Flashcards in Ischemic Heart Disease Deck (43)
What causes endothelial damage to the vessel wall?
-inflammation to the endothelium, LDL accumulates under dissected endothelium. Mfs enter and start trying to remove LDL, these Mfs turn into foam cells. This all causese ongoing inflammation which may be prone to rupture. Once it ruptures a clot is formed.
What is the difference between stable and unstable angina?
Unstable angina is when a plaque has ruptured and a clot is formed. May lead to NSTEMI and STEMI.
Stable angina is narrowing of blood vessels, the plaque is stable and is not broken open, its just blocking the vessel enough to where when that person undergoes exertion it causes sx.
Sx of Cardiac Ischemia
-substernal chest pain
-may radiate to the jaw, shoulders, arms
-threshold for angina less after meals or in the cold
-may be worse lying down (sign of severe angina, end stage)
*elderly and diabetics have less overwhelming sx typically.
How do you differentiate between stable and unstable angina based on hx questions?
-sx precipitated by stress or exertion
-relieved by rest or nitrates
-long standing greater than 1-2mo
-chest pain at rest or with minimal exertion
-new onset angina
-change in pattern of stable angina
Description of cardiac chest discomfort
History MUST contain all these components
-precipitating and alleviating factors
-characteristics of discomfort
-location and radiation
-duration: how long has it been going on, how long is each episode
-effects of nitro
Classification of typical and atypical angina
-substernal w/ cardiac characteristics to the pain
-provoked by stress or exertion
-relieved by rest or nitro
-chest pain that meets 2 or less criteria above
New York Heart Association FUnctional Status Classification of Angina
-describe each class
2. mild limitation of exercise tolerance, sx w/ ordinary exertion.
3. moderate limiation of exercise tolerance, sx with minimal exertion
4. severe limitation of activities, sx at rest.
-S4 (atrial contraction against decreased LV compliance)
-S3 (decreased systolic function)
-apical systolic murmur or Mitral regurgitation
-Paradoxically split S2 (split during expiration, left ventricle not working)
What labs do you need to order for stable and unstable angina?
same as stable + troponin and CMP.
EKG findings suggestive of ischemia
-T wave inversion, depression, flattening
- changes from previous EKG
-ST depression or elevation
How can EKG be helpful in differentiating between stable and unstable angina?
-helps confirm stable vs unstable.
* chronic stable angina should not have acute EKG changes.
Chronic Stable Angina:
-further work up
-stress testing; determin the severity of limitation of activity, assess prognosis, evaluate response to therapy.
*generally once chronic stable you dont need to do this test unless they are experiencing sx.
-cardiac catheterization: once stable chronic angina dx has been made you rarely do this.
Indications for cardiac catheterization in patients with chronic stable angina?
-persistent limiting angina despite maximal medical therapy
-stress test suggestive of high risk dz
-hx of aortic valve disease to determine if chest pain is ischemic or d/t valve dx
-worsening sx (b/c we re-categorize them to unstable angina)
Medical therapy for chronic stable angina
-calcium channel blockers
-sodium channel blockers
-antiplatelet agents (aspirin/P2Y12)
-therapuetic lifestyle changes and coronary revascularization for refractory angina.
What is the goal for medical therapy with stable angina?
-prevent chest pain
Medical conditions that may precipitate anginal attacks
What drug could be used for immediate relief of anginal sx?
short acting nitrates
-ex: sublingual nitroglycerin tablets or spray (0.4mg)
"Only antianginal agents that have been demonstrated to prolong life in patients with CAD post MI"
What is the first line therapy for treatment of angina?
-they decrease myocardial O2 consumption
What drug could you add on after all other meds have failed to control chronic stable angina sx?
-decreases calcium....decreased ventricular tension.....decreases myocardial O2 consumption
*does not lower BP or affect HR.
Coronary Vasospasm/Prinzmetals angina/Variant angina
-what is this?
-what is found on EKG?
-who is this most common in?
-this is a spasm in the coronary vessel
-EKG: ST elevation
-Most common in young women because they have smaller vasculature.
-cyclical pain over months
-Sx: chest pain without precipitating factors, may awaken pt from sleep in early morning hours.
*will have normal exercise tolerance.
Coronary Vasospasm Triggers
-exposure to cold
-vasoconstriciting meds (decongestants, cold medicine)
-beta blockers may trigger (b/c the alphas are unopposed.
Associated disorders to Coronary Vasospasm
Treatment of Coronary Vasospasm
-rule out obstructive disease with cardiac catheterization
-Calcium channel blocker and long acting nitrates
-SL nitro for acute relief
-avoid beta blockers as they leave the alpha receptors unopposed which leads to vasoconstriction
Acute Coronary Syndrome
-what is the defining factor of this?
-what are the three conditions associated with this?
-defining feature is plaque rupture
-the three conditions associated with this are
1. unstable angina
What are the high risk features of unstable angina?
-accelerating sx over the last 48 hrs
-prolonged ongoing rest pain
-new ST depression
-percutaneous coronary intervention in last 6mo
-post MI angina
-recurrent sx despite maximal medical therapy.
Definition of MI includes....
-elevated CK-MB and/or Troponin
-PLUS at least one of the following
--sx of ischemia
--EKG changes consistent with new ischemia
--New Q waves
---imaging evidence of n ew wall motion abnormality