17 and 18. Acute Coronary Syndrome and chronic coronary artery diseaes Flashcards
UA, NSTEMI, STEMI are result of:
acute atheromatous plaque rupture with variable degree of coronary lumen obstruction
Tx recommendation for ACS
Best rest, analgesics, Oxygen, Statins, Beta blockers and nitrates
With ACS, you IG will form a thrombus as a result of
Plaque rupture which causes: Platelet activation/adhesion/aggregation Activation of Coag factors
What tx would you want to give someone right away with Thrombus formation during ACS?
Antiplatelets: aspririn/Clopidigrel/Prasurgrel/Ticagrelor OR Antithrombics: heparin/LMWH/Direct thrombin inhbitors
Once we know patient has ACS… what is our goal?
Reperfusion: #1 immediate PCI and use Thrombolytics (in UA and NSTEMI, still have some flow, so give drugs and hold off on PCI>> reevaluate in few weeks) Do cardiac Catheterization: PCI or CABG
What ECG and lab findings do we expect to see in STEMI?
ST elevation (but not always) and elevated CK and CK-MB pt will have chest pain, diaphoresis, and perhaps hitsory of DM, HTN, smoking
Recommend reperfusion of infarct related to STEMI?
IV throbmolytic therapy Emergency coronary interevention
How would you get acute left to right intracardiac shunt?
IV septum rupture
What would you expect to see in pt with NSTEMI on ECG and in labs
will have elevated enZ but will NOT have elevated ST; will be DEPRESSED!
Partial thrombotic occlusion of the vessel lumen results in
NSTEMI
Role of thrombolytic agents in NSTEMI
NONE… we don’t use them
General on IHD
leading cause of death worldwide –>after 40; risk of devo CAD is 49% men and 32% women
MOst common cause of IHD
obstruction of coronary arteries by atheromatous plaque also congenital issues, vasculitis or radiation
How are ACS and IHD similar?
Both are caused by restrictive blood flow to myocardium d/t flow restrictions in coronary arteries Supply/demand mismatch
Chronic stable angina on ECG and labs?
only ST depression during episode.. goes away and CK and MB-CK are normal
How will a pt with IHD present at clinic?
chronic chest discomfort (stable angina), have heart fail, cardiac arrythmias or have sudden death. (very similar to acute MI but more chronic in nature)
What can we give to someone with Angina pectoris?
Nitroglycerin or rest
Diagnosis of CAD: Early finding on ECG Late findings on ECG
Early we see ST elevation; shows that we’ve had injury Later we will see development of Q waves
In a timeline of MI: Immidately before MI starts: Within hours after MI: Weeks later:
T wave inversion ST elevation Significant Q wave only
Leads to look at for LATERAL wall damage
V5, V6
I, aVL
Inferior wall leads
II, III, aVF
Anterior wall leads
V2-V4
Damage to LAD is likely to show up on which leads
V1-V6
I
aVL
(anterior leads)
Damage to RCA likely to show up on which leads?
Inferior ones:
II, III, aVF
Damage to CIRC likely to show up on which leads
I, aVL, V5-V6
(Lateral leads)
What type of data do we collect during stress testing?
look for ECG changes (twave inversions, ST depression or elevation)
Do imaging for wall mostion abnormalities or defect
Whats an option for stress testing in those that can’t exercise?
Dobutamine; will increase HR and contractility
Adenosine: cause arterial dilation for normal arteries, abnormal ones will not dilate
What is the Gold Standard for Diagnosis of obstructed coronary blood flow?
Angiography
lesions of >70% are considered significant
What medical tx can we give to pts with decreased cornary blood flow?
Antiplats: apsirin or ADP-R inhibitors
Beta blocks
Ca+ blockers
ACEI
Nitrates
STatins
Aspirin therapy in pts with exsisting CAD will reduce future events by:
25%
Whats all the cool shit that Beta blockers do?
Decrease O2 demand via decrease HR, BP, and contractility
Decrease V fib risk
Decrease automaticity; increased electrophysiologic threshold
Bradycardia wil prolong diastole thus improves diastolic perfusion
REDUCTION IN REMODELING and improves LV hemodynamics to reduce infarct
reduce risk of mortality after MI by 23%
Metoprolol and Carvelilol are examples of what kind of drugs?
Beta blockers
selective for beta 1
Overall effect of Ca+ Channel Blockers
reduce myocardial O2 demand and increase O2 supply
Helpful in pts with Prinzmetal
No mortality benefit, just symptom relief
When are ACE I really beneficial
For pt with low LV ejection fraction after MI… can help up to 26%
(still helpful after MI by reducing mortality by 22%)
Action of Nitrates
relax vascular smooth muscle
Mostly in the VENOUS system which reduces PRELOAD==> thus reduces myocardial wall tension and oxygen requirements
Would we do revascularization for crhonic CAD?
we can do it electivly for symtomatic lesions:
PCI such as balloon or stent or a surgical bypass
** do this AFTER we’ve tried medical therapy and antianginal therapy as well as lifestyle changes
What situations would CABG be preferred over PCI?
Left main
Triple vessel
Double vessel with proximal LAD and LVEF <50%
Diabetics
Sequela of Chronic CAD
Cardiomyopathy (heart fail)
LV aneurysms
Ventricular Arrhthmias/Sudden Death
Cardiac Arrest risk is higher post MI especially if:
Left ventricular ejection fraction is depressed
*put in implantable cardiac defribilatory if you have LVEF
