Flashcards in Ch. 38 Acute Coronary Syndrome Deck (76):
Priorities of coronary syndrome?
Perfusion and comfort
Who can have painless MI’s?
Diabetics because of neuropathy
What typically accompanies coronary events?
Insufficient 02 supply to meet requirements of myocardium
Necrosis or cell death that occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue
How much exercise per week does the American Heart Association recommends?
What is the number one cause of cardiogenic shock?
-Poor Peripheral pulses and cool skin are signs and should be reported ASAP
Chronic Stable Angina (CSA) Pectoris
- Strangling of the chest
- Temporary imbalance between coronary artery’s ability to supply 02 ad cardiac muscle’s demand for 02
- Ischemia limited in duration and does not cause permanent damage to myocardial tissue
- Fixed Arterial plaque = slight limit in activity
- Relieved by rest and nitro, maybe CCB - decreased O2 demand, vasodilation
Acute Coronary Syndrome (ACS) patho:
Disruption of an atherosclerotic plaque with platelet aggregation and formation of an intracoronary thrombus
Believe that atherosclerotic plaque and coronary artery rupture’s, resulting in platelet aggregation, thrombus formation or vasoconstriction (Fig. 38-1, pg. 769)
How much occlusion do you need before blood flow is impeded?
#1 arterial occlusion
Damage to endothelial lining of artery
Unstable angina (UA)
- New onset - after exertion/increased demands of heart
- Exertion increases 02 demand of the heart
- Pts may present w/ ST changes on a 12-lead ECG but do not have changes in troponin levels
Variant (Prinzmetal’s) angina
- Coronary artery SPASM - usually have to rest
- Chest pain or discomfort
- ST segment elevation during attacks, resolves when pain gone
Examples of unstable angina
Variant (Prinzmetal’s) angina
Patients first angina symptoms, usually after exertion or other increased demands on the heart
Chest pain that occurs in the days or weeks before an MI
How will the T-wave look in hyperkalemia?
How will the T-wave look in hypokalemia?
Myocardial Infarction (MI)
- Most serious acute coronary syndrome
- Myocardial tissue abruptly and severely deprived of oxygen
- Average age 65 in men and 72 in women
Occlusions of blood flow:
Ischemia -> Injury -> Necrosis
Non-ST Elevation MI (NSTEMI)
- Ruled in through serial lab work
- ST and T wave changes, indicates myocardial ischemia
- Trops elevate over next 3 - 12 hours
- ECG changes or elevated troponin should match history and physical
Causes of NSTEMI:
- Coronary vasospasm
- Spontaneous dissection
- Poor blood flow
What does an ST and T-wave changes on a 12 lead ECG indicate?
What does the combination of changes on the ECG and elevation in cardiac troponin indicate?
Myocardial cell death or necrosis
ST elevation MI (STEMI):
- Indicates MI or necrosis
- ST elevation (duh)
- 100% occlusion!
- Medical EMERGENCY
- Needs immediate revascularization of blocked coronary artery
What is the number one cause of MI?
V. Fib - Pericardial thump them if witness arrest
Where do MIs often begin?
With infarction of the sub endocardial layer of cardiac muscle, which has the greatest oxygen demand and the poorest oxygen demand.
Zone of Injury
Tissue that is injured but not necrotic
Zone of ischemia
Tissues that is oxygen deprived
What is released in response to hypoxia?
- Catecholamines (epinephrine and norepinephrine)
- Pain may increase heart’s rate, contractility, and afterload
- These factors increase oxygen requirements in tissue that is already oxygen deprived, which may lead to life-threatening ventricular dysrhythmias
The actual extent of the zone of infarction depends on what three factors?
1. Collateral circulation
2. Anaerobic metabolism
3. Workload demands on the myocardium
Anterior walls MI produce what?
Bradycardia in pts
A dynamic process that does not occur instantly. Rather, it evolves over a period of hours
Infarction is necrotic
Hypoxemia from ischemia may lead to what?
Local vasodilation of blood vessels and acidosis
What may cause changes in normal conduction and contractile functions?
Potassium, calcium, and magnesium imbalances, as well as acidosis at the cellular level
When does obvious physical changes occur?
- Do not occur in the heart until 6 hrs after the infarction, when infarcted region appears blue and swollen.
- These changes explain the need for intervention within the first 4 to 6 hours of symptoms onset!!!
What happens after 48 hours of an MI?
Afters 48 hours, the infected area turns gray with yellow streaks as neutrophils invade the tissue and begin to remove the new products cell
What happens by 8 to 10 days after infarction?
Granulation tissue forms at the edge of the necrotic tissue
What happens over 2 to 3 months?
- The necrotic area eventually develops into a shrunken, thin, firm scar
- Scar tissue permanently change is the size and shape of the entire left ventricle, called ventricular remodeling.
Ventricular Remodeling Definition:
Decreases and causes what?
- Scar tissue that permanently CHANGES the size and shape of the entire left ventricle
- Remodeling may decrease left ventricular function, cause heart failure, and increase morbidity and mortality
Scarred tissue on the heart:
*HINT: Fails to do something
Scarred tissue does not contract, nor does it conduct electrically.
Thus this area is often the cause of chronic ventricular dysrhythmias surrounding the infarcted zone
Obstruction of the left anterior descending (LAD) artery causes what?
- Causes anterior or septal MIs because it perfuses the anterior wall and most of the septum of the left ventricle.
- Also causes PVCs/third degree heart block (Ig part left vent. involved)
- Patients with anterior wall MIs (AWMIs) have the highest mortality rate b/c they are most likely to have left ventricular failure and dysrhythmias from damage to the left ventricular
What does the circumflex artery supply?
The lateral wall of the left ventricle and possibly portions of the posterior wall or the sinoatrial (SA) and atrioventricular (AV) nodes.
What may the pt experience with an obstruction of the circumflex artery?
May experience a posterior wall MI (PWMI) or a lateral wall MI (LWMI) and sinus dysrhythmias
In most people, the right coronary artery (RCA) supplies what?
The SA and AV nodes, as well as the right ventricle and inferior or diaphragmatic portion of the left ventricle.
Pts with obstruction of the RCA often have what?
Causes damage where in the heart?
Nurse should obtain what?
- Have inferior wall MIs (IWMIs)
- About half of all inferior wall MIs are associated w/ an occlusion of the RCA, causing significant damage to the right ventricle
- Thus it is important to obtain a “right-sided” ECG to assess for right ventricular involvement
When are dysrhythmias treated?
When they cause hemodynamic compromise, increase myocardial oxygen requirements, or predispose the pt to lethal ventricular dysrhythmias
How will a pt w/ an inferior ACS present?
Nurse should monitor what?
If pt becomes hemodynamically unstable, what can be used?
- Bradycardia and second-degree atrioventricular (AV) blocks resulting from ischemia of the AV node.
- Rhythms tend to be intermittent
- Monitor cardiac rhythm and rate and the hemodynamic status
- If pt becomes hemodynamically unstable, a temporary pacemaker may be necessary
Pts w/ anterior ACS are likely to exhibit what?
What is a serious complication in this pt? Health care provider may insert what?
What should the nurse observe for?
- Premature Ventricular Contractions (PVCs) caused by ventricular irritability
- Third-degree or bundle branch block b/c it indicates that a large portion of the left ventricle is involved. Health care provider may insert a pacemaker. Observe pt closely to detect the development of HF.
Preventions of CAD:
Risk Factors for Metabolic Syndrome:
- Pts who have 3 or more of these factors are diagnosed w/ metabolic syndrome
- HTN (B/P of 130/85 mm Hg or higher OR taking antihypertensive drugs)
- Decreased HDL levels, usually w/ high LDL (HDL <45 for men or <55 for women OR taking anticholesterol drugs)
- Increased lvl of triglycerides (Either 160 mg/dL or higher for men or 135 for women)
- Increased fasting blood glucose (Either 100 mg/dL or higher OR taking antidiabetic drugs)
- Large waist size ( 40 inches or greater for men or 35 inches or greater for women)
Sx of MI in women?
- Not always experience crushing chest pain
- Indigestion, burning, pressure
- Jaw pain
- Pain between shoulders
Atypical angina sx in women:
- Unusual fatigue
- Breaking out in cold sweats
- Sudden fatigue, NV, lightheadedness
- Anxiety, epigastric pain
- Usually NSTEMI
Inter professional collab care
- Assessment- hx, sx present delay this until stabilized
- Pain assessment
- B/P q hr, temp up after infarction-necrosis and inflamm response
- Heart rhythm and heart sounds
- S3 GALLOP- HF, serious complications of MI
- Peripheral pulses
- Skin temp
- Psych.- denial delays care, fear or anxiety
- Old people assess LOC FIRST!
- Troponin T and I
- Chest x-ray not diagnostic for MI- CHF yes
- Thallium scans-radioisotope imaging to assess ischemia or necrotic muscle tissue related to angina or MI
- Contrast-enhanced cardiovascular magnetic resonance (CMR)
- 12-lead ECG- w/i 10 min of arrival (located location of ischemia/necrosis, STEMI, NSTEMI, abn. Q-wave signals myocardial necrosis)
- Echocardiogram - visualize heart structures
- ECG should be obtained w/i 10 min w/ pt w/ chest pain
- Cardiac catheterization - exact location of obstruction
- Computed tomography coronary angiography (CTCA)
- To determine oxygen demand
- If cannot exercise- Dobutamine
What to watch w/ stents?
- Watch for bleeding, hematomas - radial artery pressure dressing- radial/femoral artery- peripheral pulses!
- Distal to puncture- cap refill, warmth, sensation
Re-occlude 50% of the time- should not have chest pain post stent placement- ECG, VS, call the MD
Nitro- Increases collateral blood flow/redistributes blood to subendocardium/dilates coronary arteries, decreases preload and afterload, no phosphodiesterase inhibitors w/i 24-48 hrs (pulmonary HTN), hold if under 100 SB/P
Morphine Sulfate- comfort/decreases 02 demand and relaxes muscles/decreases circulating catecholamines, watch SE-Narcan, 02 maintain >90%, semi Fowler’s, quiet environment
- ASA inhibits platelet aggregation/vasoconstriction Cher 325
- Glycoprotein (CP) llb/llla inhibitors-unstable angina/NSTEMI- watch for bleeding/hypersensitivity reactions
- Antiplatelet clopidogrel prevents platelet aggregation
- Beta blockers- decreases size of infarct/dysrhythmias
- ACE Inhibitors
- Reperfusion therapy
- Thrombolytic therapy-fibrinolytics-dissolve clot/restore blood flow
- Percutaneous coronary intervention- reopen coronary
- ST segment changes will resolve- ECG changes
- Heparin 3-5 days, and ASA or enoxaparin (LMWH)
Thrombolytic Therapy- Fibrinolytics
- Dissolve clot/restore blood flow
- W/i 6 hrs of even and 30 min of arrival to ED
- Watch for bleeding-OB stool, neuro changes- brain bleed, distended abdomen, H&H changes
What is the primary factor in the development of CAD?
Numerous risk factors, both nomodifiable and modifiable, contribute to atherosclerosis and subsequently to CAD
What is the most important risk factor for developing CAD in women?
Health promotion efforts are directed toward what?
Controlling or altering modifiable risk factors for CAD
Is ischemic pain, it usually improves when the imbalance between oxygen supply and demand is resolved
Rest reduces tissue demands, and nitroglycerin improves oxygen supply
Associated sx: N/V, diaphoresis, dizziness, weakness, palpitations, and SOB
- Substernal chest discomfort:
>Radiating to the left arm
>Precipitated by exertion or stress (or rest in variant angina)
>Relieved by nitroglycerin or rest
>Lasting less than 15 min.
- Few, if any, associated sx
- Pain or discomfort:
>Substernal chest pain/pressure radiating to the left arm
>Pain/discomfort in jaw, back, shoulder, or abdomen
>Occurring w/o cause, usually in the morning
>Relieved only by opioids
>Lasting 30 min or more
- Frequent associated sx:
>Feelings of fear and anxiety
S3 gallop, which often indicates HF- serious and common complication of MI
S3 heart sound is heard w/ the bell of the stethoscope over the apex of the heart
Temp elevation for several days after infarction
High as 102 F may occur in response to myocardial necrosis, indicating the inflammatory response
What is the normal right atrial pressure?
- 1 to 8 mm Hg
- Lower pressure: hypovolemia, adm. fluid bolus. Diuretics are contraindicated!!
What is a major complication related to intra-arterial blood pressure?
- Hemorrhage at the insertion site
- HR will increase while B/P decreases
What is a complication after coronary artery bypass graft surgery?
Hypertension which can be dangerous because it puts too much pressure on the suture line and causes bleeding
What does wide and large Q-waves indicated in a ECG?
- Pt had an MI in the past
- Results from MI and necrotic ventricular cells that do not conduct electrical impulses.
Contraindications to thrombolytic therapy (absolute):
-Any prior intracranial hemorrhage
-Known structural cerebral vascular lesion (arteriovenous malformations)
-Known malignant intracranial neoplasm (primary or metastatic)
-Ischemic stroke w/i 3 months EXCEPT acute ischemic stroke w/i 3 hr
-Suspected aortic dissection
-Active bleeding or bleeding diathesis (excluding menses)
-Significant closed-head or facial trauma w/i 3 months
Contraindications to thrombolytic therapy (Relative):
-Hx of chronic, severe, poorly controlled HTN
-Severe uncontrolled HTN on presentation (SBP >180 mm Hg or DBP >110)
-Hx of prior ischemic stroke w/i 3 months, dementia, or known intracranial pathology not covered in contraindications
-Trumatic or prolonged (equal or less than 10 min) CPR or major surgery (w/i 3 wks)
-Recent (w/i 2-4 wks) internal bleeding
-Non-compressible vascular punctures
-For streptokinase/anistreplase: prior exposure (>5 days ago) or prior allergic reaction to these agents
-Active peptic ulcer
-Current use of anticoagulants; the higher the INR, the higher risk for bleeding