Adams "Chest Pain" Flashcards
Heart shows something is wrong by:
chest pain
Differential of Chest pain
anxiety ASS asthma cardiomyopathy esophagitis gastroenteritis hypertensive emergency myocarditis pericarditis cardiac tamponade aortic dissection PE shingles
Brain says something is wrong by:
HA and vomiting
“Never let clothing stand between you and the diagnosis”
Shingles
“Doc, I think an elephant is on my chest and I am going to die!”
Classic MI presentation
ACS
Acute Coronary Syndrome
-non-cardiac disease
-stable angina
-unstable angina (60%
-definite ischemic event
STEMI 30%, NSTEMI 25%)
Unstable angina worries
hard to diagnose because no elevated troponin AND will go on to have an MI in next 10 days
MI Classic presentation
Hx: early AM presentation with substernal achy pressure
pain radiates to anterior neck, shoulders, left arm, and back
- “chest pain”
- dyspnea (SOB)
- nausea
- diaphoresis (sweating)
What percentage of MI presentations will have “chest pain?”
about 50%
- the other 50% will have SOB, nausea, sweating or other weird symptom
Classic MI Qs to ask
RISK FACTORS
Risk Factors for MI
- past hx of CAD
- smoker
- HTN
- elevated cholesterol
- family hx of CAD (mom died before
Typical physical exam findings of MI
*doesn’t lend much info most of the time
- chest clear
- RRR without murmur, S3, S4 or rub
- abdomen soft, guaiac negative stool
- no peripheral edema
- diaphoretic skin
Alternative presenations of MI
- no “pain”
- SOB
- sweaty
- syncope
- stroke
- palpitation
- indigestion
- weakness
- pain in referred areas, such as right arm/hand or abdomen
*use adjectives to help them describe their chest: heart burn? pressure? squeezing? burning? numbness?
Alternative presenations in populations…
- syncope and weakness in elderly
- women, young, and elderly present atypical
Alternative physical
S3: LV dysfunction
S4: decreased LV compliance
new murmur: papillary muscle tear/dysfunction
CHF: crackles, hepatojugular reflux, leg edema
___ and ___ (of ACS) can look same initially on EKG
UA and NSTEMI look same initially on EKGs
vs.
STEMI
NSTEMI and q waves…
No Q wave MI
Q wave MI
STEMI and q waves…
No Q wave MI
Q wave MI**most
Angina
- symptom rather than a diagnosis
- mismatch of oxygen demand and delivered oxygen to cardiac muscle –> ischemia (reversible)
How long does angina last
30 minutes = ischemia (no longer angina)
Types of angina
- stable angina (can be very freq and still stable, less predictive of CAD in women)
- prinzmetal’s (vasospasm, assoc with ST elevations, occurs at rest, often night, rarely with exercise)
- unstable angina (increasing duration, freq, intensity, new associated symptoms, occur with increasly less activity and rest)
*10% of unstable angina will have MI in 7 days
grade I angina
“ordinary physical activity doesn’t cause angina” (walking, stairs, etc.)
angina occurs with strenuous, rapid or prolonged exertion at work or recreation
grade II angina
“slight limitation of ordinary activity”
occurs on walking or climbing stairs rapidly, walking uphill, walk/stair after meals, cold/wind, under emotional stress, few hours after awakening
*walking more than 2 blocks on level ground and climibng more than 1 flight of ordinary stairs at normal pace and normal conditions
grade III angina
“marked limitations of ordinary physical activity”
angina occurs on walking
1-2 blocks on the level and climbing 1 flight stairs under normal conditions and normal pace
grade IV angina
“inability to carry on any physical activity w/o discomfort - anginal symptoms may be present at rest.”
Defining criteria of MI
elevation of TROPONIN and at least one of the following:
- symptoms of ischemia
- q wave development
- new ST/T wave changes or new LBBB
- intracoronary thrombus (angiogram or autopsy)
- loss of cardiac wall (ECHO)
EKG in MI
- normal in 30% of early MI
- compare to older EKGs
- if inferior MI, can get right side leads EKG looking for RV infarct
STEMIs and EKGs
- *ST elevation >0.1mV (one box) in all leads BUT V2 and V3 >0.2mV (two boxes)
- new LBBB (hard to diagnose because LBBB have ST elevation normally)
- posterior MI: unique bc “back of the heart” infarct –> ST elevations appear as ST depressions
NSTEMIs and EKGs
- T wave inversion >0.1mV (one box) with prominetn R wave or R/S wave ratio >1 in two contiguous leads
- ST depression >0.05mV in 2 contiguous leads
Troponin
- *take over time
- low sensitivity early in MI (50% at 3 hours)
- up to 7-10 days after MI
- if normal at 6 hours, AMi can be excluded (unless very high risks, then get a 12 hours also)
- false + = anything stressing the heart, such as a fib, sepsis, chronic kidney disease = troponin not specific to heart only
High sensitivity troponin
NEW KID ON THE BLOCK
- more rapidly positive
higher sensitivity at price of lower specificity (inc SNOUT, low SPIN)
- can still be normal with unstable angina
Other MI markers
- CPK-MB/CPK-MD ratio with total CPK *no longer used
- CRP: increase in mortality if elevated, but diagnostic/predictive value is not clear
- myoglobin and CK-MB isoforms not used
ECHO
specifically: if perform ECHO on patient with ongoing chest pain and find no wall motion abnormality –> low probability the chest pain is cardiac in origin
- prior heart disease –> show wall motion abnormality
- SNOUT: can be used to rule OUT if NORMAL** not an MI
When can you send a patient home with chest pain?
“Management of patient depends on potential risk of having cardiac disease.”
*HISTORY THAT IS NOT CONCERNING = WILL ALLOW YOU TO SEND A PATIENT HOME
= decision to send patient home is based on Hx
If have little chance of cardiac disease…
must have a plausible diagnosis upon discharge
- normal EKG (or no change)
- cardiac enzymges constant
- document follow up
If have possible cardiac disease…
- let history drive you
- use caution with: normal EKG, nitro trials, cocktails of lidocaine and antacid (10% MI will feel beter after gi cocktail), cardiac enzymes
- admit/discharge (have diagnosis, clear patient instrux, early follow up)
Treat low risk ACS
- ASA
- conservative observation
- repeat troponin in 6-12 hours
*possibly repeat EKG before repeat troponin (don’t be shy to ask for repeat, can see changes, eg inc ST elevations)
Treat moderate/high risk ACS
- nitroglycerin
- heparin
- repeat troponin in 6-12 hours
- possibly repeat EKG before repeat troponin (don’t be shy to ask for repeat, can see changes, eg inc ST elevations)
Manage UA/NSTEMI
- PCI (percutaneous coronary intervention) CATH LAB
- meds
Manage STEMI (ST elevations or new LBBB)
- fibrinolytics* (tPA, reteplase IF FIRST STAGES OF MI)
- PCI with dilation and stinting
- CABG (coronary artery bipass graft(s))
- meds
Give oxygen if…
hypoxic
*may be harmful if patient is normoxic (>94%): INCREASED MORBIDITY AND MORTALITY IF USE WRONGLY
Nitroglycerin if…
angina and selecively for MI
- not for RV ventricular infarct, it decreases preload and cause BP to drop
- give NO to decrease preload for CHF
Morphine if…
pain unresponsei to NO and is stopgap
*can cause hypotension
What about MONA?
The Death of MONA
***AAAAA
Keep the A = ASPIRIN
Antiplatelets
Aspirin***
Thienopyridines (CLOPIDOGREL) if unable to give aspirin, use in all patients less than 75 yo with UA/NSTEMI or STEMI
Clopidogrel
inhibits ADP (adenosine 5-diphosphate) dependent activation of glycoprotein IIb/IIIa complex = INHIBITS PLATELET AGGREGATION
also: prasugrel, ticagrelor
New MONA
Aspirin
Clopidogrel
send to cath lab
Anticoagulants
UFH (unfactionated heparin)
Enoxaparin (low molecular weight heparin)
Fondaparinus (like Enoxaparin)
Bivalirudin (direct thrombin inhibitor)
Give LMWH if…
DVT, PE
*can’t reverse, so don’t give in AMI
GIve UFH if…
unfractionated heparin, can use acutely, can reverse
Glycoprotein IIb/IIIa inhibitors
Abciximab, Eptifibatide, Tirofiban
- use primarily in conjunction with PCI
- best in acute STEMI when going to cath lab
- inhibits integrin gp IIb/IIIa receptor in platelet membrane
INHIBTS PLATELET AGGREGATION
Manage in first 24 hours
- ACE inhibitor
- B blocker (have been shown to decrease mortality after MI)
- (also aspirin, duh)
*start within first day or so
Greatest impact on morbidity and mortality in presence of acute MI
aspirin
Tako-tsubo syndrome
- “broken heart syndrome”
- MI
- heart loks like a luging balloon appearance
- surge of stress hormones cause MI
- chest pain
elvated troponin - ECHO would support wall abnormal
- HISTORY WILL HELP
- vessels will be normal, heart itself just gets stressed
- send to cath lab
Myocarditis
- 1/3 end up with significant heart issues…need transplant
- causes: parvovirus, chagas
- diffuse ST elevation***
- super high troponin
key points:
- offer other adjectives when eliciting a history
- not all patients have “chest pain”
- epigastric pain with no findings…consider cardiac ischemia
- got a lot of EKGs and repeat them
- ASA
- EKGs and labs should not be used to decide if a patient is sent home