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3 types of Acute Coronary Syndrome
Unstable Angina (USA) - out pt setting
- Non ST elevated MI (NON-STEMI) - in pt
- ST elevated MI (STEMI)
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3 types of angina
typically caused by art sclerosis
- stable= predictable
- unstable= accelerating, increased severity, not helped by Nitro
- Prinzmetals/Varient= vasospastic of coronary art and can cause heart damage
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Prinzmetal/Varient angina
- high risk for vent arrythmias that can lead to sudden cardiac death.
- can be triggered by smoke
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Left coronary artery name and supplies waht?
- the "widow maker"
- splits into the circumfelx which supplies the left ventricle
- supplies the anterior L vent, and Posterior L Vent
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right coronary artery supplies the anterior and posterior right vent, the inferior wall
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Tx of angina
1-4
- nitrates
- N+ Beta blockers to dec contract and O2 demand
- N + B + Ca chan. block
- CABG
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Tx of Prinzmetals/Vraient
NO BETA BLOCKERS
- Nitrates OR Ca blocks
- Nitrates + Ca blocks
- CABG
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remember:
Beta blocks the SNS effects on the CNS
Ca blockers cause Arterial vasodilation, which dec afterload
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Location matters as the severity and what cells are affected by an Acute MI
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need to get to hospital w/n the first 12 hours after chest pain starts to save the tissue
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common MI locations
- LAD- high mortality
- RCA
- L Cx
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Transmural
depth of the MI
- Trans= involves all three layers of heart
- ST elevation or Q waves develop with MI
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STEMI
elevated t wave indicate injury is occuring
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Non-STEMI
subendocardial= involves on the endocardium and partial wall of myocardiam
- No q-waves
- ST supression or inverse T waves
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typical MI Sx
chest pain or pressure
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atypical MI Sx
unexplained sweating, dyspnea, and nausea
- often unrecognized as cardiac
- women, elderly, and diabetics present with more atypical Sx than men
women present with N/V, jaw and/or back pain
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PQRST assessment for AMI
- Precipitating pain? Pain relief?
- Quality
- Radiate to?
- Severity 0-10
- Timing w/n 12 hours
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Calling EMS has better outcomes than driving to hosp
new rule is take 1 dose NTG then call instead of 3 doses
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when a right side MI is suspected, an 18 lead can be ordered. This is harder to diagnosis and less common
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ECG changes that help diagnos MI
- ST segment elevation or depression
- new Left BBB with QRS >1.0
- T-waves
- pathological Q waves
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summary:
STEMI
vs
Non STEMI
- STEMI= ST elevation, new LBBB, Q waves (long time)
- =Greem light, go fast to cath within first 12hrs
- N STEMI= ST depression, Twave inversion
- =Yellow light, go forward with caution
- =not strait to cath lab, Tx with meds first
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higher the ST seg, greater mortality
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cardiac markers
- Myoglobin first to rise, but not heart specific
- Troponin first heart specific marker to rise
- CPK-MB is heart specific too
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C reactive protein indicates what?
systemic inflammation
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B Natriuretic peptide indicates what?
it inc Na secretion from kidneys to dec fluid volume
- it is synthesized in cardiac vents and responds to stretch
- elevation indicates fluid overload
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Homocysteine
a corrosive acid use to predict mortality of MI event
treat with statisn
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mag and K levels decrease in MI
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golden hour, 1st 60 minutes can save a lot of muscle
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STEMI route if PCI (balloon and stent) hospital is <90 min
- strait to Cath lab for primary PCI
- supportive device
- Dx angiogram
- PCI
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STEMI route when PCI is > 120 minutes
- go to NON PCI hospital door in/out time <30min
- Transfer to PCI hospital, give thromblytic and supportive device <120 minutes
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MONA Tx of all Acute Coronary Syndromes
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Goal: destress the heart
Beta better than Ca blocks to Tx angina
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goal: hemodyn stability
- fluid volume
- vasopressor after fluid stable b/c of dec BP
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special considerations for R vent infarct (volume pump)
- inc preload
- IV fluids
- limit NTG and Morphine
- + inotropes as needed
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% of significant stenosis?
what about LCA?
sig >70%
widow maker >50% is sig
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Before a heart cath, what about the kidney needs to be considered?
- assess the creatinine levels
- hydrate with IV
- lower contrast in high risk pt's
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Statins (lipids lowers) are indicated pre-PCI and post ACS
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Anticoag before a cath is important
use multiple anti coags
DAPT= duel anti platelet therapy
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sites for heat cath
femoral and radial arteries
- radial has less complications
- femoral can have a psudoaneurysm (dilated artery from injury)
goal is increase lumen size to >50% with balloon
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if 3 of the major CA's are >70% blocked, open heart surg needed
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non medicated stent
BMS - bare metal stent
goal is to decrease vasospasm and help hold art open
clotting will occur immediatly, so anti-coag important
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Drug-eluding stent
medicated stent
- coated with drugs to dec intimal (fibrotic) tissue growth
- need to be on anticoag for longer time because the stent prevent endothelial growth which produces it's on anti-coag
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laser angioplasty can be done if CA is calcified instead of plaque
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placement of femoral cath considerations and concerns
need to be on femoral head d/t compression after removal
above head = Inc risk for retroperitonal hemorrhage
below = risk for pseudoaneurysm
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nsng care after PCI femoral
- make sure coag is back to nl before sheath removal of cath
- support site when coughing
- bedrest 6-8 hrs
- atropine at bedside
- reverse trendleberg to eat
- distal pulse and site hematoma chacks
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Intra-aortic balloon pump
inflates with diastole to inc CA bld flow
deflates at QRS to help pull blood out of L vent
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left ventricle assist device
bridge from L vent to Aorta until heart transplant is possible
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ways to prevent long term HF while in CCU
- ACE inhibitors (prils) to dec SVR, infarct size, and ventricular remoldeling
- limit fibrotic scare formation
pt will have very low BP, but this helps by dec SVR
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complications of thrombolytics
blding: assess nuero, bladder, bowel, back pain. No needle sticks
dysrhythmias
reocclusion
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how do you know if thrombolytics work?
ST segment returns, enzymes normalize
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Why use therapuetic hypothermia?
when pt was cardiac arrest or shock but was resuscitated, reprofused, and regular rhythm, BUT is still unconciaous
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