Chronic Stable Angina and Acute Coronary Syndrome Flashcards
What is chronic stable angina?
The clinical manifestation of MI that results from CAD
-MI happens when O2 demands are greater than the O2 supply
-usually happens bc 1+ coronary arteries are narrowed from atherosclerosis –> usually 70% or more (50% for L main coronary artery)
sensations of angina
intermittent chest pain that occurs over a long period with similar pattern of onset, duration , and intensity of symptoms
Onset: physical exertion, stress, or emotinal upset
Sometimes deny pain, but report presure, heaviness, or discomfort in chest –> might have dyspnea or fatigue
NO CHANGE IN BREATHING
Timing of angina pain
ECG during angina event
-lasts few mins
-goes away when you rest, calm down or use sublingual nitroglycerin
ST segment depression or T wave inversion during ischemia –> returns to normal when blood flow is restored
Silent ischemia
Ischemia that happens in absense of symptoms
-a/w DM
-confirmed with ECG
-same prognosis as regular ischemia
Prinzmetal’s (variant) angina
-rare
-happens at rest
-with or without CAD
-common w/ ppl who have migraines, Raynaud’s phenomenon, heavy smokers
-due to spasm of coronary artery from high intracellular Ca
-caused by alc/coke, vasoconstrictors, and cold
Treatment = moderate exercise, SL NTG, CCBs –> might go away by itself
Microvascular angina
-coronary MICROVASCULAR disease (syndrome X)
-chest pain w/o significant CAD or major coronary artery spasm
-s/w atherosclerosis or spasm of distal coronary branches
-common in women and happens w/ physical exertion
-treat same as CAD
Goal of treatment
reduce O2 demand or increase O2 supply
-O2
-antiplatelet and lipid-lowering drugs
-nitrates
-ACE inhibitors
-B-blockers
-CCBs
Acute care for patient with angina
-position upright and apply O2
-Assess VS and heart/breath sounds
-Continuous ECG monitor: 12 lead
-pain relief - NTG and IV opiods
-get cardiac biomarkers
-get xray
-provide support
Auscultation things
-S3 and S4
-new systolic murmur = ischemia of papillary muscle of mitral valve
Ambulatory care: Patient teaching
-Teach ab CAD, angina, risk factors, and how to avoid them (no extreme weather, rest after heavy meals)
-diet, physical activity (condition the heart- don’t stress it)
-med options
-psychological support
Drug therapy
-aspirin
-short acting nitrates
Aspirin
Short acting nitrates
-dilate peripheral and coronary arteries and collateral vessels
Sublingual nitroglycerin
-give 1 tablet or 1-2 metered sprays
-relief in 5 mins; duration 30-40 mins
-can repeat every 5 mins for up to 3 doses, then call EMS
-side effects = headache, dizziness, flushing, ortho-hypo
-can use prior to risky activity
Drug therapy: long acting nitrates
-used to reduce frequency of angina and treat Prinzmetal’s angina
-side effects = headache, ortho-hypo
Route
-oral
-NTG ointment
-transderm controlled release NTG
Allow 10-14 hr break from it to prevent NTG tollerance
Drug therapy
ACE inhibitors and ARBs
B-adrenergic blockers
ACE and ARB
-vasodilation and reduced blood volume
-prevent or reverse ventricular remodeling
-use ARB if you can’t use ACE
B-adrenergic blockers
-reduced myocardial contractility, HR, SVR, and BP
-side effects = bradycardia, hypotension, wheezing, GI issues, weight gain, depression, fatigues, and sex issues
-Don’t use if severe bradycardia or acute decompensated HF
-Use cautiously if asthma and DM
Drug management
CCBs
Lipid lowering drugs
Sodium current inhibitor
CCBs
-systemic vasodilation w/ reduced SVR
-reduced heart contractility
-coronary casodilation
-reduced HR
-causes fatigue, headache, dizziness, flushing, edema
Sodium current inhibitor
-used when inadequate response to antianginal drugs
-dizziness, nausea, constipation, headache
Diagnostic studies
-12 lead ECG
-Labs: cardiac biomarkers, lipid profile, CRP
-chest xray
-echocardiogram
-excersise stress test
-electron beam CT
-Coronary CT angiogram
Cardiac catheterizations
gold standard to identify and localize CAD
-visualize blockages
-open blockages
Coronary revascularization with PCI
-balloon angioplasty
-Intracoronary stents: bare metal or drug eluting (prevents neointimal hyperplasia)
drugs for Stent placement procedure and post procedure
-used to prevent platelet aggregation and acute stent thrombosis
During PCI
-unfractionated heparin or low-molecular weight heparin
-direct thrombin inhibitor and/or glycoprotein IIb/IIIa inhibitor
After PCI
-Dual antiplatelet therapy (DAPT) = aspirin and ticagrelor or clopidogrel
RISK OF BLEEDING
Coronary artery bypass graft conditions
-med treatments failed
-disease involves left main coronary artery or 3 vessels
-PCI can’t be done
-failed PCI or chest pain continues
good option for those w/ diabetes, LV dysfunction, CKD
Traditional CABG surgery
-arterial or venous grafts placed from aorta/branch to heart muscle distal to blockage
grafts taken from internal mammary artery, saphenous vein, and/or radial artery
This surgery requires sternotomy and cardiopulmonary bypass
Postop for CABG
ICU for 24 to 36 hrs
-hemodynamic monitoring
-arterial line for BP monitoring
-pleural and mediastinal chest tubes
-continuous ECG
-ET tube to ventilator
-epicardial pacing wires
-urinary catheter
-NG tube
**Afib is common after surgery –> start BB asap
**Post operative Cognitive Dysfunction can last months after surgery
**young ppl fare worse than old ppl (?)
Acute coronary syndrome
-prolonged ischemia
-not immediately reversible
Includes
-NonST elevation ACS = unstable angina and NSTEMI
-ST segment elevation myocardial infarction
Presentation of ACS on ECG
ST elevations on ECGs are prob STEMIS
-compare to previous ECG if possible
-ST elevation = potentially reversible MI, but will result in necrosis if untreated
UA of NSTEMI - may or may not have ST segment depression and/or T wave inversion
-if not, can’t distinguish bt the two w/o serum biomarkers
Total coronary occlusions
-heart becomes hypozic within 10 s
-anaerobic metabolism leads to lactic acid accumulation
-heart cells viable 20 mins; then irreversible damage if no collateral circulation
if reperfused, aerobic metabolism and contractility restored and cells repaired
ACS etiology and pathology
-deterioration of once stable plaque leads to rupture, platelet aggregation, and thrombus
Result
-partial occlusion of coronary artery = UA or NSTEMI
-total occlusion of coronary artery = STEMI
ACS: unstable angina
Chest pain
-new onset; occurs at rest; increase frequency/duration/ less effort
-can be first clinical sign of CAD
-pain lasting over 10 mins
unpredictable –> needs immediate treatment
-ECG show ST depression and/or T wave inversion = ischemic changes
ACS: MI
usually occur in presence of preexisting CAD
-STEMI = occlusive = ST elevation
-NSTEMI = nonocclusive
STEMI
EMERGENCY
-artery must be opened w/in 90 mins w/ either PCI or thrombolytic agent
-thrombolytic agent usually used in hospitals w/o cath lab
-Echo shows hypokinesis (bad contractility) or akinesis (no contraction) of necrotic areas
NSTEMI
still a big deal, but not as time sensitive
-Get a PCI w/in 12-72 hrs
-don’t use thrombolytics
-Echo for same reasons as STEMI
Evolution of MI
-takes hours to days
-Subendocardium gets ischemic first
-entire thickness of heart muscle becomes necrotic w/in 4-6 hrs (takes 12 hrs if only partial occlusion)
Severity is influenced by degree of collateral circulation (that’s why young ppl do worse)
Clinical manifestation of MI: pain
-severe chest pain unrelieved by rest, position change, or nitrates (often substernal or epigastric but may radiate)
-usually in the morning for more than 20 mins
-no pain if DM
Clinical manifestation of MI: SNS
releases catecholemins
-diaphoresis
-raised HR and BP
-vasoconstriction or peripheral blood vessels
-Skin is ashen, clammy, and cool to touch
Clinical manifestation of MI: Cardiovascular
-At first: high HR and BP –> then both lower (secondary to decrease in CO)
-less renal perfusion = less peeing
-crackles = LV dysfuction
-JVD, hepatic engorgement, edema
-S3 or S4
-holosystolic murmur
Clinical manifestation of MI
Nausea
Fever
Vomiting
-reflex stimulation of vomiting center by severe pain
-vasovagal reflex
Fever
-up to 100.4 in first 24-48 hrs; up to 4-5 days
-systemic inflammatory process caused by heart cell death
MI healing process
Inflammatory process
-w/in 24 hrs leukocytes infiltrate areas of necrosis
-proteolytic enzymes of neutrophils and macrophages remove necrotic tissue by day 4, resulting in thin heart wall
Catecholamine-mediated lipolysis and glycolysis for myocardiumm to use during anaerobic respiration (increases blood glucose)
Necrotic zone identifiable by ECG changes
Collagen matrix/ scar tissue laid down by day 10-14 (weak though)
Heart is vulnerable to tress –> carefully monitor patient
@6 weeks, healed, but not complient
Ventricular remodeling –> normal myocardium hypertrophies and dilates to try to compensate for infarcted muscle –> take ACE inhibitors to stop it
Complications of MIs: dysrhythmias
-most common one
-happens in 80-90% of patiets
-can be caused by ischemia, electrolyte imbalance, or SNS stimulation
-VT and VF are most common cause of death in prehospitalization period
Complications of MI: HF
Due to decreased pumping power
Left sided
-mild dyspnea, restlessness, agitation, or slight tachycardia
-pulmonary congestion on xray
-S3, S4, crackles
-nocturnal dyspnea and orthopnea
Right sided
-JVD, hepatic congestion, lower extremity edema
Complications of MI: Cardiogenic shock
Decreased O2 and nutrients related to
-severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction
Requires aggressive management to
-increase O2 delivery, decrease O2 demand, and prevent complications
-highest death rate
Complications of MI:
Papillary muscle dysfunction or rupture
LV Aneurysm
Papillary muscle
-causes acute and massive mitral valve regurgitation –> systolic murmur
-aggravates an already compromised LV = decreased CO
LV aneurysm
-myocardial wall is thin –> bulges during contraction –> might rupture and hide thrombi
-leads to HF, dysrhythmias, and angina
Complications of MI: Ventricular septal ruptures
New, loud systolic murmur
-HF and cardiogenic shock
-Needs emergency repair
-rare condition, but high death rate
Complications of MI: Pericarditis
inflammation of pericardium
-mild to severe chest pain with inspiration, coughing, or upper body movement
-feels better when leaning forward
-Pericardial friction rub, fever, low BP, ECG changes
-Treat with lots of aspirin
Complications of MI: Dressler syndrome
Pericarditis and fever that develops in 1-8 weeks after MI –> maybe autoimmune
-chest pain, fever, malaise, pericardial friction rub, arthralgia, high WBC and sedimentation rate
-Treat with high dose aspirin
Diagnostic study of MI and UA: Cardiac catheterization
Needed w/in 90 mins for STEMI (or they can have thrombolytics w/in 30 mins)
Needed w/in 12-72 hrs for UA or NSTEMI
May have PCI, medical therapy, or referral for CABG depending on findings
Emergency care for ACS
ECG
Upright position
Oxygen kept above 93%
IV access
SL NGT and Aspirin
Morphine
Statin
Care for ACS depending on ECG
If ECG shows ST elevation, take patient to cath lab for PCI or thrombolytic therapy
If ECG shows ST depression or T wave inversion, take to critical care or telemetry unit
Dysrhythmias treated according to agency
Monitor serum biomarkers
Immediate treatment for UA, NSTEMI, and STEMI
UA and NSTEMI
-heparin
-glycoprotein IIb/IIIa inhibitors before or during PCI
STEMI
-glycoprotein IIb/IIIa inhibitors during PCI
Acute care of ACS
Admit to ICU/telemetry unit
-monitor VS and pulsox
-continuous ECG
-12 lead ECG
-cardiac biomarkers
-bed rest/limit activity for 12-24 hrs and then gradually increase
Acute care drugs ACS
Heparin = UA and NSTEMI
DAPT = NSTEMI and UA with stent
Aspirin = UA
Cardiac caheterization = UA and NSTEMI (then maybe PCI, CABG, or meds)
Reperfusion therapy = STEMI
-emergent PCI
-Thrombolytic therapy
Emergent PCI
First treatment with confirmed STEMI
-goal = open blocked artery w/in 90 mins
-BSM or DES
If severe LV dysfunction, IABP and/or inotropes
Maybe emergent CABG
Advantages of PCI vs CABG
-faster reperfusion
alternative to surgery
-local anesthesia
-ambulatory sooner
-shorter LOS
-faster return to work
Complications of PCI
-dissection or rupture of artery
-abrupt closure
-acute stent thrombosis
-failure to cross blockage
-extended infarct
-in stent restenosis
Thrombolytic therapy
For STEMI
-more readily available in some places
-meds open blocked arteries by lysing thrombus
-allows for transfer to PCI hospital if possible w/in 2 hrs
Risk for bleeding
Done if chest pain less than 12 hrs and ECG shows STEMI
When reperfusion occurs
-st returns to normal
-no chest pain
-spike of serum biomarkers
-dysrhythmias sometimes
Major concern is reocclusion and bleeding
-IV heparin
-monitor for chest pain and ECG changes
Goal: limit size of infarction and give w/in 30 mins
Drug therapy
Suspected ACS
-Antiplatelet therapy, IV NTG, and atorvastatin
-Also MNA, antidysrhythmic drugs, lipid-lowering drugs, stool softeners
NSTEMI or UA
-anticoagulation and glycoprotei IIb/IIIa
MI
-DAPT, aspirin, BB, CCB, ACE inhibitor, nitrates
Nursing management:
Pain
Monitoring
Rest?
Pain: NTG, morphine, O2
Monitor:
-ECG for vfib, PVCs, VT, ST segment
-VS, I&O, O2
Rest
-promote relaxation –> gradual increase in activity
Nursing management: sex
ED drugs contraindicated with nitrates
Take prophylactic nitrates before sex
Sudden cardiac death
unexpected death from heart issues –> usually 1 hr after symptom onet
Usually dysrhythmias cause disruption in cardiac func resulting in loss of CO and cerebral flow
Most often caused by
-CAD
-structural heart disease
-conduction disturbance
Manifestations of SCD
angina, palpitations, dizziness, lightheadedness
Happens in ppl w/ old MI or acute MI
If they survive, higher risk for another event –> should get ICD after 40 days of medical therapy
LV dysfunction (EF<30%) is strong indication for ICD need
SCD diagnosis
Rule out or confirm MI
-serial cardiac biomarkers
-serial ECGs
-cardiac catheterization
-PCI or CABG if indicated
-EPS
-Outpatient monitor, Mobile Cardiac Outpatient Telemetry, or implanted monitor
Prevention of SCD
ICDs!!!!
Amiodarone
wearable cardioverter defibrillator (bridge to ICD or heart transplant)
CPR
