Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NURS 425 > Exam #2: Dysrhythmias And Cardiac Arrest > Flashcards

Exam #2: Dysrhythmias And Cardiac Arrest Flashcards

1
Q

Acute Coronary Syndrome

A

When ischemia is prolonged and is not immediately reversible, acute coronary syndrome (ACS) develops.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACS encompasses

A
  • Unstable angina (UA)
  • Non–ST-segment-elevation myocardial infarction (NSTEMI) (partial occlusion)
  • ST-segment-elevation MI (STEMI) (total occlusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Relationships among CAD, Chronic stable angina and ACS

A

On slide 12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute Coronary Syndrome: Pathophysiology

A
  • On the cellular level, the heart muscle becomes hypoxic within the first 10 seconds of a total coronary occlusion.
  • Heart cells are deprived of oxygen and glucose needed for aerobic metabolism and contractility.
  • Anaerobic metabolism begins and lactic acid accumulates.
  • In ischemic conditions, heart cells are viable for approximately 20 minutes.
  • Irreversible heart damage starts after 20 minutes if there is no collateral circulation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Location and Patterns of Angina and MI

A
  • Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms.
  • Many people with angina complain of indigestion or a burning sensation in the epigastric region.
  • The sensation may also be felt between the shoulder blades.
  • Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as not being heart related.
  • Some patients, especially women and older adults, report atypical symptoms of angina including dyspnea, nausea, and/or fatigue (This is referred to as angina equivalent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ACS: Etiology and Pathophysiology

A
  • Caused by the decline of a once stable atherosclerotic plaque. The previously stable plaque ruptures, releasing substances into the vessel. This stimulates platelet aggregation and thrombus formation.
  • This area may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI).
  • What causes a coronary plaque to suddenly become unstable is not well understood, but systemic inflammation (described earlier) is thought to play a role.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical Manifestations of ACS: Unstable Angina

A
  • New in onset
  • Occurs at rest, unpredictable
  • Increase in frequency, duration, or with less effort
  • Pain lasting > 10 minutes
  • Needs immediate treatment
  • Symptoms in women often under-recognized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical Manifestations of ACS: MI

A
  • STEMI and NSTEMI
  • Result of abrupt stoppage of blood flow through a coronary artery, causing irreversible myocardial cell death (necrosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can cause MI?

A
  • # 1 Preexisting CAD
  • STEMI - occlusive thrombus
  • NSTEMI - non-occlusive thrombus

**Read notes on PowerPoint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The earliest tissue to become ischemic in MI is the

A

Subendocardium (innermost layer of the heart muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How long does it take the heart to become necrosed if ischemia were to persist?

A
  • 4-6 hours for the entire thickness of the heart muscle to become necrosed
  • If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as 12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Read slide 18 notes

A

+look at ECG changes on slide 19 and what it represents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acute MI Classifications

A
  1. Transmural MI (all muscle layers of the heart)

2. Non-Q-wave MI: subendocardial and subepicardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

12-lead ECG in transmural MI

A

New pathological Q-waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MI Locataions

A
  • Anterior wall infarction
  • Left lateral wall infarction
  • Inferior wall infarction
  • Right ventricular infarction
  • Posterior wall infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Correlations among Ventricular Surfaces, Electrocardiographic Leads, and Coronary Arteries

A

..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If ST elevation is shown in electrocardiographic leads II, III, aVF, what area of the heart and what coronary artery is involved?

A
  • Inferior surface of left ventricle

- Coronary Artery: Right coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If ST elevation is shown in leads V5-V6, I, aVL, what area of the heart and what coronary artery is involved?

A

Lateral surface of left ventricle and left circumflex coronary artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

If ST elevation is shown in leads V2-V4, what area of the heart and what coronary artery is involved?

A

Surface of Left Ventricle: Anterior

Coronary Artery Involved: Left anterior descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If ST elevation is shown in leads V1-V6, I, aVL, what area of the heart and what coronary artery is involved?

A

Surface of Left Ventricle: Anterior lateral

Coronary Artery: Left main coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If ST elevation is shown in leads V1-V2, what area of the heart and what coronary artery is involved?

A

Surface of Left Ventricle: Can be septal or posterior

Coronary Artery: Left anterior descending or left circumflex or right coronary artery (reciprocal changes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clincial Manifestations of ACS: MI

A
  • Pain
  • Cardiovascular Changes
  • Catecholamine release and stimulation of SNS
  • Nausea and vomiting
  • Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical Manifestations of ACS - MI: Pain

A
  • Severe chest pain not relieved by rest, position change, or nitrate administration
    • Heaviness, pressure, tightness, burning, constriction, crushing
    • Substernal or epigastric
    • May radiate to neck, lower jaw, arms, back
  • Often occurs in early morning
  • Atypical in women, elderly
  • No pain if cardiac neuropathy (diabetes)

*Read notes on slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Clinical Manifestations of ACS - MI: Catecholamine Release and Stimulation of SNS

A
  • Release of glycogen
  • Diaphoresis
  • Increased HR and BP
  • Vasoconstriction of peripheral blood vessels
  • Skin: ashen, clammy, and/or cool to touch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Clinical Manifestations of ACS - MI: Cardiovascular changes

A
  • Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)
  • Crackles
  • Jugular venous distention
  • Abnormal heart sounds
    • S3 or S4
    • New murmur

*Read notes on slide!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Clinical Manifestations of ACS - MI: Nausea and vomiting

A
  • Reflex stimulation of the vomiting center by severe pain
  • Can result form vasovagal reflex from the area of the infarcted heart muscle
  • Not always seen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical Manifestations of ACS - MI: Fever

A
  • Up to 100.4° F (38° C) in first 24-48 hours

- Systemic inflammatory process caused by heart cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Myocardial Infarction Healing Process

A
  • Within 24 hours, leukocytes infiltrate the area of cell death
  • Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day → thin wall
  • Necrotic zone identifiable by ECG changes
  • Collagen matrix laid down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Myocardial Infarction Healing Process: at 10-14 days

A
  • Scar tissue is still weak.
  • Heart muscle will be vulnerable to increased stress during this time because of the unstable state of the healing heart wall.
  • Need to monitor patient carefully as activity level increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Myocardial Infarction Healing Process: By 6 weeks after MI,

A
  • Scar tissue has replaced necrotic tissue. (May be manifested by abnormal wall motion on an ECG or nuclear imaging, LV dysfunction, altered conduction patterns, HF)
  • Area is said to be healed, but less compliant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ventricular Remodeling

A

Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are complications of MI?

A
  • Dysrhythmias
  • Heart failure
  • Cardiogenic Shock
  • Papillary Muscle Dysfunction
  • Left Ventricular Aneurysm
  • Ventricular septal wall rupture and left ventricular wall rupture
  • Acute pericarditis
  • Dressler syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Complications of MI: Dysrhythmias

A
  • Most common complication
  • Can be caused by ischemia, electrolyte imbalances or SNS stimulation (H’s and T’s)
  • VT and VF are most common cause of death in prehospitalization period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Complications of MI: Heart Failure

A

-Occurs when pumping power of the heart is diminished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Symptoms of Left-sided HF

A

Mild dyspnea, restlessness, agitation, slight tachycardia initially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Symptoms of Right-sided HF

A

Jugular venous distention, hepatic congestion, lower extremity edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Complications of MI: Cardiogenic shock occurs because of

A

Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction

*Read slide notes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Complications of MI: Papillary muscle dysfunction or rupture

A
  • Causes mitral valve regurgitation
  • Aggravates an already compromised LV → rapid clinical deterioration

*Read notes on slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Complications of MI: Left ventricular aneurysm

A
  • Myocardial wall becomes thinned and bulges out during contraction
  • Leads to HF, dysrhythmias, and angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Complications of MI: Ventricular septal wall rupture and left ventricular free wall rupture

A
  • *New, loud systolic murmur
  • HF and cardiogenic shock
  • Emergency repair
  • Rare condition associated with high death rate

*Read notes on slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Complications of MI: Acute pericarditis

A
  • Inflammation of visceral and/or parietal pericardium
  • Mild to severe chest pain
  • Increases with inspiration, coughing, movement of upper body
  • Relieved by sitting in forward position
  • Assess for the presence of pericardial friction rub
  • ECG changes (STEMI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Complications of MI: Dressler Syndrome

A

Pericarditis and fever that develops 1 to 8 weeks after MI

*Read notes on slide

43
Q

Dressler Syndrome Symptoms

A

Chest pain, fever, malaise, pericardial friction rub, arthralgia

44
Q

Dressler Syndrome treatment of choice

A

High dose aspirin

45
Q

Unstable Angina and MI: Diagnostic Studies

A
  • Detailed health history
  • 12-lead ECG:
  • Serum cardiac biomarkers
  • Coronary angiography
  • Pharmacologic stress testing

*Read notes on slide

46
Q

Unstable Angina and MI Diagnostic Studies: 12 lead ECG

A
  • Compare to previous ECG
    -Changes in QRS complex, ST segment, and T wave
  • Distinguish between STEMI and NSTEMI
  • Serial ECGs reflect evolution of MI
47
Q

Serum Cardiac Biomarkers after MI

A
  • Proteins released into the blood from necrotic heart muscle after an MI.
  • These biomarkers are important in the diagnosis of MI.
  • Serial cardiac biomarkers are drawn over 24 hours (e.g., every 8 hours x3). The presence of biomarkers helps to differentiate between a diagnosis of UA (negative biomarkers) and NSTEMI (positive biomarkers).
48
Q

Serum Cardiac Biomarkers: Cardiac-specific troponin has two subtypes

A

cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)

49
Q

Serum Cardiac Biomarkers: Cardiac-specific troponin

A
  • These biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase (CK-MB).
  • Serum levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days.
50
Q

Serum Cardiac Biomarkers: CK levels

A
  • Levels begin to rise at about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours.
  • The CK enzymes are fractionated into bands.
  • The CK-MB band is specific to heart muscle cells and help to quantify myocardial damage.
51
Q

Serum Cardiac Biomarkers: Myoglobin

A
  • Is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours.
  • Although it is one of the first serum cardiac biomarkers to appear after an MI, it lacks cardiac specificity.
  • Its role in diagnosing MI is limited.
52
Q

Unstable Angina and MI Diagnostic Studies: Coronary Angiography

A
  • For patients with a STEMI
  • Not for patients with UA or NSTEMI

*Read notes

53
Q

Unstable Angina and MI Diagnostic Studies: Pharmacological Stress Testing

A

For patients with abnormal but nondiagnostic ECG and negative biomarkers (i.e unstable angina)

54
Q

ACS Interprofessional Care: Initial Interventions include

A

Pneumonic: MOANA(Morphine, Oxygen, Aspirin, Nitrogen and Ativan)

  • 12-lead ECG
  • Upright position
  • Oxygen – keep O2 sat > 93% (DO FIRST)
  • IV access (to provide access for emergency drug therapy)
  • Nitroglycerin (SL) and Aspirin (chewable)
  • Statin
  • Morphine (if pain is unrelieved by NTG)
  • Ativan (to decrease anxiety -> decreased O2 demand)
55
Q

Interprofessional Care ACS: Ongoing Monitoring

A
  • Treat dysrhythmias (amiodarone or lidocaine)
  • Frequent vital sign monitoring
  • Bed rest/limited activity for 12–24 hours (d/t decreased O2 demand)
56
Q

Intraprofessional Care ACS: For patients with UA (unstable angina) and NSTEMI

A
  • Dual antiplatelet therapy and heparin (aspirin and Clopidogrel)
  • Cardiac catheterization with PCI once stable
57
Q

Interprofessional Care ACS: STEMI

A

Reperfusion therapy or thrombocytes therapy

58
Q

Interprofessional Care ACS: Emergency PCI

A
  • Treatment of choice for confirmed STEMI
  • Goal: 90 minutes from door to catheter laboratory
  • Balloon angioplasty + stent(s)
  • Many advantages over CABG

*Read notes on slide

59
Q

Interprofessional Care ACS: Thrombocytopenia Therapy

A
  • Only for patients with a STEMI: Agencies that do not have cardiac catheterization resources
  • Given IV within 30 minutes of arrival to the ED
  • Patient selection critical

*Read notes on slide

60
Q

Interprofessional Care ACS: Thrombolytic Therapy Management

A 
-Draw blood and start 2–3 IV sites
Complete invasive procedures prior
-Administer according to protocol
-Monitor closely for signs of bleeding
-Assess for signs of reperfusion
-Return of ST segment to baseline best sign
-Hang IV heparin to prevent reocclusion

*Read notes on slide

61
Q

ACS Interprofessional Care

A
  • Thrombolytic therapy
  • Reperfusion therapy
  • Emergent PCI
  • Medications
  • Coronary Surgical Revascularization
  • Traditon CABG surgery
  • Radial Artery Graft
  • Minimally invasive direct coronary artery bypass
  • Off-pump coronary artery bypass
  • Robotic or totally endoscopic coronary artery bypass
  • Transmyocardial laser revascularization
62
Q

Interprofessional Care ACS: Coronary Surgical Revascularization is recommended for what patients?

A
  • Failed medical management
  • Presence of left main coronary artery or three-vessel disease
  • Not a candidate for PCI (e.g., blockages are long or difficult to access)
  • Failed PCI with ongoing chest pain
  • History of diabetes mellitus, LV dysfunction, chronic kidney disease
63
Q

Interprofessional Care ACS:: Drug therapy

A
  • IV nitroglycerin (NTG)
  • Morphine (relaxes smooth muscle, vasodilation)
  • β-adrenergic blockers (decreases HR and aids in decreasing remodeling)
  • ACE inhibitors (aids in decreasing remodeling)
  • Antidysrhythmic drugs (amiodarone)
  • Lipid-lowering drugs (statins)
  • Stool softeners (prevents straining and resultant vagal stimulation from the valsava maneuver)

*Read notes on slide!!

64
Q

Intraprofessional Care ACS: Nutritional Therapy

A
  • Initially NPO
  • Progress to:
    • Low salt
    • Low saturated fat
    • Low cholesterol
65
Q

Nursing Management of Chronic Stable Angina and ACS: Nursing Assessment of Subjective Data includes

A
  • Health history:
    • CAD/chest pain/angina/ MI
    • Valve disease
    • Heart failure/cardiomyopathy,
    • Hypertension, diabetes, anemia, lung disease, hyperlipidemia
  • Drugs
  • History of present illness
  • Family history
  • Indigestion/heartburn; nausea/vomiting
  • Urinary urgency or frequency
  • Straining at stool
  • Palpitations, dyspnea, dizziness, weakness
  • Chest pain
  • Stress, depression, anger, anxiety

*Read notes on slide

66
Q

Nursing Management of Chronic Stable Angina and ACS: Nursing Assessment of Objective Data

A
  • Anxious, fearful, restless, distressed
  • Cool, clammy, pale skin
  • Tachycardia or bradycardia
  • Pulsus alternans
  • Pulse deficit
  • Dysrhythmias
  • S3, S4, ↑ or ↓ BP, murmur
67
Q

Nursing Management of Chronic Stable Angina and ACS: Nursing Diagnoses

A
  • Decreased cardiac output RT altered contractility and altered heart rate and rhythm
  • Acute pain RT an imbalance between myocardial oxygen supply and demand
  • Anxiety RT perceived or actual threat of death, pain and/or possible lifestyle changes
  • Activity intolerance RT to general weakness secondary to decreased CO and poor lung and tissue perfusion
  • Ineffective health management RT lack of knowledge of disease process, etc.
68
Q

Nursing Management of Chronic Stable Angina and ACS: Planning/Overall Goals

A
  • Relief of pain
  • Preservation of heart muscle
  • Immediate and appropriate treatment
  • Effective coping with illness-associated anxiety
  • Participation in a rehabilitation plan
  • Reduction of risk factors
69
Q

Nursing Management of Chronic Stable Angina: Acute Interventions include (repeat from previous flashcards)

A
  • Upright position (easier to breathe)
  • Supplemental oxygen
  • Assess vital signs
  • 12-lead ECG (NSTEMI versus STEMI)
  • Administer NTG followed by an opioid analgesic, if needed
  • Assess heart and breath sounds
70
Q

Nursing Management for Chronic Stable Angina: Ambulatory are Includes

A
  • Provide reassurance
  • Patient teaching
    • Activity including sex (can’t exercise for 6 weeks)
    • Diet
    • CAD and angina
    • Precipitating factors for angina
    • Risk factor reduction
    • Drugs

*read notes from slide!

71
Q

Nursing Management for ACS: Acute Care - Pain

A

-Pain: nitroglycerin, morphine, oxygen

72
Q

Nursing Management of ACS: Acute care - Continued monitoring

A

ECG, ST segment, heart and breath sounds, VS, pulse ox, and I’s and O’s

73
Q

Nursing Management of ACS: Rest and comfort

A

Balance rest and activity and begin cardiac rehabilitation

*Read notes on slide

74
Q

Nursing Management of ACS: Acute Care - Anxiety Reduction

A
  • Identify source and alleviate
  • Patient teaching important

*Read notes on slide

75
Q

Nursing Management of ACS: Acute Care - Emotional and behavioral reaction

A
  • Maximize patient’s social support systems

- Consider open visitation

76
Q

Nursing Management for ACS: Coronary Revascularization - PCI

A
  • Monitor for recurrent angina
  • Frequent VS, including cardiac rhythm
  • Monitor catheter insertion site for bleeding
  • Neurovascular assessment
  • Bed rest per institutional policy
77
Q

Coronary Revascularization - CABG: The patient will have numerous invasive lines for monitoring cardiac status and other vital signs including

A

ICU for first 24–36 hours

  • Pulmonary artery catheter
  • Intraarterial line
  • Pleural/mediastinal chest tubes
  • Continuous ECG
  • ET tube with mechanical ventilation
  • Epicardial pacing wires
  • Urinary catheter
  • NG tube
78
Q

What are complications related to CPB?

A
  • Bleeding and anemia from damage to RBCs and platelets
  • Fluid and electrolyte imbalances
  • Hypothermia as blood is cooled as it passes through the bypass machine
  • Infections
79
Q

Nursing Management of ACS: CABG postoperative care

A
  • Assess patient for bleeding (incision site, check for internal bleeding signs: decrease in blood pressure, muffled heart sounds, etc; chest tube drainage (bright red indicates fresh bleed))
  • Monitor hemodynamic status (CI, preload, etc depending on line you have)
  • Assess fluid status (UO, BP, HR)
  • Replace blood and electrolytes PRN
  • Restore temperature
  • Monitor for atrial fibrillation (which is common)
  • Pain management
  • DVT prevention
  • Surgical site care
  • Pulmonary hygiene
  • Cognitive dysfunction (d/t reduced blood flow to the brain from procedure)
80
Q

Nursing Management of ACS: Surgical Site Care includes the

A
  • Radial artery harvest site
  • Leg incisions
  • Chest incision
81
Q

Interprofessional Care for ACS: Traditional Coronary artery bypass graft surgery

A
  • Requires sternotomy and cardiopulmonary bypass (CPB)
  • Uses arteries and veins for grafts: The internal mammary artery (IMA) is most common artery used for bypass graft

*Read notes for this slide

82
Q

Cardiopulmonary Bypass

A
  • Blood is diverted from the patient’s heart to a machine where it is oxygenated and returned (via a pump) to the patient.
  • This allows the surgeon to operate on a quiet, nonbeating, bloodless heart while perfusion to vital organs is maintained.
83
Q

Internal Mammary Artery for Bypass Graft

A
  • The internal mammary artery (IMA) is the most common artery used for bypass graft.
  • It is left attached to its origin (the subclavian artery) but then dissected from the chest wall.
  • Next, it is anastomosed (connected with sutures) to the coronary artery distal to the blockage.
84
Q

Saphenous Vein Grafts

A
  • Saphenous veins are also used for bypass grafts.
  • The surgeon endoscopically removes the saphenous vein from one or both legs.
  • A section is sutured into the ascending aorta near the native coronary artery opening and then sutured to the coronary artery distal to the blockage.
  • The use of antiplatelet and statin therapy after surgery improves vein graft patency.
85
Q

Radial Artery Graft

A
  • Thick muscular artery that is prone to spasm
  • Perioperative calcium channel blockers and long-acting nitrates can control the spasms
  • Patency rates are not as good as IMA but better than saphenous veins
86
Q

Interprofessional Care of ACS: Minimally invasive direct coronary artery bypass (MIDCAB)

A
  • For patients with disease of left anterior descending or right coronary artery
  • Does not involve a sternotomy and CPB

*Read notes

87
Q

Interprofessional Care for ACS: Off-pump Coronary Artery Bypass

A
  • Sternotomy
  • Performed on a beating heart (no CPB) using mechanical stabilizers.
  • Primary for patients with comorbidities who should avoid CPB.
88
Q

Off-Pump Coronary artery bypass is associated with

A

Less blood loss, less renal dysfunction, less postoperative atrial fibrillation, and fewer neurologic complications.

89
Q

Interprofessional Care for ACS: Robotic or totally endoscopic coronary artery bypass

A
  • This technique uses a robot in performing CABG surgery.
  • This procedure is done without the use of CPB or with the use of CPB using femoral access.
  • TECAB is used for limited bypass grafting.
90
Q

During coronary bypass, we want the patient to be

A

Hypothermic because it decreases oxygen demand.

91
Q

Benefits of Robotic or Totally endoscopic Coronary artery bypass

A

The benefits include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time.

92
Q

Interprofessional Care of ACS: Transmyocardial Laser Revascularization

A
  • Indirect revascularization procedure

- High-energy laser creates channels in heart to allow blood flow to ischemic areas

93
Q

Nursing Management of Acute Coronary Syndrome: Ambulatory Care includes

A
  • Cardiac rehabilitation
  • Patient and caregiver teaching
  • Physical Activity
  • Resumption of sexual activity
94
Q

Nursing Management of Acute Coronary Syndrome: Physical Activity

A
  • METs scale
  • Monitor heart rate
  • Low-level stress test before discharge
  • Isometric versus isotonic activities

*Read notes

95
Q

Nursing Management of Acute Coronary Syndrome: Resumption of sexual activity

A
  • Teach when discuss other physical activity
  • Erectile dysfunction drugs contraindicated with nitrates
  • Prophylactic nitrates before sexual activity
  • When to avoid sex
  • Typically 7–10 days post MI or when patient can climb two flights of stairs

*Read notes for more info

96
Q

Nursing Management of Acute Coronary Syndrome: Evaluation

A
  • Stable vital signs
  • Relief of pain
  • Decreased anxiety
  • Realistic program of activity
  • Effective management of therapeutic regimen
97
Q

Sudden Cardiac Death

A
  • Unexpected death from cardiac causes

- Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow

98
Q

Sudden Cardiac Death Signs and Symptoms

A

-No warning signs or symptoms if no MI
-Prodromal symptoms if associated with MI:
-Chest pain, palpitations, dyspnea
Death usually within 1 hour of onset of acute symptoms

*Read notes for more info

99
Q

Sudden Cardiac Death: Diagnostic workup to rule out or confirm MI

A
  • Cardiac biomarkers
  • ECGs
  • Treat accordingly
  • Cardiac Catheterization

*Read notes

100
Q

Sudden Cardiac Death is most commonly caused by

A
  • Ventricular dysrhythmias
  • Structural heart disease
  • Conduction disturbances

*Read notes for more info

101
Q

Sudden Cardiac Death Treatment

A

PCI or CABG

102
Q

Sudden Cardiac Death Nursing Care

A
  • 24-hour Holter monitoring
  • Exercise stress testing
  • Signal-averaged ECG
  • Electrophysiologic study (EPS)
  • Implantable cardioverter-defibrillator (ICD)
  • Antidysrhythmic drugs
  • LifeVest
  • Patient teaching

*Read notes!!

103
Q

Sudden Cardiac Death: Psychosocial adaptation

A
  • “Brush with death”
  • “Time bomb” mentality
  • Additional issues:
    • Driving restrictions
    • Role reversal
    • Change in occupation

*Read notes

NURS 425 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions