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.
2
Q
ACS encompasses
A
- Unstable angina (UA)
- Non–ST-segment-elevation myocardial infarction (NSTEMI) (partial occlusion)
- ST-segment-elevation MI (STEMI) (total occlusion)
3
Q
Relationships among CAD, Chronic stable angina and ACS
A
On slide 12
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.
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)
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.
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
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)
9
Q
What can cause MI?
A
- # 1 Preexisting CAD
- STEMI - occlusive thrombus
- NSTEMI - non-occlusive thrombus
**Read notes on PowerPoint
10
Q
The earliest tissue to become ischemic in MI is the
A
Subendocardium (innermost layer of the heart muscle)
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
12
Q
Read slide 18 notes
A
+look at ECG changes on slide 19 and what it represents
13
Q
Acute MI Classifications
A
- Transmural MI (all muscle layers of the heart)
2. Non-Q-wave MI: subendocardial and subepicardial
14
Q
12-lead ECG in transmural MI
A
New pathological Q-waves
15
Q
MI Locataions
A
- Anterior wall infarction
- Left lateral wall infarction
- Inferior wall infarction
- Right ventricular infarction
- Posterior wall infarction
16
Q
Correlations among Ventricular Surfaces, Electrocardiographic Leads, and Coronary Arteries
A
..
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
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.
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
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
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)
22
Q
Clincial Manifestations of ACS: MI
A
- Pain
- Cardiovascular Changes
- Catecholamine release and stimulation of SNS
- Nausea and vomiting
- Fever
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
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
25
Clinical Manifestations of ACS - MI: Cardiovascular changes
- 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!
26
Clinical Manifestations of ACS - MI: Nausea and vomiting
- 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
27
Clinical Manifestations of ACS - MI: Fever
- Up to 100.4° F (38° C) in first 24-48 hours
| - Systemic inflammatory process caused by heart cell death
28
Myocardial Infarction Healing Process
- 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
29
Myocardial Infarction Healing Process: at 10-14 days
- 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
30
Myocardial Infarction Healing Process: By 6 weeks after MI,
- 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
31
Ventricular Remodeling
Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle
32
What are complications of MI?
- Dysrhythmias
- Heart failure
- Cardiogenic Shock
- Papillary Muscle Dysfunction
- Left Ventricular Aneurysm
- Ventricular septal wall rupture and left ventricular wall rupture
- Acute pericarditis
- Dressler syndrome
33
Complications of MI: Dysrhythmias
- 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
34
Complications of MI: Heart Failure
-Occurs when pumping power of the heart is diminished
35
Symptoms of Left-sided HF
Mild dyspnea, restlessness, agitation, slight tachycardia initially
36
Symptoms of Right-sided HF
Jugular venous distention, hepatic congestion, lower extremity edema
37
Complications of MI: Cardiogenic shock occurs because of
Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction
*Read slide notes
38
Complications of MI: Papillary muscle dysfunction or rupture
- Causes mitral valve regurgitation
- Aggravates an already compromised LV → rapid clinical deterioration
*Read notes on slide
39
Complications of MI: Left ventricular aneurysm
- Myocardial wall becomes thinned and bulges out during contraction
- Leads to HF, dysrhythmias, and angina
40
Complications of MI: Ventricular septal wall rupture and left ventricular free wall rupture
- *New, loud systolic murmur
- HF and cardiogenic shock
- Emergency repair
- Rare condition associated with high death rate
*Read notes on slide
41
Complications of MI: Acute pericarditis
- 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)
42
Complications of MI: Dressler Syndrome
Pericarditis and fever that develops 1 to 8 weeks after MI
*Read notes on slide
43
Dressler Syndrome Symptoms
Chest pain, fever, malaise, pericardial friction rub, arthralgia
44
Dressler Syndrome treatment of choice
High dose aspirin
45
Unstable Angina and MI: Diagnostic Studies
- Detailed health history
- 12-lead ECG:
- Serum cardiac biomarkers
- Coronary angiography
- Pharmacologic stress testing
*Read notes on slide
46
Unstable Angina and MI Diagnostic Studies: 12 lead ECG
- 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
Serum Cardiac Biomarkers after MI
- 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
Serum Cardiac Biomarkers: Cardiac-specific troponin has two subtypes
cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)
49
Serum Cardiac Biomarkers: Cardiac-specific troponin
- 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
Serum Cardiac Biomarkers: CK levels
- 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
Serum Cardiac Biomarkers: Myoglobin
- 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
Unstable Angina and MI Diagnostic Studies: Coronary Angiography
- For patients with a STEMI
- Not for patients with UA or NSTEMI
*Read notes
53
Unstable Angina and MI Diagnostic Studies: Pharmacological Stress Testing
For patients with abnormal but nondiagnostic ECG and negative biomarkers (i.e unstable angina)
54
ACS Interprofessional Care: Initial Interventions include
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
Interprofessional Care ACS: Ongoing Monitoring
- Treat dysrhythmias (amiodarone or lidocaine)
- Frequent vital sign monitoring
- Bed rest/limited activity for 12–24 hours (d/t decreased O2 demand)
56
Intraprofessional Care ACS: For patients with UA (unstable angina) and NSTEMI
- Dual antiplatelet therapy and heparin (aspirin and Clopidogrel)
- Cardiac catheterization with PCI once stable
57
Interprofessional Care ACS: STEMI
Reperfusion therapy or thrombocytes therapy
58
Interprofessional Care ACS: Emergency PCI
- 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
Interprofessional Care ACS: Thrombocytopenia Therapy
- 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
Interprofessional Care ACS: Thrombolytic Therapy Management
```
-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
ACS Interprofessional Care
- 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
Interprofessional Care ACS: Coronary Surgical Revascularization is recommended for what patients?
- 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
Interprofessional Care ACS:: Drug therapy
- 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
Intraprofessional Care ACS: Nutritional Therapy
- Initially NPO
- Progress to:
- Low salt
- Low saturated fat
- Low cholesterol
65
Nursing Management of Chronic Stable Angina and ACS: Nursing Assessment of Subjective Data includes
- 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
Nursing Management of Chronic Stable Angina and ACS: Nursing Assessment of Objective Data
- Anxious, fearful, restless, distressed
- Cool, clammy, pale skin
- Tachycardia or bradycardia
- Pulsus alternans
- Pulse deficit
- Dysrhythmias
- S3, S4, ↑ or ↓ BP, murmur
67
Nursing Management of Chronic Stable Angina and ACS: Nursing Diagnoses
- 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
Nursing Management of Chronic Stable Angina and ACS: Planning/Overall Goals
- 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
Nursing Management of Chronic Stable Angina: Acute Interventions include (repeat from previous flashcards)
- 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
Nursing Management for Chronic Stable Angina: Ambulatory are Includes
- 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
Nursing Management for ACS: Acute Care - Pain
-Pain: nitroglycerin, morphine, oxygen
72
Nursing Management of ACS: Acute care - Continued monitoring
ECG, ST segment, heart and breath sounds, VS, pulse ox, and I’s and O’s
73
Nursing Management of ACS: Rest and comfort
Balance rest and activity and begin cardiac rehabilitation
*Read notes on slide
74
Nursing Management of ACS: Acute Care - Anxiety Reduction
- Identify source and alleviate
- Patient teaching important
*Read notes on slide
75
Nursing Management of ACS: Acute Care - Emotional and behavioral reaction
- Maximize patient’s social support systems
| - Consider open visitation
76
Nursing Management for ACS: Coronary Revascularization - PCI
- Monitor for recurrent angina
- Frequent VS, including cardiac rhythm
- Monitor catheter insertion site for bleeding
- Neurovascular assessment
- Bed rest per institutional policy
77
Coronary Revascularization - CABG: The patient will have numerous invasive lines for monitoring cardiac status and other vital signs including
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
What are complications related to CPB?
- 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
Nursing Management of ACS: CABG postoperative care
- 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
Nursing Management of ACS: Surgical Site Care includes the
- Radial artery harvest site
- Leg incisions
- Chest incision
81
Interprofessional Care for ACS: Traditional Coronary artery bypass graft surgery
- 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
Cardiopulmonary Bypass
- 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
Internal Mammary Artery for Bypass Graft
- 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
Saphenous Vein Grafts
- 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
Radial Artery Graft
- 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
Interprofessional Care of ACS: Minimally invasive direct coronary artery bypass (MIDCAB)
- For patients with disease of left anterior descending or right coronary artery
- Does not involve a sternotomy and CPB
*Read notes
87
Interprofessional Care for ACS: Off-pump Coronary Artery Bypass
- Sternotomy
- Performed on a beating heart (no CPB) using mechanical stabilizers.
- Primary for patients with comorbidities who should avoid CPB.
88
Off-Pump Coronary artery bypass is associated with
Less blood loss, less renal dysfunction, less postoperative atrial fibrillation, and fewer neurologic complications.
89
Interprofessional Care for ACS: Robotic or totally endoscopic coronary artery bypass
- 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
During coronary bypass, we want the patient to be
Hypothermic because it decreases oxygen demand.
91
Benefits of Robotic or Totally endoscopic Coronary artery bypass
The benefits include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time.
92
Interprofessional Care of ACS: Transmyocardial Laser Revascularization
- Indirect revascularization procedure
| - High-energy laser creates channels in heart to allow blood flow to ischemic areas
93
Nursing Management of Acute Coronary Syndrome: Ambulatory Care includes
- Cardiac rehabilitation
- Patient and caregiver teaching
- Physical Activity
- Resumption of sexual activity
94
Nursing Management of Acute Coronary Syndrome: Physical Activity
- METs scale
- Monitor heart rate
- Low-level stress test before discharge
- Isometric versus isotonic activities
*Read notes
95
Nursing Management of Acute Coronary Syndrome: Resumption of sexual activity
- 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
Nursing Management of Acute Coronary Syndrome: Evaluation
- Stable vital signs
- Relief of pain
- Decreased anxiety
- Realistic program of activity
- Effective management of therapeutic regimen
97
Sudden Cardiac Death
- Unexpected death from cardiac causes
| - Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow
98
Sudden Cardiac Death Signs and Symptoms
-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
Sudden Cardiac Death: Diagnostic workup to rule out or confirm MI
- Cardiac biomarkers
- ECGs
- Treat accordingly
- Cardiac Catheterization
*Read notes
100
Sudden Cardiac Death is most commonly caused by
- Ventricular dysrhythmias
- Structural heart disease
- Conduction disturbances
*Read notes for more info
101
Sudden Cardiac Death Treatment
PCI or CABG
102
Sudden Cardiac Death Nursing Care
- 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
Sudden Cardiac Death: Psychosocial adaptation
- “Brush with death”
- “Time bomb” mentality
- Additional issues:
- Driving restrictions
- Role reversal
- Change in occupation
*Read notes
