Acute Coronary Syndrome Flashcards
RCA
1) cardiac muscle supplied (mechanical)
2) conducting tissue supplied (electrical)
1) R atrium/ventricle, portion of posterior and inferior surface of L ventricle
2) 55% SA node, 90% AV node
LAD
1) cardiac muscle supplied (mechanical)
2) conducting tissue supplied (electrical)
1) anterior wall of right and left ventricles, intraventricular septum
2) bundle branches
Circumflex artery
1) cardiac muscle supplied (mechanical)
2) conducting tissue supplied (electrical)
1) L atrium, L lateral ventricular wall
2) 45% SA node, 10% AV node
modifiable risk factors - cardiac
- smoking
- HTN
- T2DM
- obesity
- physical inactivity
- cholesterol
non modifiable risk factors for cardiac disease
- age > 55yrs for male, 65 yrs for female
- sex
- family hx
- ethnicity (south asian, african)
acute coronary syndrome
any constellation of clinical signs or symptoms suggestive of acute MI or unstable angina
what causes signs and symptoms to present in ACS?
imbalance in coronary oxygen supply and demand lasting greater than 10 mins
continuum of ACS
1) stable angina
2) unstable angina
3) NSTEMI
4) STEMI
unstable angina
- unanticipated, occurs at rest, might be transient and ECG could be normal.
- chest pain = 10-20mins
- ischemic event is not severe enough to cause myocardial necrosis
- may be temporary ST segment depression or T-wave inversion
- does not release cardiac biomarkers; no cell death
NSTEMI
- chest pain is greater than 20mins
- ischemic changes associated with ST depression or T wave inversion persisting after pain is relieved
- release of cardiac biomarkers and cell death occurs
- usually partial occlusion
STEMI
- severe chest pain lasting greater than 30 mins
- ischemic changes that are associated with ST elevation
- release of cardiac biomarkers and cell death occurs
- usually full occlusion
angina pectoris
chest pain that is cardiac in origin. crushing chest pain with radiation down left arm
atypical presentation of ischemic symptoms include ______ and are more common in _____
- SOB, weakness, fatigue, cold sweats, n/v, indigestion, doom, neck pain
- women, elderly, people with diabetes
angina pectoris s&s
- beneath sternum radiating into jaw/neck
- upper chest
- beneath sternum radiating into left arm
- epigastric/radiating into neck, jaw, arms
- left shoulder, inner aspect of both arms
- intrascapular
referred pain with angina pectoris
heart shares dermatomes with other areas of the body, so the brain perceives the pain as coming from other areas; may think cardiac pain is jaw, arm, neck discomfort
physiology of chest pain
ischemia -> chemoreceptors and mechanoreceptors activated in the heart -> stimulation of pain receptors -> signal to brain -> pain occurs
when are chemoreceptors activated in the heart?
when bradykinin is produced
when are mechanoreceptors activated in the heart?
when ischemic injury occurs (edema, myocardial stretch)
silent ischemia
- non painful ischemia common in older adults and diabetics
- you have defective afferent nerves and an increased pain threshold with reduced pain sensitivity hence no pain
layers of the vessels of the heart
1) tunica adventitia (CT)
2) tunica media (muscle)
3) tunica intima (endothelium)
role of endothelium
- prevents thrombus formation
- mediates immune and imflmtry response
- regulates vascular tone and growth
plaque formation
- atherosclerosis occurs as a result of endothelial injury
- chronic inflammatory condition
what can endothelial injury be caused by?
- cardiac risk factors
- chronic inflmtn from bacteria, viruses
- ineffective shear stress
pathogenesis of endothelial injury
injured endothelium = fatty streaks build up consisting of cholesterol, calcium = evolve into fibrous plaque that builds up in arterial lumen = causes thrombus formation and blocks artery = release of less nitric oxide which is a vasodilator and platelet inhibitor
shear stress
drag force exerted by flow against blood vessel
high shear stress
keeps tight junctions between endothelial cells (good stress)
low shear stress
allow for gaps between the endothelial cells which allows for
the infiltration of fatty substances/streaks (bad stress)
where do plaques occur more often at?
bifurcations or in acute angle curves ( areas of more turbulent flow)
what does the thickening of arterial vessel do?
decreases blood flow through the artery affecting myocardial O2 supply and elasticity of the blood vessel
chest pain differential diagnoses
- ACS
- aortic dissection
- PE
- tension pneumothorax
- pericardial tamponade
- esophageal rupture
role of 12 lead ECG
- Central to the diagnosis and evaluation of ACS
- Other lead placement is possible (15 lead, 18 or 24 lead)
- Provides info about ST segment and T wave changes in certain views
- Leads look at specific views of the heart
- Provides info about coronary flow
disruption in specific regions
T wave changes or flattening represents…
abnormal repolarization or ischemia/ischemic periods
ST depression and T wave inversion may indicate…
- Ischemic, injury, or partial thickness
infarct - Can be a precursor to ST elevation
- Usually means that there is a partial
blockage in the artery somewhere
ST elevation means…
- infarction, lack of O2 leading to tissue death, complete blockage in artery that extends through full thickness of myocardium
Wide QRS could mean
BBB or V-paced
Q wave
- indicates tissue necrosis
- Dead spot in the area of infarcted tissue
- Appears hours into the ischemic process
- Q waves with no ST elevation indicate previous MI
anterior infarction
LAD supplies the anterior walls of the L and R ventricles and the intraventricular septum
LAD occlusion - anterior wall of LV would cause…
- decreased contractility
- pump failure/cardiogenic shock (Decreased CO)
- pulm edema
- more prone to arryhthmias like ST, BBB, VT, VF
lateral infarction
circumflex artery supplies lateral wall left ventricle and sometimes posterior wall and SA node
occlusion risks with lateral infarction
- bradyarrythmias
- posterior wall involvement
inferior infarction
RCA supplies SA node (55%), AV node, bundle of HIS (90%); R ventricle and inferior wall
occlusion risks with inferior infarction
- heart blocks, junctional
- RV failure
right ventricular infarction and occlusion risks
- RCA supplies R ventricle and inferior wall
- cardiogenic shock and preload sensitive, so nitrates are contraindicated
- rarely occurs on own; usually occurs post- inferior/posterior infarction
reciprocal changes
happen in opposite direction of where MI is occurring
Posterior lead with ST elevation might show reciprocal changes in…
anterior and septal leads
Anterior lead with ST elevation might show reciprocal changes in…
inferior or posterior
Inferior lead with ST elevation might show reciprocal changes in…
lateral
Lateral lead with ST elevation might show reciprocal changes in…
septal or inferior
Septal lead with ST elevation might show reciprocal changes in…
none
how to dx MI
- look at pt presentation
- ECG changes - must be present in 2 or more leads
- cardiac biomarkers - are they elevated?
- cardiac cath
cardiac biomarkers
trops (T & I), CK-MB
troponin
- Proteins released from damaged cardiac cells
- Troponin T
- Troponin I – cardiac muscle cells
- Specific to the heart
- Elevation indicates heart damage
what is the abnormal result for trops? what do you know about trop peak and decline?
any value greater than 0.04. wont peak right away (takes hours to days) and declines hours after to baseline
CK-MB
release with muscle breakdown
and non specific
ACS management
*MONA
- reduce demand (rest, pain meds, reassurance, manage tachyarrythmias)
- increase supply (O2, nitroglycerin)
- prevent worsening (ASA 160-325)
- remove occlusion (PCI, fibrinolytics, CABG)
what is the goal of fibrinolytics?
To restore blood flow within 90
minutes of starting therapy
what is evidence of reperfusion?
- Angiography
- No chest pain
- ST segments baseline
- Reperfusion dysrhythmias (Self limiting)
selection criteria for fibrinolytics
- > 120 min transfer to PCI center
- Recent chest pain (<12hrs)
- Persistent ST elevation or new LBBB
- Ischemic chest pain unresolved by SL nitro
exclusion criteria for fibrinolytics
- Stable clots that may be disrupted (recent surgery, facial/ head trauma within 3 months)
- Uncontrolled HTN
- Recent ischemic stroke within 3 months except acute ischemic stroke within 3hrs
- active internal bleeding
- Previous hemorrhagic stroke at any time
- known intracranial neoplasm
- known structural cerebral lesion
- suspected aortic dissection
nursing management in fibrinolytic therapy agents
- Review health authority specific protocols for ax, VS frequency, 7Rs
- Limit risk of bleeding (adequate IV access prior to giving drug, avoid brushing teeth & shaving for 48hrs, limit injections, ++ pressure after venipuncture)
- Assess for intercranial and internal bleeding (changes in LOC, new bruising, blood in urine)
- Assess for extravasation
PCI: what is it and who are good candidates?
- Gold standard to reduce infarction and ischemia in STEMI
- 120 minutes from 911 to stent
- Candidates = STEMI, NSTEMI with >70% occlusion, unretractable angina
what are the different PCIs?
- balloon angioplasty and stent placement (risk of re-thrombosis: ax for new chest pain. may be drug eluting)
- long term dual platelet therapy (ASA and ticagrelor)
- thrombectomy (removal of clots in situations of large clot burden)
Post PCI nursing management
- ax pt for angina or new ST changes (vasospasm or re-occlusion)
- monitor for/prevent worsening AKI (contract dye from fluoroscope)
- monitor PCI puncture site for hematoma and blood flow (femoral: monitor for back pain = retroperitoneal bleeding. HOB < 30. bedrest 4-8hrs. keep leg straight. frequent neurovascular checks)
coronary artery bypass graft: what is it and what does it result in?
- Results in better perfusion for patients with multiple lesions or Left main lesions
- Removal of the saphenous or internal mammary vein and grafted to create a conduit around the
lesion
what are electrical complications post ACS?
1) sinus bradycardia and AV blocks (most common with inferior MIs)
2) sinus tachy (most common with anterior MIs d/t impaired LV pumping)
3) new onset afib (higher mortality and more complications post MI)
4) ventricular dysrhythmias (almost all ppl will experience PVCs, accelerated idioventricular is second most common)
what are mechanical complications post ACS?
1) aneurysm - rupture of LV free wall
2) interventricular septum rupture
3) papillary muscle rupture
4) HF
what are the 3 main evolutionary stages in an MI?
1) acute injury: time bw acute blockage and start of tissue death (ST elevation)
2) necrosis (Q wave, dead zone)
3) resolution (2 weeks later, persistent Q waves or inverted T waves)
