ACS Flashcards
Define unstable angina
Chest pain 10-20 mins
No myocardial necrosis therefore no biomarkers released
No ST elevation, with tissue ischemia there may be ST depression or T wave inversion
Partially occluded coronary artery
Define NSTEMI
Severe chest pain lasting >20 mins
Ischemic changes associated with ST depression and T wave inversion persist even after relief of pain
Cardiac biomarkers are released
Usually mostly injury with infarction not the complete thickness of the myocardium therefore recovery of injured cells is possible
Partial occluded coronary artery
Define STEMI
Severe chest pain lasting >30 mins
Ischemic changes to myocardium are associated with ST elevation >1mm
Cardiac biomarkers are released
Tissue injury and necrosis to full thickness of myocardium
Pronounced Q wave is possible
Total vessel occlusion- pain not relieved by nitro/rest/o2
What can new BBB indicate
Anterior and or septal STEMI
non modifiable risk factors of ACS
Age M>45, F>55
First degree family hx
Race Asian, black, native
Modifiable risk factors of ACS
Tobacco use Dyslipidemia - inc LDL, dec HDL HTN Inactivity Obesity (esp abdominal) DM Stress Excessive alcohol Metabolic syndrome Depression
What cluster of symptoms represents metabolic syndrome
Abdominal obesity, high serum blood glucose, dyslipidemia, HTN
Functions of the endothelium
blood compatible container, separating it from the tissues around it
regulates vascular tone and growth
regulates thrombosis and fibrinolysis
role in immune and inflammatory reactions
Name the 4 major coronary arteries and myocardial areas they vascularize
Circumflex - L atrium, lateral and posterior LV
LAD - Septum, anterior walls of LV
RCA(R marginal) - RV, posterior and inferior LV
RCA(posterior descending) - R atrium
Name 4 major coronary arteries and conduction systems they vascularize
Cirumflex - SA Node 50% and AV node 10%
LAD - Septum - contributes to BBB
RCA(R marginal) - AV Node 90%, proximal bundle of His
RCA(post descending) - SA node 60%
which leads look at inferior heart?
II, III, aVF
which leads look at L lateral heart?
I, aVL, V5, V6
which leads look at Anterior heart
V3, V4
which leads look at septum?
V1, V2
whats the role of nitric oxide in endothelium
is released by normal non injured endothelium, regulates vasodilation and inhibits platelet aggregation
what causes endothelial injury
ineffective shear stress, modifiable and nonmedifiable risk factors, chronic inflammation from bacteria and viruses
what is shear stress
drag force exerted by blood flow on endothelium
- when shear stress is ineffective, and in areas of turbulent flow, such as at bifurcations in blood vessels plaque forms
- low shear stress allows gaps in endothelial cells, nice place for plaque formation
atypical chest pain S/S?
- feeling unwell/fatigue
- nausea/epigastric pain
- indigestion
- neck pain
- jaw pain
- SOB
- Sense of impending doom
what signs on ECG indicate MI
- ST segment elevation, 1mm up, 1.5mm from J point
- pathologic Q waves, 1/3 the length of R and one little box across
- Q wave with no ST elevation indicates previous MI
what signs on ECG indicate myocardial ischemia/injury
ST segment depression, T wave inversion
Inferior infarct caused by blockage in what coronary artery
RCA leads II, III, aVF Feeds Inferior RV, post/inf LV -dec co. pump failure and dec contractility Feeds SA node -55%, AV 90% -SA pauses/arrests -AV blocks and bradycardia
Lateral infarct caused by blockage in what coronary artery
Circumflex leads I, aVL, V5, V6 Feeds Lateral LV -some dec contractility Feeds SA node at least partially -Sinus Pauses/arrests, leading -Bradydysrhythmias in secondary pacemakers
Septal infarct caused by blockage in what coronary artery
LAD leads V1, V2 Leads to rhythm and conducting problems -BBB -Junctional/Ventricular rhythms
Anterior infarct caused by blockage in what coronary artery
LAD leads V2-V4 Can cause: -Anterior LV disfunction causing -dec contractility -pump failure - dec CO -pulm edema -Rhythm changes such us ST. VT, VF
R ventricular infarct caused by blockage in what coronary artery
RCA
Leads V1R-V6R
Often occurs in conjunction with Inferior post infarct
Sensitive to preload
Absolute contraindications of thrombolytic therapy
BASS C-N-L
- Any hx of hemorrhagic stroke
- Ischemic stroke in past 3 months (>past 3 hrs)
- Known cerebral lesion
- Known intracranial neoplasm
- Active internal bleeding
- suspected aortic dissection
- Significant closed head or facial trauma, past 3 mths
Relative contraindications of thrombolytic therapy
HACSIS HTN, AC, CPR, Stroke, Intracranial path, Sx
- Severe uncontrolled hypertension
- Hx prior ischemic stroke >3mths, other intracranial pathology e.g. dementia
- Use of anticoagulants
- Traumatic/prolonged CPR
- Major sx < 3 weeks
Nursing considerations for throbolytic reperfusion therapy
- Have adequate IV access, as should not venipuncture within 24hrs of thrombolytics
- Ensure adequate cardiac output in order for drug to circulate
- No shaving/brushing teeth 24-48 hrs
- ensure pain relief and ST segment normalization post procedure
- No automatic BP cuffs, cause hematoma
- ongoing assessment for bleeds
Mechanical complications of MI
LV wall rupture - lethal - 1%
AV septum rupture - 0.5%
Papillary rupture - lethal 5% 2-7 days post MI
NOPQRST
N-ormal baseline O-nset of pain P-resipitating/palliating factors Q-uality of pain R-egion/radiation S-everity T-iming
Complications of MI
- cariogenic shock - dec contract of LV primarily, and or dec preload from atrial failure
- mechanical complications - ruptures
- emboli - PE, DVTs
- electrical complications - dysrhythmias depending on coronary involved and node perfusion problems
Aspirin for ACS
Single most important drug to prevent mortality in ACS
Mech of Act
-Blocks formation of Thromboxane A - preventing platelet aggregation
Effect on O2 S/D
-prevents platelet aggregation, thereby increasing intraluminal flow, allowing o2 rich blood to tissues/end organs
Contraindications
-GI bleed
-hypersensitivity
Nitro for ACS
Mech of Act
-Converts to nitric oxide - potent vasodilator, primarily venous effects
Effect on O2 S/D
-Increases venous capacitance, thereby dec preload, and contractility with starling’s law, decreasing myocardial o2 demand
-Coronary vasodilation - increased (or restores) supply
Contraindications
-Avoid in RV infarct
-Avoid in cardiogenic shock
Morphine for ACS
Mech of Act
-mimics endogenous endorphins-analgesic
Effect on O2 S/D
-vasodilatory effect - increase o2 supply to myocardium
- dec afterload
-Decreased pain-dec contractility-dec o2 demand
