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Patho > Chronic Stable Angina and Acute Coronary Syndrome > Flashcards

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
Q

ACS: unstable angina

A

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
Q

ACS: MI

A

usually occur in presence of preexisting CAD

-STEMI = occlusive = ST elevation
-NSTEMI = nonocclusive

27
Q

STEMI

A

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
Q

NSTEMI

A

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
Q

Evolution of MI

A

-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
Q

Clinical manifestation of MI: pain

A

-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
Q

Clinical manifestation of MI: SNS

A

releases catecholemins
-diaphoresis
-raised HR and BP
-vasoconstriction or peripheral blood vessels
-Skin is ashen, clammy, and cool to touch

32
Q

Clinical manifestation of MI: Cardiovascular

A

-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
Q

Clinical manifestation of MI
Nausea
Fever

A

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
Q

MI healing process

A

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
Q

Complications of MIs: dysrhythmias

A

-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
Q

Complications of MI: HF

A

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
Q

Complications of MI: Cardiogenic shock

A

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
Q

Complications of MI:
Papillary muscle dysfunction or rupture
LV Aneurysm

A

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
Q

Complications of MI: Ventricular septal ruptures

A

New, loud systolic murmur
-HF and cardiogenic shock
-Needs emergency repair
-rare condition, but high death rate

40
Q

Complications of MI: Pericarditis

A

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
Q

Complications of MI: Dressler syndrome

A

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
Q

Diagnostic study of MI and UA: Cardiac catheterization

A

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
Q

Emergency care for ACS

A

ECG
Upright position
Oxygen kept above 93%
IV access
SL NGT and Aspirin
Morphine
Statin

44
Q

Care for ACS depending on ECG

A

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
Q

Immediate treatment for UA, NSTEMI, and STEMI

A

UA and NSTEMI
-heparin
-glycoprotein IIb/IIIa inhibitors before or during PCI

STEMI
-glycoprotein IIb/IIIa inhibitors during PCI

46
Q

Acute care of ACS

A

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
Q

Acute care drugs ACS

A

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
Q

Emergent PCI

A

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
Q

Advantages of PCI vs CABG

A

-faster reperfusion
alternative to surgery
-local anesthesia
-ambulatory sooner
-shorter LOS
-faster return to work

50
Q

Complications of PCI

A

-dissection or rupture of artery
-abrupt closure
-acute stent thrombosis
-failure to cross blockage
-extended infarct
-in stent restenosis

51
Q

Thrombolytic therapy

A

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
Q

Drug therapy

A

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
Q

Nursing management:
Pain
Monitoring
Rest?

A

Pain: NTG, morphine, O2

Monitor:
-ECG for vfib, PVCs, VT, ST segment
-VS, I&O, O2

Rest
-promote relaxation –> gradual increase in activity

54
Q

Nursing management: sex

A

ED drugs contraindicated with nitrates

Take prophylactic nitrates before sex

55
Q

Sudden cardiac death

A

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
Q

Manifestations of SCD

A

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
Q

SCD diagnosis

A

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
Q

Prevention of SCD

A

ICDs!!!!

Amiodarone

wearable cardioverter defibrillator (bridge to ICD or heart transplant)

CPR

Patho (44 decks)

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