Nursing mgmt of disorders of cardiac oxygenation and perfusion: Unstable angina, ACS, AMI, CAD Flashcards
1
Q
Acute coronary Syndrome (ACS)
A
Umbrella term when blood supply to the heart becomes limited or blocked
* Decreased supply/ increased demand of blood= Heart not happy causing pain
.
* Blockage is usually due to a blood clot and can be sudden and complete
* If clot forms due to plaque rupture, part of the clot may break away and block on of the coronary arteries causing the ACS
* Less commonly a spasm within the coronary artery can limit blood flow causing ACS
2
Q
What is included in ACS
A
- Angina
- Non-ST elevation MI
- ST elevation MI
3
Q
ACS due to a vasospasm
A
Often occurs due to drug use. Can spontaneously resolve
4
Q
Cause of ACS
A
Imbalance between myocardial O2 supply and O2 demand
- When the blood flow to the heart is compromised, Ischemia causes chest pain, angina
5
Q
What is anginal pain described as
A
- Tight squeezing
- Heavy pressure
- Constricting feeling on the chest
- Radiates to the jaw, neck or arm
- Elephant on the chest
Women and older adults and Diabetics may not experience the typical symptoms that are associated with MI or Angina
6
Q
What differs MI from Angina
A
Chest pain that is unrelieved from
* Rest (stable)
* Nitro
* Lasting 15 minutes or more
7
Q
Atherosclerosis
A
Deposition of fatty deposits onto the walls of arteries leading to hardening of the arteries. This both limits blood flow and limiting artery movement
* The lumen of the arteries can then become entirely blocked leading reduced blood flow to the heart leading to ACS
.
* Leading cause of death around the world
8
Q
Stable angina
A
- Also known as exertional angina
- Occurs with exercise or emotional stress
- NOT Associated with nausea, epigastric distress, dyspnea, anxiety, diaphoresis
9
Q
What relieves stable angina
A
Rest or nitro
Should resolve within 15 min
10
Q
Unstable angina
A
- Also known as pre-infarction angina
- Occurs with exercise OR rest
- But Increases in occurrence, severity, duration overtime
Occurs often due to a rupture of a plaque, with a clot forming on top the lesion, but the artery is only partially occluded
11
Q
What relieves unstable angina
A
Nitro and time
NOT relieved by rest
12
Q
Variant angina
A
Prinzmetal’s angina
* Due to a CA spasm, often occurring at rest
* Can occur due to drug use. can spontaneously resolve
13
Q
Normal EF
A
55-65%
14
Q
Exercise stress test
Dont need to know
A
Walking on a treadmill, hooked up to a monitor. This is done to make your heart beat harder. EKG is used to observe for abnormalities or ischemia/ watching for pt S+S (CP, SOB)
If you are unable to exercise meds are given instead to make your heart beat faster/harder
Positive test means more testing needs to be done (Nuclear)
15
Q
Nuclear stress test
A
- Nuclear contrast is used to take images of your heart at rest and exercising which are then compared
- Cardiologist compares the amount of blood flow through the arteries and to the muscle at rest and exercising
16
Q
Anginal pain locations
A
Jaw, chest, neck, shoulders, back, arms
Pretty much anywhere
17
Q
Risk factors for Coronary artery disease (CAD)
A
- Male/ post menopausal women
- Sedentary lifestyle
- HTN
- Dyslipidemia
- Tobacco use
- Obesity
- Excessive ETOH use
- Family history
- Metabolic disorders (DM, hyperthyroid)
- Meth or coke use
18
Q
Myocardial infarction (MI)
A
- May occur without cause in the morning or after rest
- Relieved only by opiods (pain)
- Manifestations last longer than 30 min
- Associated with nausea, epigastric distress, dypnea, anxiety, diaphoresis
19
Q
Goals to treat unstable angina
A
Decrease O2 demand
Increase O2 supply
20
Q
Meds given to treat unstable angina
A
- Nitro
- Aspirin (ASA)
- Beta blockers (BB)
- Statins
- Antiplatelets
- Anticoagulants
- Glycoprotein llb/llla inhibitors
21
Q
Acute MI
A
- Plaque ruptures and thrombus formation occurs
- This completely occludes the artery
- This causing ischemia and necrosis of the myocardium that was supplied by that vessel
22
Q
Etiology of acute MI
A
- Atherosclerotic plaque formation
- Inflammatory response
- Thrombus formation
- Platelet aggregation
- Decreased O2 delivery through the coronary arteries
- Decreased O2 to the myocardium
- Ischemic cascade (Sequence of events)
- Cell death to the myocardium
- MI
23
Q
Left anterior descending (main) artery
A
- Supplies the anterior side of the heart
- “Widowmaker”
- If this becomes occluded you’re kinda screwed
24
Q
Circumflex artery
A
Goes around the circumference of the heart
25
Right coronary artery
Supplies the RV, RA and SA and AV nodes
26
Physical assessment of acute MI
* Pale, cool and clammy
* Tachycardia
* Tachypnea
* Diaphoretic
* N+V
* Decreased LOC
* Or none, women and elderly people can present entirely different
27
Subjective reporting of acute MI
* Anxiety, feeling of impending doom
* CP w/wo radiation, substernal or precordial
* Crushing or aching pressure on the chest
* Nausea
* Dizziness
* Women can have atypical angina with pain, beneath shoulders, ache in jaw area, or sensation of choking with exertion
28
Diagnosis of the type of ACS: Unstable angina, EKG/Biomarkers
* Pt has S+S of coronary ischemia but EKG and biomarkers show no evidence of MI
29
Non ST elevation Myocardial infarction (NSTEMI)
* Pt has elevated biomarkers (Troponin)
* No evidence on the EKG of an acute MI
* May be less damage to the myocardium
30
ST elevation myocardial infarction (STEMI)
* EKG shows ST elevation, indicating an acute MI
* Needs to be shown in 2/12 leads
* Can indicate significant myocardial damage is happening
* STEMI means the infarction is occurring now
| Time is muscle
31
Is ischemia reversible
* Yes, infarction is not reversible however so you want to catch it before it progresses
* When cardiac muscle suffers injury, cardiac enzymes are released into the bloodstream which are biomarkers for MI
32
Myocardial Ishemia
Abrupt interruption of O2 to the heart produces myocardial ischemia, which can lead to infarction
33
MI, area of infarction development
* Infarction develops over minutes to hours
* Early recognition and treatment of an acute MI are needed to prevent death
* Time is muscle
34
Cardiac Markers: Myoglobin
* Earliest marker of injury to cardiac or skeletal muscle
* Levels are no longer evident after 24 hours
35
Cardiac Markers: Creatine kinase-MB
* Peaks at 24 hours or after after onset of CP
* Levels are no longer evident after 3 days
36
Cardiac Markers: Troponin I
* Any positive value indicates damage to the cardiac tissue, is a concern and needs to be reported
* Levels are no longer evident after 7-10 days
37
Cardiac Markers: Troponin T
* A protein that is found in cardiac muscle, usual levels are super low (0-0.04 nanograms per ml). which makes it difficult to test with standard equipment. **Troponin T test is highly sensitive**
* Any positive value indicates damage to the cardiac tissue, is a concern and needs to be reported, **14 ng/L indicates heart dmg or a heart attack is likely**
* Levels are no longer evident after 10-14 days
38
What level of troponin T indicates heart dmg or a MI is imminent
14 ng/L and above
39
How soon should an ECG be done after arriving to the ER
10 Min after arriving to the ER or reporting pain
40
P wave
Atrial contraction
41
P wave
Atrial contraction
42
QRS complex
Contraction of the ventricles
43
T wave
Relaxation of the ventricles
44
What can you gather of a MI if you monitor a ECG over time
* Location
* Evolution
* Resolution
45
How can we view how an MI changes over time
ECG changes seen via the leads that view the heart
46
First signs of acute MI on ECG
* T wave
* ST segment
47
ST depression
Indicates the presence of ischemia causing CP, can be sign of angina
48
T wave inversion
* Area of injury becomes ischemic, myocardial repolarization is altered+delayed, leading to the T wave to invert
* Indicates the presence of ischemia causing CP or angina , Which can be indicative of MI
49
ST segment elevation
* Injured cells depolarize normally, however depolarize more rapidly than normal cells causing the ST segment to rise at least 1 mm
* Indicates **acute** injury
* MI can be indicated by ST elevation see in 2 contiguous leads
* Measured at the J point
50
Abnormal Q wave
* Appearance of abnormal Q waves is another indicator of MI
* Develop 1-3 days after because there is no depolarization through dead tissue
*** Indicate necrosis**
* Long q wave
* Indicates a prior or old infarction, not acute
51
Echocardiogram
* Ultrasound of the heart used to look at the structure and function, giving info on the valves , and blood flow
* Gives EF
52
Acute MI (AMI)
* Area of infarction developing over minutes to hours
* Area of muscle tissue becomes deprived to O2, causing cell death
* Time is muscle
53
AMI diagnosis
* Presenting symptoms
* 12 lead EKG
* Lab test: cardiac biomarkers
Prognosis depends on the severity of CA obstruction and presence of Myocardial dmg
54
J point
Point right after the QRS complex
55
12 Lead EKG: What measures the Inferior wall
II , III, aVF
56
12 Lead EKG: What measures the Lateral Wall
I, aVL, V5, V6
57
12 Lead EKG: What measures the Septal wall
V1, V2
58
12 Lead EKG: What measures the Anterior wall
V3, V4
59
In a patient with a STEMI, ST elevation is shown in the anterior leads (V2, V3, V4). What can be shown shown in the Inferior leads (II, III, aVF)
ST depression. In pt with STEMI there can be reciprocal changes in opposite leads
60
New/Significant Q wave
0.04 seconds or >25% of the R wave height
Q wave drops down further
61
How is a Non-ST elevation MI (NSTEMI) diagnosed
Abnormal blood levels of cardiac biomarkers
62
How are MI classified
Affected area
* Anterior, lateral, inferior or posterior
EKG changes
* STEMI or NSTEMI
Time frame within the progress of the infarction
* Acute, evolving, old
63
78 year old women with
* CP, Dyspnea
* EKG; nonspecific changes
* HS troponin: 112
NSTEMI
64
49 y/o, male
* CP, dyspnea
* EKG with ST elevation on leads II, III, aVF, troponin pending
Inferior stemi
65
65 y/o woman
* CP, Dyspnea
* Normal EKG
* Troponin 0.08
??? Angina or another reason causing symptoms. Needs further workup
Could be
* GERD
* Anxiety
* Musculoskeletal
66
Treatment Guidelines for acute MI
Rapid transport to hospital
*12 lead EKG to be read within **10 min**
* Obtain labs for cardiac biomarkers
* Routine medical interventions: O2, nitro, morphine, ASA, BB, Ace/arb within 24 hours, anticoagulated with heparin and platelet inhibitors (Plavix), Statin
* Evaluate need for indications for reperfusion therapy (PCI, thrombolytics)
* Continue therapy as indicated: IV heparin, lovenox, bivalirudin, Clopidogrel, llb/llla inhibitors, "Bedrest for 12-24 hours" statin at discharge
67
Coronary angiogram (cardiac cath)
* Invasive diagnostic procedure used to evaluate the presence and degree of CAD
* Essentially they insert a cath into either your femoral or radial and inject dye around your heart, which is then read under essentially an X ray (fluoroscopy) to see the degree of stenosis
* Used to diagnose degree of stenosis and see what procedures the pt can more forward with
68
Nursing actions: Coronary angiogram
* Informed consent: make sure the pt knows the procedure
* Keep pt NPO for 8 Hours or per cardiologist
* Assess for iodine or shellfish allergy (Myth but she taught it) and or a latex allergy
* Ensure recent labs are done, notify provider if renal function is abnormal. Start IVF if ordered
69
Nursing actions: Post coronary angiogram
* Assess the site, either radial or femoral for any bleeding/hematoma, check pulses
* Ensure any new med orders have been done
* Admin IVF
* If no HF or Fluid overload push PO fluids (Helps eliminate the contrast from the system)
* If pt is found to need surgery make sure meds are reviewed by the provider (anti plt may need to be stopped)
70
Emergent percutaneous coronary intervention (PCI)
* pts with stemi need to be taken to cardiac cath lab for immediate PCI (If indicated)
* prefered treatment for acute MI, treating the underlying atherosclerotic lesion
* Because the duration O2 deprivation determines cardiac cells that can die, time from arrival to ER to PCI insertion should be less than 60 min
71
Percutaneous coronary intervention (PCI)
* Opens up the arterial occlusion and promotes reperfusion to the area deprived of o2, stent can be bare metal or drug alluding
Its a balloon that is inflated to open a stent and then withdrawn
* Can cause MI or Stroke
* Restenosis can occur as well
72
Thrombolytics in acute MI
* Given when PCI is not available or is too long of a wait time
* Agents are admined IV according to protocol to dissolve the thrombus, limiting the size of infarction and preserving ventricular function
* Thrombolytics dissolve the clot but do not correct the underlying issue. Pt is to be referred to cardiac angio after
* Should be given within **30 min** of onset of symptoms for best results (Door to needle time)
* Used as a bandage till they can get the issue corrected
73
Which thrombolytics are given for acute MI
* Alteplase, Reteplase, Tenecteplase
74
Indications for administration of thrombolytics
* CP>20 min, unrelieved by nitro
* ST elevation in 2 contiguous leads
* 12 hrs from onset of pain
75
**Absolute** contraindications for thrombolytics
* Active bleeding
* Known bleeding disorder
* History of hemorrhagic stroke
* History of intracranial vessel malformation
* Recent surgery or trauma
* Uncontrolled HTN
* Pregnancy
76
Nursing considerations: Thrombolytics
* Minimize punctures
* Avoid IM injections
* Start IV lines before giving drugs: One line for blood draws
* Monitor for arrhythmias and hypotension
* Monitor for reperfusion (Resolution of pain or ST changes)
* Assess for S+S of bleeding
* Treat major bleeding by stopping the thrombolytics, applying pressure and contacting the provider
77
Complications of acute MI
1. Location: Anterior, Lateral, Inferior
2. Amount of myocardial dmg
3. Other comorbidities: ie renal issues, then needing complex PCI
4. Ischemic mitral regurgitation: Mitral valve doesn't work properly and causes regurg, and pulmonary edema
5. Ventricular aneurysm
6. Pseudoaneurysm
78
LV injury to the heart: AMI
Can decrease CO, causing HF which can progress to Cardiogenic shock
79
Complications of acute MI: Ventricular aneurysm
* Occurs when a weakened section of the wall of one of the ventricles expands, and bulges in the area of infarct. Occurring as early as 48 hours-2wks of postinfarction
* Mgmt is with medical treatment, directed to the anticoagulation
* Mgmt also includes surgical resection of an aneurism in a large aneurysm or of there is worsening condition
80
What is the prevalence of arrhythmias after a STEMI
78-83% of pt. This occurs due to reperfusion injury and ongoing myocardial ischemia
81
Dysrhythmias: Anterior wall MI
(V3, V4)
* More myocardial dmg
* **LV dysfunction**
* **Ventricular arrhythmias**
82
Dysrhythmias: Inferior wall MI
(II, III, aVF)
* **Bradyarrhythmias**
* **Heart block**
* RV infarction (<10% mortality)
83
Dysrhythmias: Lateral wall MI
( I, aVL, V5, V6)
* Usually seen with other infarctions
* Iso Lateral MI can be seen with occlusion of obtuse marginal, or diagonal branch occlusions
84
Med adherence with AMI
* 31% of pts stopped taking at least one med in 6 mo post AMI
* Super important to keep med adherence or else you're having another MI
85
Nitroglycerin
* **Reduces myocardial O2 demand, lessening ischemia**
* Fast acting vasodilator (arteries, veins and arterioles)
* Reduces BP and prevents vasospasm
* First line agent for angina, for mgmt of CP due to ACS
* Short acting nitrate, is used to reduce cardiac workload in selected patients
* Decreases LV preload AND afterload
* Doesn't fix actual issue but provides relief
Can be given basically any route PO, transdermal
86
Nitro admin: adults
* 1 Tab, under the tongue or between the check at the first sign of an anginal attack
* 1 tab every 5 min up to 15 min (15 min is when its considered MI)
* **If pain is unrelieved in 5 min call 911, and go to the hospital**
* Do NOT take more than 3 tabs in 15 min
* **Nitro lowers BP, when the pt takes it make sure they sit down or else they can pass out**
87
Nitro contraindications
* SBP: <90 mmHg
* BP decreases 30 or more below baseline
* Severe bradycardia (<50 bpm)
* Tachycardia
* Within 24-48 hours of a pt taking a phosphodiesterase inhibitor
88
Phosphodiesterase inhibitor
Viagra
Its a vasodilator, when taken with nitro it can crash BP
89
Morphine sulfate
* Opioid used to treat moderate to severe pain
* Produces analgesia, resp depression, euphoria, sedation, and **decreases myocardial O2 consumption** GI motility
* Caution with asthma or emphysema due to risk of resp depression
90
Beta Blockers (BB)
* End in lol
* Decreases the afterload of the heart making O2 demand less.
* In acute MI: BB decrease the infarct size and improve survival rates
* Dont give if apical is less than 60
91
Nursing actions: Beta blockers (BB)
* BB can cause bradycardia and hypotension **(Hold for apical pulse under 60 and notify provider)**
* Monitor pt with asthma closely, while cardioselective BB are prefered (metoprolol) some BB are not cardioselective and can affect the lungs as well
* Use with caution in pt with CHF
* Monitor for decreased LOC, Crackles in the lungs and chest discomfort
92
Patient education Beta blockers
* Change position slowly, notify provider of weight gain, dyspnea or edema
93
Med mgmt of AMI: Ace inhibitors or ARBS
* Reduce myocardial infarction size
* Improve ventricular remodeling
* Prevents remodeling of cells associated with HF
Both are beneficial in reducing morbidity and mortality in post infarction patients
94
Med mgmt of AMI: Calcium channel blockers
* **Used selectively,** reducing the myocardial O2 demand
* Increases blood supply in ischemic heart disease associated with Coronary artery spasms
* Helps with vasospasm
95
Med mgmt of AMI: **Statins**
* Lower LDL cholesterol
* Improve endothelial function, reducing inflammation
* Reduce thrombus formation
* Lowers risk of heart attack and stroke
96
Antiplatelet agents: P2Y12 Inhibitors
* Aspirin and clopidogrel prevent plt from forming together reducing arterial clotting
* Aspirin prevents vasoconstriction, meaning it should be given with nitro on the onset of CP in addition to its anti clotting effects
97
Antiplatelet agents: Nursing actions
* Anti-plt agents can cause GI upset, use with caution in pt with history of GI ulcers
* Tinnitus is a manifestation of aspirin tox
* Patient education: Knowing bruising and bleeding risk
* If aspirin is prescribed as well, choose the enteric coated aspirin, take with food to minimize GI upset
98
Manifestation of Aspirin tox
Tinnitus, let the provider know
99
Clopidogrel
* Plavix
* Anticoagulant, makes plt less sticky
* 75mg daily
* Used in pt that have underwent stenting
| Alert provider if they have bleeding or blood in stool
100
Prasugrel
* Effient
* 10 mg daily
* Increased risk of bleeding, contraindicated in those with history of bleeding / TIA
* Contraindicated in those older than 75
| Alert provider if they have bleeding or blood in stool
101
Ticagrelor
* Brilinta
* 90 mg **BID (2x a day)**
* faster onset, decreased mortality in CV pts
* Side effects include SOB
| Alert provider if they have bleeding or blood in stool
102
Most important thing for pt on antiplt agents
* Take meds as prescribed, if they have a stent if they don't take the meds they may cause restenosis, MI and death
103
Anticoagulants
* Heparin
* Enoxaparin
* are used to prevent clots and prevent larger clots from forming
* Main side effect is bleeding
104
Glycoprotein llb/llla inhibitors
* Prevent the binding of fibrinogen to plt, blocking clot formation
* Given IV
* Monitor for bleeding and anemia, and thrombocytopenia
105
Things that need to be monitored for ACS
* BP, urine, OP, serum sodium, Potassium and creatine, bleeding
106
Tobacco effect on vasculature
* Constricts and causes inflammation leading to clot formation
