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NSG 478 > Nursing mgmt of disorders of cardiac oxygenation and perfusion: Unstable angina, ACS, AMI, CAD > Flashcards

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

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2
Q

What is included in ACS

A
  • Angina
  • Non-ST elevation MI
  • ST elevation MI
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3
Q

ACS due to a vasospasm

A

Often occurs due to drug use. Can spontaneously resolve

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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
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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

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6
Q

What differs MI from Angina

A

Chest pain that is unrelieved from
* Rest (stable)
* Nitro
* Lasting 15 minutes or more

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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

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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
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9
Q

What relieves stable angina

A

Rest or nitro
Should resolve within 15 min

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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

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11
Q

What relieves unstable angina

A

Nitro and time

NOT relieved by rest

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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

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13
Q

Normal EF

A

55-65%

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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)

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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
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16
Q

Anginal pain locations

A

Jaw, chest, neck, shoulders, back, arms

Pretty much anywhere

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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
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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
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19
Q

Goals to treat unstable angina

A

Decrease O2 demand
Increase O2 supply

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20
Q

Meds given to treat unstable angina

A
  • Nitro
  • Aspirin (ASA)
  • Beta blockers (BB)
  • Statins
  • Antiplatelets
  • Anticoagulants
  • Glycoprotein llb/llla inhibitors
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21
Q

Acute MI

A
  1. Plaque ruptures and thrombus formation occurs
  2. This completely occludes the artery
  3. This causing ischemia and necrosis of the myocardium that was supplied by that vessel
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22
Q

Etiology of acute MI

A
  1. Atherosclerotic plaque formation
  2. Inflammatory response
  3. Thrombus formation
  4. Platelet aggregation
  5. Decreased O2 delivery through the coronary arteries
  6. Decreased O2 to the myocardium
  7. Ischemic cascade (Sequence of events)
  8. Cell death to the myocardium
  9. MI
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23
Q

Left anterior descending (main) artery

A
  • Supplies the anterior side of the heart
  • “Widowmaker”
  • If this becomes occluded you’re kinda screwed
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24
Q

Circumflex artery

A

Goes around the circumference of the heart

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25
Q

Right coronary artery

A

Supplies the RV, RA and SA and AV nodes

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26
Q

Physical assessment of acute MI

A
  • Pale, cool and clammy
  • Tachycardia
  • Tachypnea
  • Diaphoretic
  • N+V
  • Decreased LOC
  • Or none, women and elderly people can present entirely different
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27
Q

Subjective reporting of acute MI

A
  • 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
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28
Q

Diagnosis of the type of ACS: Unstable angina, EKG/Biomarkers

A
  • Pt has S+S of coronary ischemia but EKG and biomarkers show no evidence of MI
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29
Q

Non ST elevation Myocardial infarction (NSTEMI)

A
  • Pt has elevated biomarkers (Troponin)
  • No evidence on the EKG of an acute MI
  • May be less damage to the myocardium
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30
Q

ST elevation myocardial infarction (STEMI)

A
  • 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

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31
Q

Is ischemia reversible

A
  • 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
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32
Q

Myocardial Ishemia

A

Abrupt interruption of O2 to the heart produces myocardial ischemia, which can lead to infarction

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33
Q

MI, area of infarction development

A
  • Infarction develops over minutes to hours
  • Early recognition and treatment of an acute MI are needed to prevent death
  • Time is muscle
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34
Q

Cardiac Markers: Myoglobin

A
  • Earliest marker of injury to cardiac or skeletal muscle
  • Levels are no longer evident after 24 hours
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35
Q

Cardiac Markers: Creatine kinase-MB

A
  • Peaks at 24 hours or after after onset of CP
  • Levels are no longer evident after 3 days
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36
Q

Cardiac Markers: Troponin I

A
  • 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
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37
Q

Cardiac Markers: Troponin T

A
  • 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
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38
Q

What level of troponin T indicates heart dmg or a MI is imminent

A

14 ng/L and above

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39
Q

How soon should an ECG be done after arriving to the ER

A

10 Min after arriving to the ER or reporting pain

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40
Q

P wave

A

Atrial contraction

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41
Q

P wave

A

Atrial contraction

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42
Q

QRS complex

A

Contraction of the ventricles

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43
Q

T wave

A

Relaxation of the ventricles

44
Q

What can you gather of a MI if you monitor a ECG over time

A
  • Location
  • Evolution
  • Resolution
45
Q

How can we view how an MI changes over time

A

ECG changes seen via the leads that view the heart

46
Q

First signs of acute MI on ECG

A
  • T wave
  • ST segment
47
Q

ST depression

A

Indicates the presence of ischemia causing CP, can be sign of angina

48
Q

T wave inversion

A
  • 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
Q

ST segment elevation

A
  • 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
Q

Abnormal Q wave

A
  • 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
Q

Echocardiogram

A
  • Ultrasound of the heart used to look at the structure and function, giving info on the valves , and blood flow
  • Gives EF
52
Q

Acute MI (AMI)

A
  • Area of infarction developing over minutes to hours
  • Area of muscle tissue becomes deprived to O2, causing cell death
  • Time is muscle
53
Q

AMI diagnosis

A
  • Presenting symptoms
  • 12 lead EKG
  • Lab test: cardiac biomarkers

Prognosis depends on the severity of CA obstruction and presence of Myocardial dmg

54
Q

J point

A

Point right after the QRS complex

55
Q

12 Lead EKG: What measures the Inferior wall

A

II , III, aVF

56
Q

12 Lead EKG: What measures the Lateral Wall

A

I, aVL, V5, V6

57
Q

12 Lead EKG: What measures the Septal wall

A

V1, V2

58
Q

12 Lead EKG: What measures the Anterior wall

A

V3, V4

59
Q

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)

A

ST depression. In pt with STEMI there can be reciprocal changes in opposite leads

60
Q

New/Significant Q wave

A

0.04 seconds or >25% of the R wave height
Q wave drops down further

61
Q

How is a Non-ST elevation MI (NSTEMI) diagnosed

A

Abnormal blood levels of cardiac biomarkers

62
Q

How are MI classified

A

Affected area
* Anterior, lateral, inferior or posterior

EKG changes
* STEMI or NSTEMI
Time frame within the progress of the infarction
* Acute, evolving, old

63
Q

78 year old women with
* CP, Dyspnea
* EKG; nonspecific changes
* HS troponin: 112

A

NSTEMI

64
Q

49 y/o, male
* CP, dyspnea
* EKG with ST elevation on leads II, III, aVF, troponin pending

A

Inferior stemi

65
Q

65 y/o woman
* CP, Dyspnea
* Normal EKG
* Troponin 0.08

A

??? Angina or another reason causing symptoms. Needs further workup

Could be
* GERD
* Anxiety
* Musculoskeletal

66
Q

Treatment Guidelines for acute MI

A

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
Q

Coronary angiogram (cardiac cath)

A
  • 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
Q

Nursing actions: Coronary angiogram

A
  • 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
Q

Nursing actions: Post coronary angiogram

A
  • 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
Q

Emergent percutaneous coronary intervention (PCI)

A
  • 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
Q

Percutaneous coronary intervention (PCI)

A
  • 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
Q

Thrombolytics in acute MI

A
  • 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
Q

Which thrombolytics are given for acute MI

A
  • Alteplase, Reteplase, Tenecteplase
74
Q

Indications for administration of thrombolytics

A
  • CP>20 min, unrelieved by nitro
  • ST elevation in 2 contiguous leads
  • 12 hrs from onset of pain
75
Q

Absolute contraindications for thrombolytics

A
  • Active bleeding
  • Known bleeding disorder
  • History of hemorrhagic stroke
  • History of intracranial vessel malformation
  • Recent surgery or trauma
  • Uncontrolled HTN
  • Pregnancy
76
Q

Nursing considerations: Thrombolytics

A
  • 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
Q

Complications of acute MI

A
  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
Q

LV injury to the heart: AMI

A

Can decrease CO, causing HF which can progress to Cardiogenic shock

79
Q

Complications of acute MI: Ventricular aneurysm

A
  • 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
Q

What is the prevalence of arrhythmias after a STEMI

A

78-83% of pt. This occurs due to reperfusion injury and ongoing myocardial ischemia

81
Q

Dysrhythmias: Anterior wall MI

A

(V3, V4)
* More myocardial dmg
* LV dysfunction
* Ventricular arrhythmias

82
Q

Dysrhythmias: Inferior wall MI

A

(II, III, aVF)
* Bradyarrhythmias
* Heart block
* RV infarction (<10% mortality)

83
Q

Dysrhythmias: Lateral wall MI

A

( 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
Q

Med adherence with AMI

A
  • 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
Q

Nitroglycerin

A
  • 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
Q

Nitro admin: adults

A
  • 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
Q

Nitro contraindications

A
  • 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
Q

Phosphodiesterase inhibitor

A

Viagra
Its a vasodilator, when taken with nitro it can crash BP

89
Q

Morphine sulfate

A
  • 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
Q

Beta Blockers (BB)

A
  • 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
Q

Nursing actions: Beta blockers (BB)

A
  • 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
Q

Patient education Beta blockers

A
  • Change position slowly, notify provider of weight gain, dyspnea or edema
93
Q

Med mgmt of AMI: Ace inhibitors or ARBS

A
  • 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
Q

Med mgmt of AMI: Calcium channel blockers

A
  • Used selectively, reducing the myocardial O2 demand
  • Increases blood supply in ischemic heart disease associated with Coronary artery spasms
  • Helps with vasospasm
95
Q

Med mgmt of AMI: Statins

A
  • Lower LDL cholesterol
  • Improve endothelial function, reducing inflammation
  • Reduce thrombus formation
  • Lowers risk of heart attack and stroke
96
Q

Antiplatelet agents: P2Y12 Inhibitors

A
  • 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
Q

Antiplatelet agents: Nursing actions

A
  • 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
Q

Manifestation of Aspirin tox

A

Tinnitus, let the provider know

99
Q

Clopidogrel

A
  • 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
Q

Prasugrel

A
  • 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
Q

Ticagrelor

A
  • 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
Q

Most important thing for pt on antiplt agents

A
  • Take meds as prescribed, if they have a stent if they don’t take the meds they may cause restenosis, MI and death
103
Q

Anticoagulants

A
  • Heparin
  • Enoxaparin
  • are used to prevent clots and prevent larger clots from forming
  • Main side effect is bleeding
104
Q

Glycoprotein llb/llla inhibitors

A
  • Prevent the binding of fibrinogen to plt, blocking clot formation
  • Given IV
  • Monitor for bleeding and anemia, and thrombocytopenia
105
Q

Things that need to be monitored for ACS

A
  • BP, urine, OP, serum sodium, Potassium and creatine, bleeding
106
Q

Tobacco effect on vasculature

A
  • Constricts and causes inflammation leading to clot formation

NSG 478 (23 decks)

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