest and decrease with exercise
24
Q
reversible perfusion defects need?
A
catheterization, catheterization indicates which pts get bypass vs angioplasty vs medication alone
25
the 2 diff methods of detecting ischemia in terms of using nuclear isotopes or echo are essentially equal in terms of sensitivity and specificity
exercise thallium=exercise echo
dipyridamole thallium=dobutamine echo
26
coronary angiogrpahy
used to detect the anatomic location of coronary artery disease
a test to detect the presence of narrowing that is best managed with surgery, angioplasty or other methods
sometimes is it used if noninvasive tests like ekg or stree testing ore queivoal
most accurate method of detecting cad
27
angiography determines
bypass surgery vs angioplasty
28
stenosis less than 50% is
insignificant
surgically correctable disease begins with at least 70% stenosis
29
with 1 or 2 vessel disease on agniography
stent placement
30
with 3 vessel disease, left main or 2 vessel disease in diabetics
CABG
31
holter monitoring is used mainly for
rhythym evaluation
32
holter monitoring
continuous ambulatory ekg monitor that records the rhythym
useually 24 but can be used up to 72 hours
detects rhythym disorders like a fib, flutter, ectopy like premature beates, or v tach
it does not detect ischemia and is not accurate for evaluating the st segment
33
echocardiography is to evaluate
valve function
wall motion
and ef
34
dont put pts on a treadmill if
they are currently having chest pain
35
overview of treatment of chest pain
know what medications will lower mortality, dont need dose but know route of administration
36
nitro is used orally or by patch with
chronic angina
37
nitro is used as sl paste or iv with
acute angina
38
nonsepficie bta blockers such as propranolol are not used routinely in
cardiology
39
antiplatelet therapy
all pts with acute coronary syndromes (acs) should receive 2 antiplately meds immediatly upone arrival in the ed
the meds should be a combo of aspirin and either clopidogrel prasugrel or ticagrelor
all 3 inhibit the p2y12 receptor on the platelet
the use of 2 meds is for cute presentation and for coronary stenting not chronic or stable cad
40
antiplatelet therapy when angioplasty and stenting is planned
use ticagrelor or prasugrel, these best prevent restenosis of stenting
41
clopidogrel is used in
combo with aspirin on all acs
aspirin intolerance or allergy
recent angioplasty with stenting
is it rarely associated with ttp
42
best mortality benefit in chronic angina
aspirin and beta blockers
43
prasugrel
a thienopyridine medication in same class as clopidogrel
indicated as antiplatelet med that has its best evidence for use in those undergoing angioplasty and stenting
dangerous in pts 75 and older bc of hemorrhage and stroke
44
ticlopidine
used to inhibit platelets in the rare pt who is intolerant of both aspirin and clopidogrel
you cannot use if the reason for aspirin and clopidogrel intolerance is bleeding since it will inhibit platelets as well
causes neutropenia and ttp
45
ranolazine
additional therapy for angina fefractory or persistent through other treatment
46
ace inhibitors and arbs
low ejection fraction/systolic dysfunction (best mortality benefit)
regurgitant valvular disease
cough is the most common adverse effect of acei in up to 7% of pts
if causing hyperkalemia then switch to hydralazine and nitrates
47
hydralazine
direct acting arterial vasodilator
decreases afterload and has been shown to have a clear mortality benefit in pts with systolic dysfunction
should be used with nitrates to dilate the coronary arteries so that blood is not stolen away from coronary perfusion when afterolad is decreased with hydralazine
48
statins tip
cad with any ldl
the goal is at least an ldl
49
guidelines for using statins
when the ldl is above 100
cad with any ldl level
goal of ldl below 70 for those with cad and diabetes
everyone will agree that the goal for ldl with cad is below 100
50
cad equivalents for statin use
try to get ldl below 100
pad
carotid disease (not stroke)
aortic disease (artery not the valve)
stroke
dm
51
what is clear with lipid management
no cutoff point at which to start statins in those with cad stroke or pad, but they should all be on a statin
should not really be asked this on a test bc it is unclera the goal for ldl levels either below 70 or 100
is is clear that only statins are asociated with a definite mortality benefit in the managment of hyperlipidemia in any circumstance
52
most common adverse effects of statins
liver dysfunction will occure in 1% and they will get elevated transaminases
myositis elevation of cpk or rhabdomyolysis occurs in .1% of pts
dont routinely check for cpk unless symptoms are present
test ast and alt routinely even w/o symptoms
53
other lipid lowering therapies
niacin, gemfibrozil, cholestyramine and ezetimibe all have beneficial effects on lipid profiles but none are initial therapy bc they have a mortality benefit on cad
nicain and givric acid derivatives like gemfibrozil have some mortality benefit but not as much as the statins
statins ahve an antioxidant effect on the endothelial lining of the coronary arteries that gives a benefit that transcends simply lowering the ldl number
only use when cant get ldl down with statin or they are intolerant to statins with liver failure myositis or allergic
54
niacin
associate with glucose intolerance, elevation of uric acid level, and itchiness from atransient release of histamine
excellent drug to add to statins if full lipid contorl is not achieved with statins
although statins exercise and cessation of tobacco will all raise the hdl level nicain will raise hdl more
55
gemfibrozil
fibric acid derivatives lower triglyceride levels somewhat more than statins, but lower tris alone has not proven to be as sueful as the straightforward mortality benefit of statins
use caution when adding fibrates to statins bc of an increased risk of myositis
56
cholestyramine
bile acid sequestrant has significant interactions with other meds in the gut and may block their absorption
can cause constipation and flatus
57
ezetimibe
lowers ldl without any evidence of actual benefit to teh pt
ldl elvels are an imperfect marker of benefit with cholesterol lowering therapies
no better than a placebo with mi stroke or death
58
what is clear with lipid lowering therapy
statins lower mortality the most
adverse effects of other agents are well established
59
statin ae
elevation of transaminases (lfts)
myositis
60
niacin ae
elevation in glucose and uric acid level
pruritus
61
fibric acid derivatives ae
increased risk of myositis when combined with statins
62
cholestyramine ae
flatus and abdominal cramping
63
ezetimibe ae
well tolerated and nearly useless
64
check ast and alt when using
statins
65
dihydropyridine ccbs may increase mortality in pt with
cad bc of their effect in raising heart tartes
reflex tachycardia
66
none of the ccb have been shown to lower mortality in
cad
67
although ccbs are negative inotropes
they acutally increase myocardial o2 consumption because of reflex tachycardia
68
bottom line is do not routinely use ccbs in
cad
69
ccbs verapamil and dilitazem are used in pts who cannot tolerate b blockers bc of
severe asthma
70% of people with reactive airway disease can toerate beta1 specific blockers
70
use ccbs (verapamil and diltiazem) in CAD only with:
severe asthma precluding the use of beta blockers
prinzmetal variant angina
cocaine induced chest pain (bblockers are ci)
inability to control pain with maximum medical therapy
71
adverse effects of ccbs
edema
constipation (verapamil most often)
heat blocke (rare)
72
revascularization
angiography is indipsensible in evaluating a pt for the possibility of revasuclarizations which is either coronary bypass surgery or angioplasty
symptoms alone cannot tell the number of vessels involved what vessels or the degree of stenosis
73
cabg
lowers mortality only in a few specific circumstances with very severe disease such as:
3 vessels with at least 70% stenosis in each vessel
left main coronary artery occlusion
two vessel disease in a pt with dm
persistent symptoms despite maximal medical therapy
74
cabg long term mortality
benefit is greater with the most severe disease such as those with left v dysfunction. the immediate operative moratlity may be greater in pts with an ef below 35% but in the long term those surviving hte procedure will do better in those with 3 vessel and left v dysfunction
75
cabg internal mammary artery grafts
last on avg 10 years before they occlude
76
cabg saphenous vein grafts
remain patent reliably for only 5 years
77
PCI
is commonly referred to as angioplasty
intervention is more precise bc there are other interventions besides angioplasty
it is the best therapy in acs esp in those with st segment elevation
78
the mortality benefit of pci is hard to demonstrate in
chronic stable angina
79
maximal medical therapy with aspirin b blockers acei/arbs and statins has been proven to have equal or evern superior benefit compared to pci in
stable cad
pci is more definitive in terms of decreaseing dependence on meds and decreaseing frequency of painful angina episodes
80
ACS
definition
it is impossible to determine the precise etiology of acs from history and physical exam alone
81
ACS
risk factors
same as cad
htn dm tobacco
82
why are acs associate with an s4
bc of ischemia leading to noncompliance in the lv
s4 gallop is the sound of atrial systole as blood is ejected form the atrium into a stiff v
83
pulsus paradoxus
a decrease in p of greater than 10 mm hg on inspiration
associated with cardiac tamponade
84
kussmaul sign
an increase in jvp on inhalation most often assocaited with constrictive pericaditis or restrictive cardiomyopathy
85
triphasic scratchy sound
pericardial friction rub
mi (dressler syndrome), occurs several days after an MI and is much rarer than simple ventricular ischemia
86
continous machinery murmur
pda
87
there are no specific physical findings that allow you to answer a most likely diagnosis question in terms of st elevation or depression w/out
an ekg
88
a displaced pmi
is characteristic of lvh as well as dilated cardiomyopathy
it cannot occur with an acs
89
leads v2-v4
anterior wall of lv
worst place to have mi
mortality is 30-4-% within 1 year
90
leads 2 3 and avf
inferior all of of lv
mortality is 5% within 1 year
91
pr interval grater than 200 milliseconds
first degree heart block
little pathologic potential, esp when isolated
92
pvcs and apcs
are associated with the later development of more severe arrhythymias but no additional therapy is needed if magnesium and paotssium levels are normal
we dont like to see pvcs but theri presence does not require any changes in management
93
st depression in v1 and v2
suggestive of a posterior wall mi
bc the lead are read in opposite direction of the rest of the leads
low mortality and no additional therapy is needed
94
rbbb
benign compared to a new leftbb
95
most important step for an acute mi
give aspirin, lowers mortality
morphine oxygen and nitro should all be given but they do not lower mortality and so they are not as important as aspirin
give apsirinr simultaneously while activating the cath lab
96
when do you give clopidogrel with acute mi
when pt cant tolerate aspirin or has undergone agnipolasty with stenting
97
always initate therapy and testing before what with mi
move the pt
98
b blockers and mi
they lower mortality but are not critically dependant on time
same thing with acei and statins
99
EKG and mi
time to becoming abnormal
duration of abnormality
immediately at onset of pain
st elevation progresses to q waves over several days to a week
100
myoglobin and mi
time to becoming abnormal
duration of abnormality
1-4 hours
1-2 days
101
ck-mb
time to becoming abnormal
duration of abnormality
4-6 hours
1-2 days
102
troponin and mi
time to becoming abnormal
duration of abnormality
4-6 hours
10-14 days
103
the use of troponing level is not without its difficulties
troponin cannot distinguish a reinfarction occuring several days after the first event
renal insufficiency can result in false positive tests since troponin is excreted through the kidney
104
MI reinfarction
when a pt has a new episode of pain within a few days of the first cardiac event the management is:
perfomr an ekg to detect new st segment abnormalities
check ck-mb levels, after a few days from initial infarction they go back down and so an elevation will tell you it is a new infarction
105
mi icu monitoring
placed here after initial management is put in place
continuous rhythm monitoring improves survival and outcome
the most common cuase of death in the first several days after an mi is ventricular arrhythmia (tach and fib)
rapid performance of electrical cardioversion or defib is available
106
ck mb should be gone in
24-48 hours
107
st elevation mi treatment
initially with aspirin
clopidogrel is often used if there is an allergy to aspirin but prasugrel and ticagrelor are alternatives to clopidogrel that are superior if stenting happens
108
angiolplasty is superior to thrombolytics in terms of:
survival and mortality benefit
fewer hemorrhagic complications
likelihood of developing complications of mi (less arrhythmia less chf fewer ruptures of septum free wall and papillary muscle ruptures)
109
door to balloon or pci time is
less than 90 minutes
110
complications of pci
rupture of coronary artery on inflation of balloon
restenosis (thrombosis) of the vessel after the angioplasty
hematoma at the site of entry into the artery
only 20% of us hosptials can do angioplasty bc they have no cath lab
111
how to reduce the risk of restenosis after pci
the palcement of drug eluting stents aht inhibit the local t cell response (paclitaxel, sirolimus)
112
rate of restenosis within 6 monts of pci
no stenting 30-40%
bare metal stent 15-30%
drug eluting stent
113
what do you do if pt has ci to thrombolytics
transfer somewhere with a cath lab
114
absolute ci to thrombolytics
major bleeding into the bowel (melena) or brain (any type of cns bleeding)
recent surgery (within the last 2 weeks)
htn above 180/110
nonhemorrhagic stroke within the last 6 months
115
heme positive brown stool is not a ci to use
thrombolytics
116
the mortality benefit of thrombolytics extends out to
12 hours from the onset of chest pain
50% improvement rate if given within 2 hours
should receive thrombolytics withing 30 minutes of coming through the door
117
MI treatment indications and benefits
aspirin
everyone
the best initial therapy
118
MI treatment indications and benefits
clopidogrel or prausgrel or ticagrelor
those underoing angioplasty or stenting
second antiplatelet drug with aspirin
119
MI treatment indications and benefits
beta blockers
everyone
effect is not dependent on time
started any time during admission
120
MI treatment indications and benefits
acei/arb
everyone
benefit best with ejection fraction below 40%
121
MI treatment indications and benefits
statins
everyone
goal ldl
122
MI treatment indications and benefits
oxygen,nitrates
everyone
no clear mortality benefit
123
MI treatment indications and benefits
heparin
after thrombolytic/pci to prevent restenosis
inital therapy with st depression and other nonst elevation events (unstable angina)
124
MI treatment indications and benefits
ccb
cant use beta blockers
cocaine induced pain
prinzmetal or vasospastic variant angina
125
door to needle time
under 30 minutes
126
when the pt has acs and there is no st segment elevation (so if the pt has depression) there is no benefit from what?
thrombolytic therapy or pci
give heparin instead
127
glycoprotein IIb/IIIa inhibitors
abciximab tirofiban eptifibatide
used in coronoray syndromes in those who are to undergo angioplasty and stenting
are not benefical in acute st elevation infarctions unless underoing stenting or angioplasty
inhibit the aggregation of platelets
lead to a reduction in mortality in those with st depression particularly in pts whose troponin or ckmb levels rise and who then develop a mi requiring pci with stenting
128
Cardiac events when to use aspirin
stable angina
unstable angina/non-st elevation MI
st elevation mi
129
Cardiac events when to use beta blockers
stable angina
unstable angina/non-st elevation MI
st elevation mi
130
Cardiac events when to use nitrates
stable angina
unstable angina/non-st elevation MI
st elevation mi
131
Cardiac events when to use heparin (enoxaparin)
unstable angina/non-st elevation MI
st elevation mi
132
Cardiac events when to use GPIIb/IIIa
unstable angina/non-st elevation
133
Cardiac events when to use thrombolytics
st elvation mi, but not as good as pci
134
Cardiac events when to use ccbs
never
135
Cardiac events when to use warfarin
never acutely
136
Cardiac events when to use antiplatelet drug
unstable angina/non-st elevation MI
st elevation mi
137
tpa (thrombolytics) are only beneficial with
St elevation MI
138
heparin is best for
non st elevation mi
139
GPIIa/IIIb inhibitors are best for
non st elevation mi and those undergoing pci and stenting
140
what has no clear mortality bneefit in ACS
ccb and warfarin
141
low molecular weight heparin is superior to
unfactionated heparin in terms of mortality benefit
142
absolute contraindications to stenting
major bleeding (bowel/brain)
recent surgery (less than 2 weeks)
severe htn (greater than 180/110)
nonhemorrhagic stroke (less than 6 months)
143
In non-st elevation ACS, when all medications have been given and the pt is not better
urgent angiography, and possible angioplasty (PCI) should be done
```
no better means:
persistent pain
s3 gallop or CHF developing
worse EKG changes or sustained ventricular tachycardia
rising troponin levels
```
144
starving hearts have v tachy
open it fast with PCI
145
complications of acute mi are an excellent source of
what is the most likely diagnosis
146
sinus bradycardia
very common in assocaition with mi bc of vascular insufficiency of the SA node
147
3rd degree (complete) AV Block
cannon A waves, produced by atrial systole against a closed tricuspid valve, the tricuspid valve is closed bc the of the 3rd degree AV block causes the atria and ventricles to contract seperately and out of coordination with each other
148
Cannon A Wave
3rd degree block
the bounding jugulovenous wave bouncing up into the neck
look for an association with right ventricular infarction and 3rd degree AV block
all symptomatic bradycardias are treated first with atropine and then by placing a pacemaker if the atropine is not effective
149
Tachycardia causes
R ventricular infarction
tamponade/free wall rupture
ventricular tachycardia/ventricular fibrillation
valve or septal rupture
150
Right ventricular infarction
association with new inferior wall mi and clear lungs
you cannot get blood into the lungs if the blood cannot get into the heart
diagnose by flipping ekg from usual left side of chest to the right side, st elevation in RV4 is the most specific finding
151
the Right coronary artery supplies
Right Ventricle
AB node
inferior wall of heart
-this is hwy up to 40% of inferior wal mi will have a right ventricular infarction
152
How to treat RV infarction
high volume fluid replacement
dont use nitroglycerin they worsen cardiac filling
153
Tamponade/free wall rupture
it usually takes several days after an infarction for the wall to scar and weaken enough for it to rupture
look for sudden loss of pulse
lungs are clear
cause of pulseless electrical activity
diagnose with emergency echo
emergency pericardiocentesis is done on the on the way to the OR
154
ventricular tachy/ventricular fibrillation
both can cause sudden death and there is no way to distinguish them without an ekg if they cause sudden loss of pulse. both are treated with cardioversion/defibrillation
155
Valve or septal rupture
both present with new onset of a murmur and pumonary congestion. mitral regurgitation murmur is best heard at the apex with radiation to the axilla. ventricular septal rupture is best heard at the lower left sternal border
156
most accurate test for valve rupture and septal rupture
echocardiogram
157
look for a step up on oxygen saturation as you go from the right atrium to the right ventricle to hand you the diagnosis of
septal rupture
158
intraaortic balloon pump
is the answer when there is acute pump failure from an anatomic problem that can be fixed in the operating room
IABP contracts and relaxes in sync with natureal heartbeat, it gives a push forward to the blood
159
IABP is never a
permanent device, it serves as a bridge to surgery for valve replacement or transplant for 24-48 hours
160
Extension of the infarction/reinfarction
when a pt presents with either an inferior or anterior infarction, it is common for a second event to infarct a second geographic area of the heart
look for recurrence of pain new rales on exam a new bump up in ckmb and even sudden onset of pulmonary edema
repeat ekg and reterat with angioplasty and sometimes thrombolytic in addittion to usual meds (asprin, metoprolol nitrates, ACE, statins)
161
aneurysm/mural thrombus
detected with echocardiography. most aneursyms do not need specific therapy, treated with heparin and followed by warfarin
162
bradycardia, cannon a waves
third-degree AV block
163
no cannon A waves
sinus bradycardia
164
sudden loss of pulse, jugulovenous distention
tamponade/wall rupture
165
IWMI in history, clear lungs, tachycardia, hypotension with nitroglycerin
RV infarction
166
new murmur, rales/congestion
valve rupture
167
new murmur, increase in oxygen saturation on eneterin the right ventricle
septal rupture
168
loss of pulse, need ekg to answer question
ventricular fibrillation
169
Detection of persistent ischemia
everyone gets a stress test prior to discharge
the stress test determines if angiography is needed
angiography determines the need for revascularization such as angioplasty or bypass surgery
170
do not do a stress test if the pt remains
symptomatic, go straight to angiography
171
do not do agniography if reversible sign of myocardial ischemia are
absent
there is no point in revascularizine to mycardium that is dead (infarcted)
172
Post MI stress test
identify those with residual ischeia prior to leaving the hospital. do not just cath (angiography) everyone
173
postinfarction routine medications
```
everyone should go home on:
aspirin
beta blockers (metoprolol)
statins
ACEI
clopidogrel or prasugrel or ticagrelor: for those intolerant of aspirin or post-stenting
ARBs: those with a cough on ACEI
```
174
ACEI are best for anterior wall infarctions bc
of the high likelihood of developing systolic dysfunction
175
dipyridamole is never the right choice for
CAD
176
Prphylactic antiarrhythmic medications
do not use amiodarone, flecainide, or any rhythm-controlling medication to prevent the development of ventricular tachycardia or fibrillation
do not be fooled by the question describing frequent PVCs and ectopy.
prophylactic antiarrhythmics increase mortality
177
sexual issues postinfarction
tested very frequently, know these things
do not combine nitrates with sildenafil, can get hypotension bc they are both vasodilators
erectile dysfunction postinfarction is most commonly from anxity, however of all the medications that cause erectile dysfunction beta blockers is the most common
the pt does not have to wait after an MI to reengage in sexual activity. if the pt is symptom free, sexual activity may begin immediatly . this is bc sexual activity usually does not last long enough to constitute an excessive increase in myocardial oxygen consumption
if the post mi stress test is described as normal the pt can renegage in any form of exercise program as tolerated including sex
178
Congestive Heart Failure
definition
sob (dyspnea) is the essential fature of cgf
it is a dysfunction of the heart as a pump of blood, resulting in an insufficent oxygen delivery to tissues accompanie by the accumulation of fluid in the lungs
systolic dysfunction is a low ef
dyastolic dysfunction is the inability of the heart to relax and receive blood, ef is normal and can even be increased
179
Postinfarction Routine Medications
everyone goes home on
aspirin
beta blockers (metroprolol)
statins
ACE inhibitors
clopidogrel or ticagrelor or prasugrel: only if intolerant to aspirin
ARBs: if you get a cough with ACEI
180
Ace inhibitors are best for?
bc of the high likelihood of developing systolic dysfunction
anterior wall infarctions
181
Prophylactic antiarrhythmic medications
do not use amiodarone, flecainide, or any rhythm-controlling medication to prevent the development of ventricular tachycardia or fibrillation.
182
prophylactic antiarrhythmics increase
mortality
183
do not be fooled by the question describing frequent pvcs and
ectopy
184
dipyridamole is never the right choice for
cad
185
Causes of systolic dysfunction
htn
htn resulting in a cardiomyopathy or abnormality of the myocardial muscle is the most common cause of chf
initially when caused by htn there is preservation of the ef, over time the heart dilates resulting in systolic dysfunction and low ejection fraction
186
valvular heard disease of all types results in
chf
187
causes of systolic dysfunction
mi
very common cause of dilated cardiomyopathy and decreased ef
188
ch in us adults is the most common cause of
being admitted to the hospital
admitted repeatedly due to complications
189
Infarction>?>?>?
dialtion, regurgitation, chf
190
common causes of chf
infarction, cardiomyopathy, and valve disease account for most cases (over 95%)
```
alcohol
postviral myocarditis (idiopathic)
radiation
adriamycin (doxyrubicin)
chagas disease and other infection
hemochromatosis (and causes restrictive cardiomyopathy
thyroid disease
peripartum cardiomyopathy
thiamine deficiency
```
191
CHF presentation
major
dyspnea (sob), is the indispensible clue (on exertion)
pulmonary edema (clinical diagnosis)
Look for what is the most likely dx question, dont lead labs and test just physical and history
192
chf presentation
others
orthopnea
peripheral edema
rales on lung exam
jvd
paroxysnal nocturnal dyspnea
s3 gallop
193
Most likely dx for dyspnea,
sudden onset clear lungs
pulmonary embolus
194
Most likely dx for dyspnea,
sudden onset, wheezing, increased expiratory phase
asthma
195
Most likely dx for dyspnea,
slower, fever, sputum, unilateral rales/rhonchi
pneumonia
196
Most likely dx for dyspnea,
decreased breath sounds unilaterally, tracheal deviation
pneumothorax
197
Most likely dx for dyspnea,
circumoral numbness, caffeine use, hx of anxiety
panic attack
198
Most likely dx for dyspnea,
pallor, gradual over days to weeks
anemia
199
Most likely dx for dyspnea,
pulsus paradoxus, decreased heart sounds, jvd
tamponade
200
Most likely dx for dyspnea,
palpitations, syncope
arrhythmia of almost any kind
201
Most likely dx for dyspnea,
dullness to percussion at bases
pleural effusion
202
Most likely dx for dyspnea,
long smoking hx, barrel ches
copd
203
Most likely dx for dyspnea,
recent anesthetic use, brown blood not improved with oxygen, clear lungs on auscultation, cyanosis
methemoglobinemia
204
Most likely dx for dyspnea,
burning building or car, wood burning stove in winter, suicide attempt
co
205
the s4 heart sound comes during
pq interval
206
the s3 heart sound comes during
tp interval
207
chf diagnostic tests differences
know the setting like er vs office
presence of acute symptoms of dyspnea at the time of presentation
208
every pt with chf must undergo
echocardiography to evaluate ef
209
echocardiography
most important of all tests for chf
most reliable way to distinguish between systolic and diastolic dysfunction (xray ekg and bnp and anp cannot)
210
best initial test for ef
transthoracic echo
211
most accurate test for ef
multiple gated acquisition scan (muga) or nuclear ventriculography
212
transesophageal echo
is more accurate than transthoracic echo and muga or nuclear ventrulography in evaluation heart valve function and diameter
however it is not necessary for evaluatig chf
213
when should you answer nuclear ventriculography
nucelar testing for the best precision is rarely needed , but if a person is received chemo (doxorubicin) or you are trying to give the max amount of chemo to cure a lymphoma but ensure you are not causing cardiomyopathy
214
nuclear ventriculography gives precise evaluation of
wall motion abnormalities
215
when do you answer BNP
in a pt with acute sob in whome the etiology of the dyspnea is not clear and you cannot wait for an echo to be done, a normal bnp excludes chf and the reason behind the dyspnea
216
Test to determine cause/etiology of chf
ekg
mi
heart block
217
Test to determine cause/etiology of chf
chest cray
dialted cariomopathy
218
Test to determine cause/etiology of chf
hotler monitor
paroxysmal arrhythmias
219
Test to determine cause/etiology of chf
cardiac catherterization
precise valve diameters
septal defects
220
Test to determine cause/etiology of chf
CBC
anemia
221
Test to determine cause/etiology of chf
thyroid function
both high and low thyroid levels can cause CHF
222
Test to determine cause/etiology of chf
endomyocardial biopsy
rarely done
excludes infiltrative disease such as sarcoidosis or amylid when other sites for biopsy are inconclusive
biopys is mosst accurate test for some infections
223
Test to determine cause/etiology of chf
swan-ganz right heart catheterization
distinguishes chf from ards, not routine
224
Treatment for systolic dysfunction (low ef)
acei or arb
bblockers
spironolactone
diuretics
digoxin
225
acei and arbs with chf
give to all pts with systolic dysfunction at any stage of the disease, benefits occur with any drug in the class
226
bblockers with chf
there is only evidence that the following drugs will offer benefit
metoprolol b1 antagonist
bisoprolol b1 antagonist
carvedilol nonspecific bblocker and alpha1 antagonist
227
benefits of bblockers in chf is
antiischemic effect
decrease in heart rate leading to decreased oxygen consumption
antiarrhythmic effect
228
what is the most common cause of death from chf
arrhythmia/sudden death
ischemia>ventricular arrhythmias>sudden death
bblockers can stop this
229
do not give blockers with acute
chf
230
spironolactone in chf
beneficial bc it inhibits the effects of aldosterone
only effective in advanced and serious stages of CHF (3 and 4)
ae: hyperkalemia and gynecomastia
not used at a high enough dose to exhibit diuretic activity
231
what is the management of a pt with severe chf who develops gynecomastia
switch spironolactone to eplerenone
232
diuretics control symptoms of chf they do not
improve mortality
233
diuretics in chf
inital therapy of chf with low ejection fraction often includes a loop diuretic in combo with an ace or arb
use any loop
spr
234
Digoxin in chf
does not lower mortality in chf (know this)
used to control sympotms of dyspnea, and will decrease hospital admissions
235
do positive inotropes lower chf mortality?
digoxin, milrinonr, amrinone, and dobutamine
no they do not
236
what do you do if pt has elevated k in serum and they are on lisinopril for chf
switch it for hydralzine and nitro
these have been shown to increase survival with systolic dysfunction
237
candesartan is associated with
hyperkalemia
238
know what drugs lower mortality in
chf
239
Devices for CHF Treatment
implantable defibrillator
biventricular pacemaker
240
implantable defibrillator
for those with ischemic cardiomyopathy and an ef below 35%. these devics have s much as a 25% relative reduction in the risk of death. remember that arrhythmia and sudden death is the most common cause of death in CHF
241
Biventricular pacemaker
indicated in those with dilated cardiomyopathy and an ef under 35% and a wide QRS above 120 milliseconds who have persistent symptoms
it resynchronizes the heart when there is a conduction defect. many pts who would otherwise be heading to a cardiac tranplantation have had their symptoms markedly improved with the biventricular pacemaker
242
do not confuse the biventricular pacemeaker with a
dual chamber pacemaker with a wire in both an atrium and a ventricle
243
ccb's provide no clear benefit in
systolic dysfunction, some ccb's can actually raise mortality
244
CHF Transplantation
when maximal medical theraphy (ACEI, BB, Spironolactone, diuretics, and digoxin) and possible the biventricular pacemaker fail to control symptoms of CHF, then the only alternative is to seek cardiac transplantation
245
Routine anticoagulationwith warfarin is always? in the absence of a clot in the heart
wrong
246
Drugs that have mortality benefit in systolic dysfunction
```
ACEI/ARB
beta blockers
spironolactone or eplerenone
hydralazine/nitrates
implantable defibrillator
```
247
Treatment for diastolic dysfunction (CHF with preserved ejection fraction)
beta blhave clear benefit
digoxin has no clear benefit
diurectics are used to control symptoms of fluid overload
ACEi and ARBs havve unclear benefit in diastolic dysfunction
248
do not confuse diastolic dysfunction with
HOCM
249
HOCM
congenital disease with an asymmetrically enlarged (hypertrophic) septum leading to an obsruction of the left ventricular outflow tract.
diuretics are contraindicated bc they increase the obstruction
250
clearly beneficial in diastolic dysfunction
beta blockers and diuretics
251
clearly not beneficial in diastolic dysfunction
digoxin and spironolactone
uncertain: ACEI, ARs and hydralazine
252
Acute Pulmonary Edema
definition
pulmonary edema is the worst or most severe from of CHF. pulmonary edema is the rapid onset of fluid accumulating in the lungs
253
Acute pulmonary edema
presentation
acute onset of SOB associated with:
```
rales
JVD
S3 gallop
Edema
Orthopnea
```
there can be ascites and enlargement of the liver and spleen if there has been sufficient time for the chronic passive congestion of the right side of the heart to prevent filling of the heart
254
Acute Pulmonary Edema
Diagnostic Tests
```
Brain natriuretic peptide
cxr
oximetry/arterial blood gases
EKG
Echocardiography
```
255
BNP for pulmonary edema
this is used if the diagnosis of the etiology of the sob is not clear. a normal BNP level excludes pulmonary edema
256
CXR for pulmonary edema
you will see vascular congestion with filling of the blood vessels towards the head (cephalization of flow). ordinarily, most flow in the lungs is at the bases bc of simple gravity. in more chronic cases, there will be enlargement of the heart and pleural effusions
257
oximetry/arterial blood gases for pulmonary edema
hypoxia is expected. until the acute disease is extremely severe, there is also respiratory alkalosisbc of hyperventilation. bc of the increased respiratory rate, carbon dioxide leaves more easily than oxygen enters the bloodstream.
258
EKG for pulmonary edema
most important test to do acutely, bc the ekg can lead to a change in immediate therapy
if atrial fibrillation, atrial flutter, or ventricular tachycardia is the cuase of pulmonary edema, the first thin to do is to perfomr rapid, synchronized cardioversion in order to restore atrial systole and to return the atrial contribution to cardiac output. normally atrial systole contributes only 10% to 20% of cardiac output. if the heart is diseased from dilated cardiomyopathy, decreased ejection fraction, or valvular heart disease, then the atrial conribution to cardiac output.
259
if acute pulmonary edema is from an arrhythmia the fast way to fix it is with
cardioversion
260
Echocardiography for pulmonary edema
this should be done in all pts to determine if there is systolic or diastolic dysfunction. this makes no difference acutely if there is pulmonary edema bc the initial therapy does not differ.
261
best initial therapy for acute pulmonary edema
to remove a large volume of fluid from the vascular space so diuretics
oximetry should be done but should not alter acute management bc we now must give oxygen bc the pt complains of sob and she is hyperventilating
echo should be done but it doenst need to be done urgently
ramipril or any other acei or arb should be used if there is systolic dysfunction with a low ejection fraction, but it does not make a diff in an acutely stable pt (the sam eis true of metoprolol)
262
nesiritide is a therapeutic iv for of atrial natriuretic peptide
nesiritide functions in much the same was as nitrates. bc is is only a weak diuretic there is no proven mortality benefit in pulmonary edema
263
pulmonary edema treatment
preload reduction
positive inotropic agents
afterload reduction
264
pulmonary edema
preload reduction
initial therapy is:
oxygen
loop diuretics such as furosemide or bumetinide
morphine
nitrates
removing 1 or 2 liters of fluid from the vascular space and the lungs is the best thing that can be done acutely to decrease symptoms
265
pulmonary edema
positive inotropic agents
dobutamine can be used in the acute setting of pts placed in the ICU when their sob did not respond to therapy acutely with preload reduction
amrinone and milrinone are phosphodiesterase inhibitors that perfrom the same role. they increase contractility and decrease afterload
digoxin is a positive inotrope that increases contractility but it will not have this effect for several weeks after starting its use. there is no benefit of using digoxin in the acute setting
266
pulmonary edema
afterload reduction
acei and arbs are used on discharge for long-term use in all pts with systolic dysfunction and low ejection fraction. in an acute setting nitroprusside and intravenous hydralazine can be used.
267
Valvular Heart Disease
Definition
all valvular heart disease can be congenital in nature.
rheumatic fever can lead to any form of valve disease but ms is the ost common
aging can automaticallybe associated with as
regurgitant disease is most commonly caused by htn and ischemic heart disease
infarction automatically leads to regurgitation, which leads to dilation
268
all forms of valvular heart disease are associated with
SOB and many signs and symptoms of CHF
only the murmurs are specific in terms of presentation
269
lesions of the right side of the heart
tricuspid and pulmonic valve
increase in intensity or loudness with inhalation
inhalation will increase venous return to the right side of the heart
270
lesions of the left side of the heart
mitral and aortic
increase with exhalation
exhalation will squeeze blood out of the lungs into the left side of the heart
271
best initaial test for valvular heart disease
echocardiogram
272
most sensitive and specific test for valvular heart disease
transesophageal is better than transthoracic
273
most accurate test for valvular heart disease
catheterization
allows the most precise measurement of valvular diameter, as well as the exact pressure gradient across the valve
274
what test is not specific in regard to valvular heart disease
ekg, it shows hypertrophy of chambers but you cannot confirm a diagnosis of valvular disease with it
275
xray evaluation of cardiac chamber size is neither the
most accurate or the best initial test
276
treatment for vlavular heart disease
all of them are assocaited with fluid in the lungs to use diuretics
ms dilate with a balloon
as needs surgical removal
regurgitant lesion respond best to vasodilator therapy with ACEi ABs nifedipine or hydralazine
surgical replacement of regurgitant lesions must be done before the heart diltes too much, if it dose surgery wont help
if the myocardium stretches too much it wont go back to normal
when the end systolic diameter expands you must replace the valve
277
Mitral Stenosis
Definition/Etiology
most often caused by rhuematic fever, making it uncommon in the US
critical narrowing is valve surface area that is less than 1cmsquared
treat if it is symptomatic, dont treat if asymptomatic
278
look for pregnancy and immigran in the hx as a clue to answering what is the most likely diagnosis to?
Mitral stenosis
279
pregnancy related cardiomyopathy
pregancy is associated with a 50% increase in plasma volume which must travers a narrow valve
also during delivery contraction of the uterus can squeeze as much as 500 ml extra blood into cirucaltion
280
most pts with mitral stenosis are
immigrants to us from places where rhuematic fever is still common
281
mitral stenosis often present sin
young adult pts
282
Mitral stenosis presentation
SOB and CHF as well as
dysphagia from left atrium pressing on esophagus
hoarseness from la pressing on laryngeal nerve
atrial fibrilation and stroke from enormous la
hemoptysis
283
Mitral stenosis physical findings
murmurs in diastole, just after an opening snap. squatting and leg raising increase the intesnity from increased venous return to the heart
284
mistral stenosis diagnostic tests
echo
ekg
cxr: la hypertrophy
285
mitral stenosis echo
tte is the best initial test
tee is more accurate test
catheterization is the most accurate diagnostic test
these rules are true for all valvular diseases
286
mistral stenosis ekg
atrial rhythm disturbance, particularly atrial fibrillation, is very common. left atrial hypertrophy shows up as a biphasic p wave in leads v1 and v2
287
mitral stenosis cxr
straightening of the left heart border
elevation of the left main stem bronchus
second bubble behind the heart
288
mitral stenosis treatment
diuretics and sodium restirction (when fluid overload is present in the lungs)
balloon valvuloplasty (done with a chatheter)
valve replacement (only when a cahteter procedure cannot be done)
warfarin for atrial fibrillation (to an inr of 2-3)
rate control of afib (with digoxin, beta blockers, or diltiazem/verapamil
289
Aortic Stenosis definition/etiology
aortic stenosis can be caused by a congenital bicuspid valve or with increasing clacification as people age
290
Aortic stenosis presentation
Angina: most common presentation
Syncope
CHF: poorest prognosis with 2 year average survival
291
aortic stenosis murmur
as systolic, crescendo decrescendo murmur peaking in a diamond shape in mid systole
hear best at the 2nd right intercostal space and radiates to the carotid artery
valsalva and standing improve or decrease the intesity of the murmur from decreased venous return to the heart
handrip softens the murmur bc of decreased ejection of blood
292
aortic stenosis diagnostic tests
tte then tee hten catheterization
293
aortic stenosis ekg
lvh
s wave in v1 plus an r wave in v5 greater than 35 millimeters
294
Aortic stenosis treatment
valve replacemnt is the only trule effective therapy for as
diuretics can be used to decrease chf but pts do not tolerate volume dpeletion very well
balloon valvuloplasty is not routinely done for as. this is bc the main mechanism for developing as is calcifications which does not improve very well with balloon valvuloplasty, balloon catheter procedures are done only if surgery is not an option secondary to the instability or fragility of the pt
295
mitral regurgitation definition/etiology
mr is an abnormal backward flow of blood thorugh a mitral valve that does not fit together. htn, endocarditis, myocardial infarction iwth papillary muscle rupture, or any other reason that the heart dilates will lead to MR
296
mitral regurgitation presentation
mr presents with the same signs and symptoms as CHF. the only unque findings is the murmur, which is pansystolic (holosystolic), obscuring both S1 and S2.
the murmur radiates to the axilla
handgrip will worsen the murmur by pushing more blood backwards thorugh the valve, handgrip increases afterload and will worsen the urmurs of both aortic regurg and mitral regurg
squatting and leg raising will also worsen mr by increaseing venous return to the heart
all left sided murmurs except mitral valve prolapse and hypertrophic obstructive cardiomyopathywill increase with expiration
297
mr is diagnosed with
echo
298
mitral regurgitation treatment
Vasodilators: ACE ad ARBs are best, they decrease the rate of progression of a regurgitant valve
Digoxin and diuretics may be used sometimes as htey would b ein any form of CHF
Valve replacement is indicated when the heart starts to dilated. do not wait for left vetricular end systolic diameter to become too large bc the damage will be irreversible, if it is above 40 mm or the ef drops below 60%, surgical valve repair or replacement is indicated
299
Aortic Regurgitation
Definition/etiology
AR is caused by anything that makes the heart or aorta dilated in size:
mi
htn
endocarditis
margan syndrome or cystic medial necrosis
inflammatory disorders usch as ankylosing spondylitis or Reiter Syndrome
syphilis
300
AR
Presentation
```
CHF
wide pulse pressure
water-hammer (wide-boudning) pulse
quincke pulse (pulsations in nail bed)
hill sign (BP in legs as much as 40 mmhg above arm BP)
head bobbing (de musset sign)
```
301
AR
Murmur
it gives a diastolic, decresecendo murmur heard best at the lower left sternal border.Valsalva and stanidn make it better. handgrip which increaes afterload by compressing the arteries of the arms make it worse
302
AR
diagnostic tests
Echo
ekg and cxr may show LVH
303
AR
Treatment
ACEi/ARBS or nifedipine as vasodilators will increase forward flow of blood and delay progression
digoxin and diuretics have littley benefit
surgical vvalve replacement is used when there is acute valve rupture such as with mi. rpelace or repair the valve before the left ventricle dialtes excessively. ef less than 55% or left ventricular end systolic diameter greater than 55 mm. repairing hte valve means tightening the ends of the valve with sutures this decrease regurg w/o the need for anticoagulation
304
Mitral valve prolapse
definition/etiology
mvp is so common as to be considered a normal anatomic variant occurring in as much as 2-5% of the populations, particulary in women. other causes are marfan and ehlers danlos syndrome
305
mvp
presentation
most often asymptomatic, usually not associated with chf
most common:
atypical chest pain
palpitations
panic attack
306
mvp
murmur
midsystolic click that when severe is assocaited with amurmur just after the click from mitral regurgitation
valsalva and standing which decrese venous return tot he heart will worsen mvp
anything htat increase left ventricular chamber size like squatting or handgrip improves mvp
307
mvp
diagnostic tests
cho is best
catheterization is done rarely bc you rarely replace the valve
308
cardiomyopathy
definition
abnomral function of the heart muscle, the origins of all defects are in an abnomrally contracting or relaxing myocardium
309
cardiomyopathy etiology
dilated, systolic dysfunction and low ejection fraction are often used interchangeably
hypertrophic cardiomyopathy is often interchaged with diastolic dysfunction, cardiac failure with preserved ef
310
cardiomyopathy
presentation
sob worsened by exertion
edema
rales
jvd
311
best initial test for cardiomyopathy
echo it is also the most accurate
ekg and cxr are unspeficif but still are perfroed
312
cardiomyopathy treatment
diuretics for all of them
the onl real function difference in the management of pts is their treatment for each kind
313
murmurs that do not increase with expiration
hocm
mvp
314
dilated cardiomyopathy
etiology
```
alcohol
postviral myocrditis
radiation
toxins like doxorubicin
chagas disease
```
315
dilated cardiomyopahty
presentation
dyspnea gallop edema and thoser symptoms like chf
316
dilated cardiomyopathy
diagnostic tests
cho then ekg and cxr are not specific
317
dilated cardiomyopathy
treatment
ACEi arbs bblockers (metoprolil or carvedilol) spironolactone all lower mortality
diuretics and digoxin are used to control symptoms
if the qrs is wider than 120 use a bivientricular pacmeaker that improves symptoms and survival
automated implantable cardioverter/defibrillator has morality benefit in some pts
318
hypetrophic cardiomyopathy
definition/etiology
most common cause of cardiomyopahty
in hcm a rxn to stressors on the heart such as htn, the heart hypertrophies to carry the load but then has a hard time relaxing in diastole, then the pt becomes sob
in hocm it is a gneetic dosrder with an abnomral shape sto the septum of the heart that forms an anatomic obstruction bewtween the setum and the valve leaflet to block blood leaving hte heart
319
difference between hcm and other forms of cardiomyopathy
s4 gallop
fewer signs of right heart failure such as ascites and enlargment of the liver and spleen
320
hocm
dyspnea
chest pain
syncope and lightheadedness
sudden death in athletes
worse with anything that increases heaert rate (dehydration diuretics and exercise)
worse with anything that decreases left ventricular chamber size (acei arbs digoxin hydralazine, valsalva, and standing suddenly)
321
hocm diganostic tests
echo is the best initial test
the septum is 1.5 times the thickness of the posterior wall
322
hypertrophic cardiomyopathy treatment
beta blockers are the best initial therapy for hocm and hcm
negative inotropis like verapamil and disopyramide are helpful
diuretics may help in hcm but they are ci in hocm
323
hocm specific thearpy
implantable defibrillators - shoudl be used in any hocm pt with syncope
ablation of the septum shoudl first be tried with a catheter placing absolute alcohol in the muslce causing samll infarctions. if sx persist surgical myomectoy removing part of the septum is the ultimate therapy
324
systolic anterior motion (sam) of the mitral valve is classic for?
hocm
it contributes to obstruction
325
catheterization is the most accurate test for
determining the precise gradients of pressure across the chamber
326
hypertrophic cardiomyopathy ekg
nonspecific st and t wave changes are common
lvh is common
ekg can be normal in a quarter
327
septal q waves are common in
hocm but no in mi
328
digoxin and sprinolactone are definitely always wrong in
hypertrophic cardiomyopathy
329
surgical myomectomy is the therapy for hypertrophic cardiomyopathy only if
all medical and catheter procedures fail
330
hypertrophic cardiomyopathy therapy
b blocerks
diuretics
ace and arb ar unclear
331
dilated cardiomyopathy therapy
```
bblockers
diuretics
ace and arb
spironolactone
digoxin
```
332
in hocm acei and diuretics definitely
do not help this is the majore difference between hocm and hcm
333
restrictive cardiomyopathy
definition
combines the worst apsects of both dilated and hypertrophic cardiomyopathy, the heart neither contracts nor relaxes normally bc it is infiltrated with substances creating immobility
334
restrictive cardiomyopathy
etiology
sarcoidosis
amyloid
hemochromatosis
endomyocardial fibrosis
scleroderma
335
restrictive cardiomyopathy
presentation
dyspnea is most common complaint with signs of r heart failure like edema ascites jvd and liver and spleenomegaly
pulmonary htn is common bc of an increase in wedge pressure
336
kussmaul sign
increase in jvp on inhalation is common in restrictive cardiomypathy
337
restrictive cardiomyopathy
diagnostic tests
echo is best initial
ekg show low voltage
ef may be normal or elevated
amyloid presents with speckling of the septum on echo or mri
most accurate itest in an endomyocardial biopsy (rarley done they usually take a bipsy from somerhwer else in the body)
338
restrictive cardiomopathy
treatment
treat the underlying cause
diuretics may relieve some of the pulmonary htn and signs of right heart failure
thre is no other clear therapy
339
more blood increase all murmurs except
mvp and hocm
340
squatting/leg raising effect on murmurs
increases: mitral and aortic stenosis, mitral and aortic regurgitation
decreases: mvp and hoxm
341
standing/valsalva effect on murmur
increases: mvp and hoxm
decreases: mitral and aortic stenosis, mitral and aortic regurg
342
standing and valsalva do what to venous return to the heart
decreases
343
standing from a squatting psoition will
open the venous capacitance vessels of the legs
344
valsalve is exhalation against a closed glottis
this increases intrathoracic pressure, when this happens it makes it harder for blood to return to the right side of the heart
345
standing or valvsalva=
diuretic use
these ar esimilar to using a diuretic. stenotic and regurgitant murmurs are all treated iwth diuretics and or salt restirciton so the anuevers of standing and valsalva will improve them
mvp and hocm have worsening of thei cardiac physiology with diuretics. diuretics decrease left ventricular chamber size, and owrse the regurgitation of mvp and the obstruction of hoxm. hence standing and valsalva will worsen them
346
less blood decreases all murmurs except
mvp and hocm
347
handip and amyl nitrate on murmurs
the contraction of the muslces of the arms will compress the arteries of the upper extrmeity such as the brachial radial and ulnar arteries . this increases afterload by obstructing the ability of blood to empty the heart
amyl nitrate is a direct arteriolar vasodilator. amyl nitrate stimulates the effect of ACE inhibitors or ARBS on the heart. any valvular disease that is treated with an acei/arb will improve with amyl nitrate. Improve means a softer murmur.
348
handgrip=
fuller left ventricle
349
amyl nitrate=
acei=emptier left ventricle
350
handgrip decreases
left ventricular emptying
351
amyl nitrate increases
left ventricular emptying
352
handgrip and amyl nitrate have no meaningful effect on
mitral stenosis, in hte same way ACEi has no meaningful effect on MS
353
handgrip and amyl nitrate effect on AS
Hand grip: decreases
Amyl nitrate: increases
354
handgrip and amyl nitrate effect on ms
Hand grip:no effect
Amyl nitrate: no effect
355
handgrip and amyl nitrate effect on ar
Hand grip:increases
Amyl nitrate: decreases
356
handgrip and amyl nitrate effect on mr
Hand grip: increases
Amyl nitrate: decreases
357
handgrip and amyl nitrate effect on mvp
Hand grip: decreases
Amyl nitrate: increases
358
handgrip and amyl nitrate effect on hoxm
Hand grip: decreases
Amyl nitrate: increases
359
manuever are like treatment
since regurgitant lesions are treated with ACEi, ARBs, and nifedipine as vasodilators, it is understandable that amyl nitrate decreases the intesnity of these lesions, since it increases the forward flow of lbood and decreases the regurgitant, backward flow of blood
handrgip decreases ventricular empying by increasein afterlaod. this will ipmrove the lesions of MVP and HOCM. a biggr fuller heart improves the obstruction of HOCM. with amyl nitrate, the emptier heart is samller such as would occur with diuretics, dehydration, and tachycardia. thiat is why amyl nitrate will worsen MVP and HOCM
360
handrip impvoes hoxm bc the heart is
larger (more full), which decreases the obstruction
361
Pericardial disease
the causes of pericardititis, pericardial tampnae and constictive pericarditis have considerable overlap. if the etiology of pericarditis is assocaited with the extravasation of a great deal of fluid, then tamponade can occur. if the cause of pericarditis is chronic then pts can develop the fibrosis and calcification of the pericardium that leads to constrictive pericaditis.
362
pericarditis
any infection, inflammatory disorder, connective tissue disorder, trauma to the chest, or cancer of an organ anatomically near the heart can cause pericariditis. the most common infection is viral however staphylococcus, streptococcus, fungi, and othe ragents can cause pericarditis in the sam waythat virtually any infection can cause pneymonia. sle is the most common connective tissue dorder, but wegeners granulomatosis, goodpasture syndrome, ra, polyarteritis nodosa and other diosrders can cause pericarditis
363
what is the most likely diagnosis
pericarditis
sharp chest pain that changes in intensity with respiration as well as the position of the body
pain is worse by lying glat and improved by sitting up. this is probably from a change in the level of tension or stretch of the pericardium
ekg shows st segment elevation in all eads, but the most specific finding is pr segment depression
364
colchicine decreases recurrences of
pericarditis
365
pereicarditis treatment
treat the underlying cause. for the majority, no clear cause is identified, and these "idiopathic" cases are generally presumed to be viral in etiology with coxsackie b virus. these cases are treated with nsaids such as ibu naproxen indomehtacin or any other drug in the class. colchicine decreases recurrences. if a choice calls for nsaid and colchicine is is the correct answer
366
pericardial tamponade
definition/etiology
any of the cuaes of preicarditis can extravasate enough fluid to cause tamponade. compression of the chambers of the heart starts on the right side bc the walls are thinner. as little as 50ml of fluid accumulating acutely can cause tamponade. if accumulating over weeks to monthes the pericardium will stretch to accomodate as much as 2 liters of fluid. tamponade can also be from trauma with a bleed into the pericardium this requires emergent thoracotomy
367
physical findings with tamponade
pulsus paradoxus - decrease of more than 10 mmhg in blood pressure on inhalation
368
cardiac tamponade most likely dx
hypotension
tachycardia
distended neck veins
clear lungs
369
most appropriate test for cardiac tamponade
echo
370
cardiac tamponade diagnostic tests
ekg: electrical alternans (different heights of QRS complexes between beats)
CXR: enlarged cardiac shadow expanding in both directions (globular heart)
Echo: right atrial and ventricular dastolic collapse
Right heart catheterization: equalization of pressures in diastole
371
Cardiac tamponade treatment
percardiocentesis: needle drainage will rapidly reexpand the heart
iv fluids
a hole or window placed into the pericardium for recurrent cases
372
diuretics will decrease intracardiac filling pressure and may markedly worsen
the collapse of the right heart
373
constrictive pericarditis
any cause of pericarditis can result in sufficient calcification and fibrosis to prevent filling of the right side of the heart if it is chornic, such as tuberculosis
374
constrictive percarditis
what is the most likely dx
signs of right heart failure such as:
edema
ascites
enlargement of the liver and spleen
jvd
is is a combination of physical finding and calcification on cxr
375
what findings are most likely to be assocaited with this pts
constrictive pericarditis
kussmaul sign: increase in JVD on inhalation (normally the neck veins should go down on inhalation)
knock: this is an extra heart sound in dastole from ventricular filling. as the heart fills to its maximum, it hits the stiff, rigid pericardium with a knock
376
diagnostic tests for constrictive pericarditis
best initial test is cxr, it shows the calcification and fibrosis
CT and MRI are moth more accurate, but would not be done if a chest xray were not done first
an echocardiogram is often indispensible in order to exclude right entricular hypertrophy of cardiomyopathy as a cause of the presentation. the myocardium moves nomrally in those with constrictive pericarditis
377
constricitve pericarditis treatement
Diuretics: used first to decompress the filling of the heart and relieve edema and organomegaly
surgical removal of the pericardium
378
Peripheral Artery Disease
definition and etiology
stenosis of peripheral arteries with the same causative factors as cad and carotid disease such as:
diabetes mellitus
hyperlipidemia
htn
tobacco smoking
379
what is the most likely diagnosis
pad
leg pain in the calves with exertion, relieved by rest
loss of hair follicles, sweat glands, and sebaceous glands
skin becomes smooth and shiny
380
spinal stenosis pain is worse when walking
down hills bc of leaning back
381
diagnostic tests
pad
best inital test is the ankle brachial index, normally equal or slightly greater in the ankles bc of gravity. if the difference is greater than 10% (ABI less than 0.9) then disease is present
most accurate test is an angiogram but this is not necessary unless specific revascularization will be done
382
Treatment
| pad
best inital therapy is: aspirin, stopping smoking, cilostazol
sinlge most effective medication is cilostazol
surgery is done to bypass stenosis if these medical therapies are not effective
383
routine screening for pad
there is none bc there is no mortality benefit to be obtained
384
in all major vascular disease, control each of the following:
BP
LDL below 100
Diabetes
385
calcium blockers do not help
PAD
386
Aortic Disease tip
the most frequently tested points regarding aortic disease are:
diagnosis and treatment of acute dissection
screening recommendations
387
Best initial test for Chest pain with pain also between the scapulae
although ont as sensitive as other tests the cxr may show wiedening of the mediastinum which is an excellent clue as to the presence of aortic dissection
388
key points for presence of aortic dissction
pain between the scapulae
difference in bp between the arms
389
most accurate test for aortic dissection
angiography, most sensitive and specific
also the ost invasive and most lilely to have allergic reaction and renal faiulre to contrast
390
there is no difference in the accuracy of what tests for aortic dissection
MRA, CT or TEE
391
in aortic dissetion the most important step is to control what?
BP, do this with
bblockers (decreases the shearing forces that are worsening the dissection, must be started before nitroprusside to protect agaisnt relfex tachycardia or nitro)
nitroprusside
surgical correction
392
screening for aortic anuerysm
men over 65 who have smoked with US
393
new onset of backpain in a pt over 65
do an us to rule at aaa
394
worst form of heart disease in pregnancy
peripartum cardiomyopathy, if you get this with persistent lv dysfunction, you will make it worse if you get pregnant again
395
Peripartum Cardiomyopathy
it is unknown why there are antibodies made against the myocardium in some prenant women. the LV dysfunction is often reversible and short tem. if the LV dysfunction does not improve then the person must undergo cardiac transplantation
396
medical therapy for peripartum cardiomyopathy
same as for dilated cardiomyopathy
```
ACEi/ARB
bblockers
spironolactone
diuretics
digoxin
```
397
repeat pregnancy in peripartum cardiomyopathy will provoke
enormous antibody production against the myocardium
398
when does peripartum cardiomyopathy develop
after delivery in most cases, why you cane use acei or arbs
399
eisenmerger syndrome
development of a right to left shunt from pulmonary htn, develops in a person with a ventricular septal defect who has significant left to right shunting htat eventually leads to the development of pulmonary htn, when pulmonary htn becomes very severe then the shunt reverses and right to left shunting develops
400
if peripartum cardiomyopahty isnot one of the choices in asking "what is teh worst cardiac disease in pregnant women?" then l
eisenmenger
401
pregnancy increases plasma volume by 50%
ms will worsen but not as much as peripartum cardiomyopathy or eisenmenger
