Professional Documents
Culture Documents
emotional stress
CT scan calcium scores
PET scan
Takosubo
STsegement elevation in V2 to V4, troponin levels rise, coronary angiography is
normal including absensce of vasospasm. Echo shows Apical LV ballooning
Mechanism presumed to be massive catecholamine discharge
for a calm and quiet person--not sued to be upset and highly emotional
Unreliable (Unproven) Risk Factors for CAD--factors that if seen in a question should be
ignored
Homocysteine (dx test only for folate or B12 deficiency)--it goes up in both
Chlamydia infection
C-reactive protein
No clear benefit in therapeutic intervention on these factors
Tip: the most common wrong answer
If the risk factor question involves:
family history
mistaking CAD in elderly relatives as a risk for patient
Stopping smoking results in the most immediate benefit in CAD (risk goes down literally
goes down within 10 minutes of stopping)
If you stop smoking, your risk factor for lung cancer goes down to nearly to that of those
who never smoked within 7 years
What is the most likely diagnosis
Ischemic pain-- dull/sore; squeezing (pressure-like)--its a muscle!
Location of ischemic pain is substernal...not left sided (rarely) !!
Qualities that go against ischemic:
Sharp, knife-like or pointlike
Lasts a few seconds (vs 10-20 minutes)
Three features help tell whether or not the pain is ischemic in nature:
1. Changes w respiration (pleuritic)--worse when take breath (pleural, pneumo)
2. Changes with position of body (pericardial)
3. Changes with touch of chest wall (tenderness)
Each (pleuritic, positional, tender) excludes ischemia with 95% negative
predictive value (NPV)
<10% with chest pain in ED end up having an MI
50% have no cardiac disease at all
MCC of chest pain that isnt ischemic in nature is GI-related (reflux, ulcers, gallbladder)
Location of ischemic pain is substernal...not left sided!!
Reflux hits the CN 9, 10 supplying bitter taste to the back of the tongue
MI can cause fever...all clots and blood collections can cause fevers! PE, MI, etc
infarction = irreversible
ischemia is reversible wall motion or thallium uptake between rest and exercise.
Infarction is irreversible or fixed.
Cant exercise? (cant get it up to the maximal HR, also readable EKG)
Use chemicals- Persantine (dipyridamole) or adenosine (these increase perfusion of
heart) with nuclear isotopes (eg thallium or sestamibi)
OR
Dobutamine in combination with echocardiography
Dobutamine simulates exercise--it increases myocardial oxygen
consumption
provokes ischemia
ischemia decreases wall motion on echocardiogram
**Dipyridamole may provoke bronchospasm. Avoid in asthmatics!
Dipyridamole is a PDEi that increases cyclic AMP, which
induces bronchospasm
Therefore, in asthmatics used dobutamine echo or
sestalium ?
Tip: Nuclear and Echo are equal in sens and spec (sensitivity = specificity)
Exercise Thallium = Exercise Echo
Dipyridamole Thallium = Dobutamine Echo
Treatments
Single most tested concept on step 3 cardio is which medications lower mortality--know
this!!!
Chronic angina (NOT an acute coronary syndrome)
Aspirin --most important bc decrease mortality and delay progression of
disease
Beta-blockers --most important bc decrease mortality and delay progression of
disease
Note: NONspecific beta blockers (eg propanolol) are NOT used routinely
in cardiology!
Propanolol is used for things like panic attack, essential tremor,
migraine ppx, thyroid storm
Metoprolol is used in cardiology--its a B1 specific drug
Nitroglycerin--used for chest pain, but does nothing for mortality
Chronic Stable Angina
Oral
Transdermal patch
Acute Coronary Syndrome
Sublingual
Paste (on chest wall)
Intravenous--ICU
Clopidogrel
used in all forms of acute MI in combination w
ith aspirin (not used
alone unless intolerant of aspirin!)
note: this has changed from previous recommendations that
stated this was only for those intolerant of aspirin
aspirin intolerance substitute (eg allergy)
recent angioplasty with stenting-- decreases restenosis
bare metal stent 1:3 will restenosis, but if use aspirin and
clopidogrel it decreases the restenosis rate to 15-20%
coated stent with aspirin and clopidogrel decreased restenosis
rate to 5-10%
Adverse Effects
Rare Thrombotic Thrombocytopenic Purpura
Prasugrel--lowers mortality
Antiplatelet medication for use in (along with aspirin):
angioplasty & stenting
all acute MI
intolerant of aspirin (so, can use as single agent)
NOTE: > 75 have an increased risk of hemorrhagic stroke!!
if pt is 75 or older use clopidogrel instead
ACE inhibitors or ARBs (angiotension receptor blockers)
used in all acute MIs
Low EF/systolic dysfunction (dilated CM) (best mortality benefit)
Regurgitant valvular disease--delays progression
Most common AE
ACEi only: 7% pts cough switch to ARBs (-sartans)
ACEi & ARBs: hyperkalemia switch to hydralazine & nitrates (afterload
reduction) (ACEi & ARBs increase K by inhibiting aldosterone)
do not answer add kayexalate (potassium-binding resin)--it is not
enough to say remove K from the body--you should eliminate the
cause and get an alternative replacement for the indication
give insulin and glucose to drive K into cells is not the right
answer unless you have an acute situation or EKG abnormalities
Statins (HMG-CoA reductase inhibitors)
When do they lower mortality the most? When you have C
AD w LDL
>100mg/dL HY!!
LDL >70: Treat when patient has CAD & DM together
remember: youre tested on National guidelines from n
onbiased federal
organizations-- not private organizations like ACC
Everyone will agree:
With CAD, goals of LDL at least <100 mg/dL
With CAD & DM, goals of LDL at least <70 mg/dL
CAD Equivalents
Use Statins to bring LDL down to <100 if:
Peripheral artery disease (PAD)
Carotid disease (NOT stroke)
Aortic disease (aortic ARTERY, not valve :)
Diabetes mellitus
MC AE of Statins?
Liver dysfunction!!
get LFT before initiating and during course of tx w statins
MC wrong answer to this question is Rhabdomyolysis (elevated
CPK)--this occurs in less than 1/10th of 1% of users (Liver dysfunction is
20-30x more frequent vs rhabdomyolysis)
do not need to follow CPK
CABG
Lowers mortality only with:
3 vessels with >70% stenosis in each
Left main occlusion
2 vessels with diabetes
persistent symptoms despite maximal medical therapy
all in combo with LV dysfunction
Benefit greatest with LV dysfunction
Internal mammary artery grafts last 10 years
Saphenous vein grafts last 5 years
Percutaneous Coronary Intervention (PCI) (Angioplasty)
Which circumstances does PCI lower mortality the most?
Intervention best therapy in acute coronary syndromes
Particularly, those with ST Elevation ACS
MC Wrong answer is in 1-2 vessel coronary disease
The main indication for using angioplasty is to acutely reverse a clot or
plaque rupture that happened within the hour. And although we use it to
decrease symptoms stable angina in 1-2 vessel disease, but it hasnt
been shown to lower mortality in chronic stable angina--may not be
normal, but have compensated--and no mortality benefit over meds
Maximal medical therapy with aspirin, BB, ACEi/ARBs, and statins has
proven benefit thats >
PCI in stable CAD
PCI decreases dependence on medication
PCI decreases frequency of angina episodes
Moreover, PCI best in ACS particularly with ST segment elevation. PCI
doesnt provide clear mortality benefit for stable patients
Systolic Dysfunction:
Low EF and dilation of heart
Diastolic Dysfunction:
EF is preserved...heart cant relax and receive blood
Important bc treatments are considerably different
MCC of CHF is HTN leading to diastolic dysfunction. Pt with MI can develop CHF rapidly
but far more people with hypertension where you initially have a preservation of EF. But,
overtime, the heart dilates up resulting in systolic dysfunction and low EF. This is simply
much more common than people who have MIs.
Valvular heart disease of all types results in CHF
MI is a very common cause of dilated CM and decreased EF
overall mortality from MI is considerably decreased by
Thrombolytics and angioplasty decrease it by 25% RRR
Aspirin, clopidogrel 25%
BB 10, 20, 30%
ACEi 10-20%
Statins 10%
As MI deaths continue to go down, the number of patients living with CHF goes up
Infarction (tissue dies) always dilates automatically lesions start to separate valve
leaflets regurgitation CHF
Less common causes of CHF (SOB, edema, orthopnea)--not dx tests to confirm/
determine these etiologies (except for hemochromatosis). Endomyocardial biopsy is
most accurate test is rarely if ever one. Hypertension and ischemia are far more
common causes fo CHF...take this list and add it up and multiple it by 10...still not as
common. The management and treatment is the same for all of these except for
revascularization.
EtOH
Postviral (idiopathic) myocarditis
Radiation
Adriamycin (doxorubicin) use
Chagas disease and other infections (doesnt present with chest pain, presents
with dilated CM...in south america :)
Hemochromatosis (also causes restrictive cardiomyopathy)
High iron, low iron binding capacity, high ferritin, 282Y mutation
Thyroid disease (hyper or hypo cause myopathy)
Peripartum CM
Thiamine deficiency-wet beri beri (rare)
In addition to dyspnea on exertion look for:
orthopnea is the positionality of SOB--one of the m
ost unique features of CHF.
when you lie flat, blood pools in your lungs (worse when lying flat, relieved when
sitting up)
Peripheral edema
Rales on lung exam