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Chronic Stable Angina and Acute Coronary Syndrome Flashcards

1
Q

What is chronic stable angina?

A

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)

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2
Q

sensations of angina

A

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

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3
Q

Timing of angina pain
ECG during angina event

A

-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

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4
Q

Silent ischemia

A

Ischemia that happens in absense of symptoms
-a/w DM
-confirmed with ECG
-same prognosis as regular ischemia

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5
Q

Prinzmetal’s (variant) angina

A

-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

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6
Q

Microvascular angina

A

-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

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7
Q

Goal of treatment

A

reduce O2 demand or increase O2 supply

-O2
-antiplatelet and lipid-lowering drugs
-nitrates
-ACE inhibitors
-B-blockers
-CCBs

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8
Q

Acute care for patient with angina

A

-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

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9
Q

Auscultation things

A

-S3 and S4
-new systolic murmur = ischemia of papillary muscle of mitral valve

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10
Q

Ambulatory care: Patient teaching

A

-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

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11
Q

Drug therapy
-aspirin
-short acting nitrates

A

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

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12
Q

Drug therapy: long acting nitrates

A

-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

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13
Q

Drug therapy
ACE inhibitors and ARBs
B-adrenergic blockers

A

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

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14
Q

Drug management
CCBs
Lipid lowering drugs
Sodium current inhibitor

A

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

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15
Q

Diagnostic studies

A

-12 lead ECG
-Labs: cardiac biomarkers, lipid profile, CRP
-chest xray
-echocardiogram
-excersise stress test
-electron beam CT
-Coronary CT angiogram

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16
Q

Cardiac catheterizations

A

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)

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17
Q

drugs for Stent placement procedure and post procedure

A

-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

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18
Q

Coronary artery bypass graft conditions

A

-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

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19
Q

Traditional CABG surgery

A

-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

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20
Q

Postop for CABG

A

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 (?)

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21
Q

Acute coronary syndrome

A

-prolonged ischemia
-not immediately reversible

Includes
-NonST elevation ACS = unstable angina and NSTEMI
-ST segment elevation myocardial infarction

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22
Q

Presentation of ACS on ECG

A

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

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23
Q

Total coronary occlusions

A

-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

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24
Q

ACS etiology and pathology

A

-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

25
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
26
ACS: MI
usually occur in presence of preexisting CAD -STEMI = occlusive = ST elevation -NSTEMI = nonocclusive
27
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
28
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
29
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)
30
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
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
Complications of MI: Ventricular septal ruptures
New, loud systolic murmur -HF and cardiogenic shock -Needs emergency repair -rare condition, but high death rate
40
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
41
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
42
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
43
Emergency care for ACS
ECG Upright position Oxygen kept above 93% IV access SL NGT and Aspirin Morphine Statin
44
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
45
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
46
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
47
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
48
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
49
Advantages of PCI vs CABG
-faster reperfusion alternative to surgery -local anesthesia -ambulatory sooner -shorter LOS -faster return to work
50
Complications of PCI
-dissection or rupture of artery -abrupt closure -acute stent thrombosis -failure to cross blockage -extended infarct -in stent restenosis
51
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
52
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
53
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
54
Nursing management: sex
ED drugs contraindicated with nitrates Take prophylactic nitrates before sex
55
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
56
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
57
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
58
Prevention of SCD
ICDs!!!! Amiodarone wearable cardioverter defibrillator (bridge to ICD or heart transplant) CPR

Patho (44 decks)

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