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Pn3 - RN > T3 Acute Coronary Syndrome > Flashcards

T3 Acute Coronary Syndrome Flashcards

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1
Q

Includes stable angina and acute coronary syndromes (ACS)

  • Insufficient oxygen 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?
A

Ischemia*

Infarction*

Coronary artery disease

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2
Q

Broad term that includes chronic stable angina and ACS.

It affects the arteries the provide blood, oxygen, and nutrients to the myocardium.

When blood flow is blocked ischemia and/or infarction occur.

??? is also called coronary heart disease (CHD) or heart disease and is the single largest killer of men and women in all ethnic groups.

A

Coronary artery disease

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3
Q

Temporary imbalance between coronary artery’s ability to supply oxygen and cardiac muscle’s demand for oxygen

Ischemia limited in duration and does not cause permanent damage to myocardial tissue*

Improves with nitro and rest*

Chest discomfort that occurs with moderate to prolonged exertion. Pattern is familiar to the patient: frequency, duration, and intensity remain the same.

Results in slight limitation of activities
Fixed atherosclerotic plague
Usually relieved by rest or nitro

Rule out musculoskeletal pain

A

CSA -chronic stable angina pectoris

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4
Q

Includes:*

  • Unstable angina
  • Acute myocardial infarction

Believed that atherosclerotic plaque in coronary artery ruptures, resulting in platelet aggregation, thrombus formation, or vasoconstriction

The amount of disruption determines the degree of obstruction
The artery has to have at least 40% plague accumulation before it starts to block blood flow.

A

Acute coronary syndrome

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5
Q

Typical symptoms of ACS?

A

Chest discomfort
Shortness of breath
Nausea
Considerations (women, DM)*

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6
Q

Chest pain that occurs at rest or with exertion and causes activity limitations*

Includes a variety of disorders*:

  • New-onset angina
  • Variant (Prinzmetal’s) angina
  • Pre-infarction angina

Patients present with ST changes on 12-lead ECG, but will not have changes in troponin or CK levels*

Unlike chronic angina, the number of attacks and intensity increases over time.

Pressure may last longer than 15 minutes

Poorly relieved by nitro or rest
Ischemia is present but not severe enough to cause detectable myocardial damage

A

Unstable angina

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7
Q

first episode of angina, usually after exertion

A

New onset angina:

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8
Q

caused by coronary artery spasm and occurs after rest

A

Variant

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9
Q

chest pain that occurs in the days or weeks before MI

A

Pre-infarction

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10
Q

Most serious acute coronary syndrome

Myocardial tissue abruptly and severely -deprived of oxygen*

Occlusion of blood flow
-Ischemia ➡ injury ➡ necrosis

Two types:*
STEMI
NSTEMI

A

Acute MI or AMI

Undiagnosed or untreated angina leads to MI

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11
Q

NSTEMI

Ecg changes ?

Lab photos ?

Causes?

A

Non-ST segment elevation MI

ST and T wave changes

  • ST depression
  • Inverted T wave

Troponin elevates over 3-12 hours

Causes: vasospasm, dissection, sluggish blood flow

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12
Q

STEMI

EKG changes

Indications

Causes

A

ST elevation MI
ST elevation in two correlated leads on EKG

Indications MI/necrosis

Causes: rupture of fibrous atherosclerotic plaques and platelet aggregation and thrombus

The thrombus causes 100% blockage. Medical emergency and requires immediate revascularization

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13
Q

Zone of ischemia, zone of injury, and zone of infarction, shown through ECG waveforms and reciprocal waveforms corresponding to each zone.

Initial area of infarction (zone of necrosis)
Zone of injury: tissue is injured but not necrotic
Zone of ischemia: tissue is oxygen deprived

The patients response to an MI depends on which artery was obstructed and which part of the ventricle was damaged.

Left anterior descending (LAD) feeds the anterior/septal wall of left ventricle. Highest mortality rate due to left ventricular failure. Widow maker

Right coronary artery (RCA) feeds SA and AV nodes

Infarction does not occur instantly, evolves over several hours

Zone of ischmiea:??

Zone of injury: ??

Zone of necrosis: ??

A

Zone of ischmiea: t-wave inversion

Zone of injury: ST elevation

Zone of necrosis: abnormal Q

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14
Q

MI highest mortality rate d/t

The patients response to an MI depends on ?

A

Highest mortality rate due to left ventricular failure. Widow maker

which artery was obstructed and which part of the ventricle was damaged.

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15
Q

Cause and genetic risk for atherosclerosis

A 
Non-modifiable 
-Age
-Gender
-Family history
-Ethnic background
Prevalence higher in Mexican Americans, American Indians, and Alaska Natives
————

Atherosclerosis is the primary factor in development of CAD.

Age is the most important risk factor for developing CAD in women. Average age for men is 65 and women is 72

Metabolic syndrome is recognized as a risk factor for CV disease. Table 38-1, patients have 3 or more factors have metabolic syndrome

Hypertesion, decreased HDL, increased triglycerides, increased fasting BG, large waist size

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16
Q

MI

Initial area of infarction
Zone of injury:
Zone of ischemia:

A

Initial area of infarction (zone of necrosis)
Zone of injury: tissue is injured but not necrotic
Zone of ischemia: tissue is oxygen deprived

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17
Q

Modifiable risk factors of MI

A 
Elevated serum cholesterol
Cigarette smoking
Hypertension
Impaired glucose tolerance/DM
Obesity
Excessive alcohol
Limited physical activity
Stress

Diabetes mellitus

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18
Q

Health promotion and maintenance of mi

A

Directed towards altering modifiable risk factors
Implement health teaching
STEMI is common cause of sudden cardiac death
-95% of SCD do not survive (v-fib)
-AED use in community

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19
Q

Mi physical assessment

Hx?

When to delay interventions for tx?

? is common in the first few hours after an MI

A 
If symptoms are present: delay until interventions for symptoms relief, vital signs, or dysrhythmias*
-History
-Physical assessment
Pain assessment
BP and HR
Heart rhythm and heart sounds
Peripheral pulses
Skin temperature
Detailed pain assessment

History: full PQRST of pain: goal is pain free. Family history, risk factors, tobacco use

Rapid physical assessment is critical: differentiate among types of chest pain

Sinus tach with PVCs is common in the first few hours after an MI

Chart 38-2 symptoms list compared between angina and MI

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20
Q
  • 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 minutes
  • Few, if any, associated symptoms
A

Angina

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21
Q
  • Pain or discomfort:
  • Substernal chest pain/pressure radiating to the left arm
  • Pain or discomfort in jaw, back, shoulder, or abdomen
  • Occurring without cause, usually in the morning
  • Relieved only by opioids
  • Lasting 30 minutes or more
  • Frequent associated symptoms:
  • Nausea/vomiting
  • Diaphoresis
  • Dyspnea
  • Feelings of fear and anxiety
  • Dysrhythmias
  • Fatigue
  • Palpitations
  • Epigastric distress
  • Anxiety
  • Dizziness
  • Disorientation/acute confusion
  • Feeling “short of breath”
A

MI

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22
Q

Important to differentiate between muscular pain and cardiac pain

How?

A

True

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23
Q

Common in women and diabetics

Symptoms:
Indigestion
Aching jaw
Unusual fatigue
Dyspnea
A

Atypical angina

24
Q

Mi Psychosocial assessment

A

Denial
Fear
Anxiety
Depression

Denial: story
Average patient waits 2 hours to seek help

25
Q

MI laboratory assessments

A

Laboratory*

-Troponin T and troponin I

Imaging assessment

12-lead electrocardiograms
-Within 10 minutes*

Cardiac catheterization*

  • Determine extent and location
  • Can lead to PCI (percutaneous coronary intervention) or CABG

Troponin is specific to MI and cardiac necrosis, rise quickly
Chest xrays to rule out other causes but not diagnostic of MI

EKGs are essential! To diagnose STEMI, location

Stress test: evaluate EKG changes during activity

26
Q

Ekg changes in MI

When do angina associated ekg changes go away?

A

Stable angina episodes result in ST depression, T-wave inversion, or both*

Variant angina causes ST elevation

Infarction causes ST elevation in STEMI but is absent in NSTEMI*

Q wave due to necrotic cells

EKG changes associated with angina subside when pain is gone

27
Q

Priority problems in MI

A

Acute pain

Decreased myocardial tissue perfusion

Decreased functional ability

Decreased ability to cope

Potential for dysrhythmias

Potential for heart failure

28
Q

Pain prevention Interventions for MI

A 
Pain management*
MONA*
Morphine sulfate
Oxygen
Nitroglycerin
Aspirin

Position of comfort; semi-Fowler’s position

Quiet and calm environment

Assess pain using PQRST

29
Q

Time window for interventions for MI

A

4-6 hour window for PCI for NSTEMI, 60-90 minutes for STEMI

30
Q

Pain relief does what for MI

A

increases oxygen supply and decreases myocardial oxygen demand.

31
Q

Nitro: increases collateral blood flow and dilates coronary arteries. Decreaes myocardial oxygen demand by peripheral vasodilation

Considerations for nitro:

A

blood pressure,

IV access,
interacting drugs,

3 doses total, 5 min apart,

headache,

pins and needles sensation

Sit down

32
Q

Drug relaxes smooth muscle, decreases myocardial oxygen demand.

A

Morphine

33
Q

Oxygen for hypoxia (keep greater than 90%). Use of oxygen in the absence of hypoxemia

Decrease oxygen =

A

increases coronary vascular resistance, decreases coronary blood flow, and increases mortality

34
Q

Other interventions and drug therapy for MI

A

-Increasing tissue perfusion

-Drug therapy* (Chart 38-4)
ASA
Glycoprotein (GP) IIb/IIIa inhibitors
Antiplatelets
Beta blockers (BBs)*
Angiotensin receptor blockers (ARBs)
Angiotensin converting enzyme inhibitors (ACEIs)

ASA 81-324 mg baby aspirins chewed, inhibits platelet aggregation and vasoconstriction, antiplatelet effect begins with 1 hour

Glycoprotein inhibitors (reopro, integrillin) prevents fibrinogen from attaching to platelets. Maintain patency of artery

Antiplatelets (Plavix, p2y12 inhibitors) given with initial loading dose followed by daily dose. Prevent platelets from aggregating, shown to decrease risk of recurrent MI

Anticoagulation: prevent clot formation

Beta blockers: decrease the size of the infarct, decrease vent dysrhythmias, and decrease mortality rates. The heart can perform more work without ischemia. Read beta blocker section on 777

ACE or ARBs within 48 hours if ejection fraction is less than 40% and have HTN, diabetes, kidney disease, etc

Calcium channel blockers: promote vasodilation and perfusion. Indicated for variant angina, not indicated after MI unless beta blockers are contraindicated

Statins: reduce risk of recurrent MI

35
Q 
ASA
Glycoprotein (GP) IIb/IIIa inhibitors
Antiplatelets
Beta blockers (BBs)*
Angiotensin receptor blockers (ARBs)
Angiotensin converting enzyme inhibitors (ACEIs)
A

ASA 81-324 mg baby aspirins chewed, inhibits platelet aggregation and vasoconstriction, antiplatelet effect begins with 1 hour

Glycoprotein inhibitors (reopro, integrillin) prevents fibrinogen from attaching to platelets. Maintain patency of artery

Antiplatelets (Plavix, p2y12 inhibitors) given with initial loading dose followed by daily dose. Prevent platelets from aggregating, shown to decrease risk of recurrent MI

Anticoagulation: prevent clot formation

Beta blockers: decrease the size of the infarct, decrease vent dysrhythmias, and decrease mortality rates. The heart can perform more work without ischemia. Read beta blocker section on 777

ACE or ARBs within 48 hours if ejection fraction is less than 40% and have HTN, diabetes, kidney disease, etc

Calcium channel blockers: promote vasodilation and perfusion. Indicated for variant angina, not indicated after MI unless beta blockers are contraindicated

Statins: reduce risk of recurrent MI

36
Q

Reperfusion therapy in MI

A

Thrombolytic therapy: uses fibrinolytics to dissolve thrombi (TPA IV or intracoronary)

PCI is defitive treatment. Includes balloons, stents, etc. IV heparin is used after PCI to maintain patent artery

37
Q

Percutaneous coronary intervention 1-4?????

Invasive but nonsurgical, perform within 90 minutes.
Combines clot retrieval and stent placement

Patients benefit from PCI if they:

A

Coronary angiogram:

have single of double vessel, discrete proximal, noncalcified lesions or clots.

38
Q

??? keep artery open.
Without ??? the artery would reocclude.

Patients with PCI need dual antiplatelet therapy (ASA and antiplatelet)

A

Coronary stent

39
Q

A client is scheduled for a cardiac angiogram. Which of the following should the nurse instruct the client about this diagnostic test?

A

A. It is noninvasive.

B. Contrast dye is injected.

C. Clients can move about after the procedure.

D. General anesthesia is used.

40
Q

Most common type of cardiac surgery and most common procedure for older adults
The occluded vessels are bypassed with patients own vessel grafts or synthetic grafts. Internal mammary artery is graft of choice and has excellent patency rates.

A

Coronary Artery Bypass Graft

41
Q

Cardiopulmonary bypass

Postoperative care

A

Chest tube care
Pacer wires
Manage fluid and electrolyte imbalance

42
Q

Other potential complications*

Of Cardiopulmonary bypass?

A 
Hypothermia
Hypotension/Hypertension
Dysrhythmias
Cardiac tamponade
Sternal infection
Pain
43
Q

MI surgical management

A

Minimally invasive direct coronary artery bypass (MIDCAB)

Endoscopic vessel harvesting

Transmyocardial laser revascularization

Off-pump coronary artery bypass

Robotic heart surgery

44
Q

Post MI interventions

Most desired outcome?

A 
Increasing functional ability
-Cardiac rehabilitation
Increasing ability to cope
Identifying and managing dysrhythmias*
-Dysrhythmias are the leading cause of prehospital death in most patients with ACS.

Monitor for heart failure*

Cardiac rehab actively assists patient with achieving and maintaining a vital and productive life

Learn to cope with cardiac event and lifestyle changes. Allow expression of anxiety, assess coping mechanisms

Most desired outcome is free of dysrhythmias: identify and managed early. Dysrhythmias ar leading cause of prehospital death. 95% of sudden cardiac arrests are vfib

Manage heart failure: decreased cardiac output is common. Most severe case is cardiogenic shock and causes most inhospital deaths after ACS.

45
Q

A 70 year-old man has been having periods of chest pain and pressure that have been ignored until he became short of breath and diaphoretic with the episode of chest pain. The patient called 911 and was taken to the ED
As his ED nurse, what is your first action in response to his report of chest pain?
The provider prescribes nitroglycerin. What assessment will you perform before giving nitro and why? What route do you anticipate?
What other drugs might be ordered?
The patients EKG shows ST elevation and the patient has elevated troponins. What do you anticipate in the care of this patient?

A

?

46
Q

Monitoring/managing heart failure

S/s

A

Decreased cardiac output due to heart failure is a common complication after an MI *

  • Left ventricular dysfunction
  • Rupture of intraventricular septum

Symptoms include: pulmonary edema (crackles), frothy sputum, wheezing, tachypnea

Monitor for cardiogenic shock*
-Cold, clammy skin, poor peripheral pulses, agitation, pulmonary congestion, tachypnea, hypotension, tachycardia, decreased urine output

47
Q

Managing hf with drugs?

A 
Heart failure is classified as class I-IV. Class I is lowest  and can be treated with preload reduction, diuretics, nitrates.
Class II and III require more aggressive treatment such as afterload reduction and enhanced contractility.

Inotropes such as dobutamine and milrinone increase of contraction (may increase oxygen demand)
Class IV is cardiogenic shock. Necrosis of more than 40% of left ventricle

Right ventricular failure: 1/3 of patients, inferior MI. clear lungs, JVD. Give fluids

48
Q

Inter professional care with MI

A

Cardiac rehab
Medication education
Risk factor modification
When to seek medical care

*Risk factor modification is essential

Seeking medical assistance: HR less than 50, wheezing, weight gain >1-2 lbs, increased nitro use, shortness of breath, dizziness,
Chest pain not relieved after nitro

49
Q

Paramedics arrive at the ED with a 78-year-old man who presents with severe chest pain. In triage, he reports that he experienced chest pain for several hours before calling 911. He reports that he takes “heart medications” but he does not know their names. He rates his chest pain as a 9 on a 0-to-10 scale. Patient history includes an MI 6 years ago that resulted in stent placement for severe CAD. One stent was placed in the LAD and another in his circumflex artery. He states that his health care provider told him he also has heart failure.

What laboratory tests do you anticipate the provider will order for this patient?

A

ANS: While there is no single ideal test to diagnose MI, the most common laboratory tests include troponins T and I, creatine kinase-MB (CK-MB), and myoglobin. These cardiac markers are specific for MI and cardiac necrosis. Troponins T and I and myoglobin rise quickly. CK-MB is the most specific marker for MI, but does not peak until about 24 hours after the onset of pain. CAD, coronary artery disease; LAD, left anterior descending artery.

50
Q

Two hours later, the patient is admitted to the cardiac stepdown unit with orders for a saline lock, cardiac diet, and oxygen at 2 L per nasal cannula with follow-up cardiac enzymes, and 12-lead ECG in 6 hours. One hour later, the patient reports severe shortness of breath. His oxygen saturation has dropped to 88%, BP is 96/54, and his monitor shows sinus tachycardia with a rate of 114. He reports mild chest pain.

What do you suspect is happening to the patient at this time?
The patient’s laboratory values include troponin T 0.6 mg/mL. What is your best interpretation of this finding?

A

ANS:
Based on the history of the recent CP and now increased shortness of breath with hypoxemia, the nurse can conclude that the patient may be experiencing heart failure.
Troponin T is elevated. This substance is not found in healthy patients; any rise indicates cardiac necrosis or acute MI.

51
Q

You immediately notify the provider and within 45 minutes, the patient is transferred to the CCU for close monitoring. He is in serious condition and has developed crackles bilaterally, and his chest pain level has increased.

What medications do you anticipate will be ordered for this patient? (Select all that apply.)

Morphine
Furosemide (Lasix)
Atenolol (Tenormin)
Prednisone (Deltasone)
Acetaminophen (Tylenol)
A

ANS: A, B, C

Based on the assessment findings, several medications will be ordered including IV diuretics (furosemide) and supplemental oxygen. If congestion and shortness of breath become critical, the patient may need to be placed on a ventilator until the fluid volume overload is under control. Once-a-day beta-adrenergic blocking agents (atenolol) decrease the size of the infarct, the occurrence of ventricular dysrhythmias, and mortality rates in patients with MI. A cardioselective beta-blocking agent is usually prescribed within the first 1 to 2 hours after an MI if the patient is hemodynamically stable. Beta blockers slow the heart rate and decrease the force of cardiac contraction. Medical interventions aim to relieve pain and decrease myocardial oxygen requirements through preload and afterload reduction. IV morphine is used to decrease pulmonary congestion and relieve pain.

52
Q

The next morning, the patient is taken to the cardiac catheterization laboratory. The cardiologist finds that there is an 80% blockage in the proximal LAD coronary artery.

Which procedure is most likely to be performed to correct this condition?

Coronary atherectomy
Coronary artery bypass graft surgery
PTCA with coronary artery stent placement
Percutaneous transluminal coronary angioplasty (PTCA)

A

ANS: C

The most common complication of PTCA is re-blockage of the coronary artery. For this reason, a coronary stent is placed to keep the re-opened artery from closing again.

53
Q

The patient’s condition improves, and he is returned to the cardiac stepdown unit. He is to be discharged after 6 days in the hospital.

What patient teaching should you provide before he is discharged from the hospital?

A

ANS:
Assist the patient in securing personal medical identification alert devices that provide information regarding his heart condition.
In collaboration with the interdisciplinary health care team, assess the patient for activity tolerance and help design an appropriate exercise regimen.
Teach about the signs and symptoms of cardiovascular disease and when to seek medical assistance.
Instruct him about all of his current medications and the most common side effects.
Give him printed information as needed.
Teach him the importance of decreasing the risk for CAD.
Be sure that he has adequate support at home after discharge from the hospital.

54
Q

A woman has been experiencing atypical angina. What symptoms would the nurse anticipate? (Select all that apply.)

Vomiting
Indigestion
Aching jaw pain
Depression
Irregular bowel movements
Decreased patterns of activity
A

ANS: B, C, F

Rationale: Many women experience atypical angina which manifests as indigestion, pain between the shoulders, an aching jaw, or a choking sensation that occurs with exertion. These symptoms typically manifest during stressful circumstances or during activities of daily living. Woman may curtail activity (decreased patterns of activity) as a result of the angina, and health care providers need to ask about changes in routine.

55
Q

Identify the laboratory test that is most specific for myocardial infarction and cardiac necrosis.

Troponin
HDL
CK-MB
CK

A

ANS: A

Troponins T and I are not found in healthy patients, so any rise in values indicates cardiac necrosis or acute MI. Specific markers of myocardial injury, troponins T and I, have a wide diagnostic time frame, making them useful for patients who present several hours after the onset of chest pain. Even low levels of troponin T are treated aggressively because of increased risk for death from cardiovascular disease (CVD). Prior to the development of highly sensitive troponin levels, providers relied upon creatinine kinase (CK), its isoenzyme (CK-MB), and myoglobin to assist with diagnosis of acute myocardial infarction. Use of these cardiac markers is no longer recommended (Amsterdam, 2014; Jaffe & Morrow, 2015).

56
Q

A patient presents to the ED and is diagnosed with an acute MI. The patient’s spouse asks what type of damage has been caused by the “heart attack.” What is the appropriate nursing response?

“The pain is controlled, so there is no damage.”
“It will take years to know the extent of the damage to the heart muscle.”
“The medication will dilate the blood vessels and any damage will be corrected.”
“A heart attack evolves over several hours. We won’t know the extent of the damage immediately.”

A

ANS: D

Infarction is a dynamic process that does not occur instantly. The MI evolves over a period of several hours. Controlled pain does not indicate that there is no cardiac muscle damage. The medications do vasodilate to prevent further damage. They do not correct damage that has already been incurred.

Pn3 - RN (25 decks)

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