Chapter 33- Coronary Artery Disease and Acute Coronary

Fall 2010 -‐ Spring 2020

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Coronary Artery Disease and

Acute Coronary Syndrome (MI) Fall 2019 -‐ Spring 2020 1

OXYGENATION NEEDS

•  Ven2la2on •  Perfusion •  Diffusion *What concept is involved? *Your pa2ent reports having CP, what do you do? *What nursing physical assessments are involved?

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Coronary Artery Disease (CAD)

Stages of Atherosclerosis (Fig. 33-‐1 pg. 703)

Atherosclerosis –major cause of CAD •  Begins as soQ

deposits of fat that harden with age

•  Referred to as “hardening of arteries”

•  Characterized by lipid deposits within in2ma of artery

•  Endothelial injury and inflamma2on play a major role in development

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•  E2ology and Pathophysiology


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Which pa2ent is most at risk for developing coronary artery disease? a.  A hypertensive pa2ent who smokes cigareZes b.  An overweight pa2ent who uses smokeless

tobacco c.  A pa2ent who has diabetes and uses

methamphetamines d.  A sedentary pa2ent who has elevated

homocysteine levels


Audience Response Question

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Risk Factors for CAD

•  Nonmodifiable risk factors –  Age –  Gender –  Ethnicity –  Family history –  Gene2c predisposi2on

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Risk Factors for CAD •  Major modifiable risk factors

–  Elevated serum lipids •  Cholesterol >200 mg/dL (5.2

mmol/L) •  Triglycerides >150 mg/dL (3.7

mmol/L) •  High-‐density lipoproteins (HDL) •  Low-‐density lipoproteins (LDL)

–  Hypertension –  Tobacco use

•  Second-‐hand smoke •  All lead to vessel inflammation

and thromobosis –  Physical inacDvity –  Obesity


•  Contribu2ng modifiable risk factors –  Diabetes –  Metabolic syndrome –  Psychologic states –  Homocysteine level –  Substance abuse “Arterial damage”

•  RN has major role in teaching health-‐promo2ng behaviors

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The nurse determines that teaching about implemen2ng dietary changes to decrease the risk of CAD has been effec2ve when the pa2ent says, a.  “I should not eat any red meat such as beef, pork, or lamb.” b.  “I should have some type of fish at least 3 2mes a week.” c.  “Most of my fat intake should be from olive oil or the oils in

nuts.” d.  “If I reduce the fat in my diet to about 5% of my calories, I

will be much healthier.”


Audience Response Question

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Coronary Artery Disease E2ology and Pathophysiology

•  C-‐reac2ve protein (CRP) – Protein produced by liver – Nonspecific marker of inflamma2on –  Increased in many pa2ents with CAD – Chronic exposure to CRP linked with unstable plaques and oxida2on of LDL cholesterol

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Coronary Artery Disease E2ology and Pathophysiology

•  Collateral circula2on –  Arterial anastomoses within coronary circula2on

–  Increased with chronic ischemia

– May be inadequate with rapid-‐onset CAD

–  Old vs. young

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Clinical Manifesta2ons of CAD Angina = Chest Pain

•  Chronic and progressive disease •  Can be acute for varying reasons, important to rule out MI

• O2 demand > O2 supply → myocardial ischemia

• Angina = clinical manifesta2on •  Occurs when arteries are blocked 70% or more •  50% or more for leQ main coronary artery

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LocaDons and PaGerns of Angina and MI Fig 33-‐3 pg. 712

•  Some patients, especially women and older adults, report atypical symptoms of angina including dyspnea, nausea, and/or fatigue.

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Chronic Stable Angina Types of Angina

•  Silent ischemia –  Diabe2c neuropathy –  Confirmed by ECG changes

•  ST segment depression and/or T-‐wave inversion

•  Prinzmetal’s (variant) angina –  Occurs at rest –  Spasm of a major coronary artery (calcium channel blockers)

–  CAD may or may not be present

•  Microvascular angina –  CP occurs in absence of significant CAD or coronary spasm of a major coronary artery

–  CP related to myocardial ischemia associated with atherosclerosis or spasm of the small distal branch vessels of the coronary microcircula2on

–  Preven2on and treatment follows CAD recommenda2ons

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Acute Coronary Syndrome Fig 33-‐7 pg. 718


Relationships among coronary artery disease, chronic stable angina, and acute coronary syndrome.

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Clinical Manifesta2ons of CAD Chronic Stable Angina

•  IntermiZent CP that occurs over a long period with same paZern of onset, dura2on, and intensity of symptoms

•  Provoked by physical exer2on, stress, emo2onal upset

•  Few minutes in dura2on, subsides when precipita2ng factors resolved

•  Control with drugs (i.e. nitroglycerin)

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Nursing and Interprofessional Care: CAD

•  Physical fitness –no maZer what age, but will differ – FITT formula: 30 minutes most days plus weight training 2 days a week

– Regular physical ac2vity contributes to • Weight reduc2on • Reduc2on of >10% in systolic BP •  Increase in HDL cholesterol

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Nursing and Interprofessional Care: CAD

•  Nutri2onal therapy (Lower LDL) – ↓ Saturated fats and cholesterol

– ↓ Red meat, egg yolks, whole milk

– ↓alcohol and simple sugars

•  ↑ Complex carbohydrates and fiber

(whole grains, fruits, vegetables, and fiber) •  ↑ Omega-‐3 faZy acids (AHA recommends ea2ng tofu, soybean, canola, walnut, flaxseed because these products contain alpha-‐linolenic acid , which becomes omega-3 fatty acid in the body. Fall 2019 -‐ Spring 2020 16

Nursing and Interprofessional Care: CAD – DRUG THERAPY

•  Lipid-‐lowering drug therapy – If diet and exercise ineffecDve –  Sta2ns –atorvasta2n (Lipitor), simvasta2n (Zocor)

•  Inhibit cholesterol synthesis, decrease LDL, increase HDL

•  Monitor for liver damage and myopathy

•  An2platelet therapy –  ASA (81 mg or 325 mg) –  Clopidogrel 75 mg

*Explain the mechanism of ac2on

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Chronic/Unstable Angina Interprofessional Care: Drug Therapy

•  Goal: ↓ O2 demand and/or ↑ O2 supply

•  Short-‐ac2ng nitrates SL NTG –  Dilate peripheral and

coronary blood vessels –  Give sublingually or by spray –  If no relief in 5 minutes, call

EMS; if some relief ,repeat every 5 minutes for maximum 3 doses

–  Pa2ent teaching –  Can use prophylac2cally

•  Long-‐ac2ng nitrates –oral, NTG ointment, Transdermal controlled-‐release NTG –  To reduce angina incidence –  Main side effects: headache

(Tylenol), orthosta2c hypotension

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Chronic Stable Angina Interprofessional Care: Drug Therapy

•  ACE and ARBs: –  benazepril (Lotensin) –  enalapril (Vasotec) –  lisinopril (Zestril) –  losartan (Cozaar)

•  β-‐Blockers: –  atenolol (Tenormin) –  metoprolol (Lopressor)

•  Calcium channel blockers: –  dil2azem (Cardizem) –  amlodipine (Norvasc) –  nifedipine (Procardia)

•  Lipid lowering drugs –  atorvasta2n (Lipitor) –  simvasta2n (Zocor)

•  An2platelets –  aspirin –  clopidogrel

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Chronic Stable/Unstable Angina Interprofessional Care: Diagnos2c Studies

– Chest x-‐ray – 12-‐lead ECG – Laboratory studies –lipid profile, CRP, BMP, CBC coags, cardiac enzymes

– Echocardiogram – Exercise stress test (physical/pharmacologic)

•  For pa2ents with abnormal but nondiagnos2c ECG and nega2ve biomarkers

– Coronary CT Angiography (CCTA)

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Chronic Stable/Unstable Angina Nursing/Interprofessional Care: Diagnos2c

Studies •  Cardiac catheteriza2on/

coronary angiography –  Visualize blockages (diagnos2c)

–  Open blockages (interven2onal)

•  Percutaneous coronary interven2on (PCI)

•  Balloon angioplasty •  Stent

*For pa2ents with a STEMI *Not for pa2ents with UA or NSTEMI

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Pre-‐PCI and Post-‐PCI With Stent Placement Fig 33-‐6 pg. 718

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Nursing Management Coronary revasculariza2on: PCI

– Monitor for recurrent angina – Frequent VS –per protocol, including cardiac rhythm

– Monitor catheter inser2on site for bleeding • Want to achieve hemostasis (sandbags)

– Neurovascular assessment – Bed rest per ins2tu2onal policy

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Nursing Management Chronic Stable/Unstable Angina

•  Acute Interven2on – Upright posi2on – Supplemental oxygen – Assess vital signs, cardiac monitor, IV access – 12-‐lead ECG – Administer NTG followed by an opioid analgesic, if needed

– Assess heart and breath sounds – Admission to hospital for observa2on

•  Interven2onal cardiac catheteriza2on

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Nursing Management Chronic Stable/Unstable Angina

•  Ambulatory Care – Provide reassurance, decrease stress response – Pa2ent teaching

•  CAD and angina •  Precipita2ng factors for angina •  Risk factor reduc2on •  Drugs (substance abuse)

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Acute Coronary Syndrome E2ology and Pathophysiology

•  Result – Par2al occlusion of coronary artery: UA or NSTEMI – Total occlusion of coronary artery: STEMI


Deteriora2on of once stable

plague Rupture Platelet

aggrega2on Thrombus

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Clinical Manifesta2ons of ACS Unstable Angina

•  New in onset, occurs at rest

•  Increase in frequency, dura2on, or with less effort

•  Pain las2ng > 10 minutes •  Needs immediate

treatment that is different from unstable angina

•  Symptoms in women oQen under-‐recognized as heart related

•  Severe CP not relieved by rest, posi2on change, or nitrate administra2on

•  Heaviness, pressure, 2ghtness, burning, constric2on, crushing

•  Substernal or epigastric •  May radiate to neck, lower jaw, arms, back

–  OQen occurs in early morning

–  Atypical in women, elderly –  No pain if cardiac neuropathy (diabetes)

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Clinical Manifesta2ons of ACS Myocardial Infarc2on (MI)

•  Result of abrupt stoppage of blood flow through a coronary artery, causing irreversible myocardial cell death (necrosis) –  Preexis2ng CAD –  STEMI -‐ occlusive thrombus

–  NSTEMI -‐ non-‐occlusive thrombus

•  ST-‐elevaDon and non-‐ST-‐elevaDon –  Changes in QRS complex, ST segment, and T wave

–  Serial ECGs reflect evolu2on of MI

–  Dis2nguish between STEMI and NSTEMI/UA for dx and tx purpose

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Unstable Angina and MI Diagnos2c Studies

STEMI •  Usually have a

complete coronary occlusion.

•  ST elevation is first seen on the 12-lead ECG.

•  Within few hours to days, T-wave inversion and pathologic Q waves develop.

NSTEMI or UAUA •  Usually have transient

thrombosis or incomplete coronary occlusion.

•  These patients often develop ST depression or T wave inversion on the initial ECG.

•  They usually do not develop pathologic Q waves.

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Myocardial Infarc2on From Occlusion (Fig 33-‐11 pg. 724

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Clinical Manifesta2ons of ACS Myocardial Infarc2on

•  Catecholamine release and s2mula2on of SNS –  Diaphoresis –  Increased HR and BP –  Skin: ashen, clammy, and/or cool to touch

•  Cardiovascular –  Ini2ally, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)

–  Crackles, JVD –  Abnormal heart sounds

•  S3 or S4 •  New murmur

•  Nausea and vomi2ng –  Reflex s2mula2on of the vomi2ng center by severe pain

–  Vasovagal reflex •  Fever

–  Up to 100.4° F (38° C) in first 24-‐48 hours

–  Systemic inflammatory process caused by heart cell death

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Myocardial Infarc2on Healing Process

•  Within 24 hours, leukocytes infiltrate the area of cell death

•  Neutrophils and macrophages begin to remove necro2c 2ssue by fourth day → thin wall

•  Necro2c zone iden2fiable by ECG changes

•  Collagen matrix laid down •  10 to 14 days aQer MI, scar

2ssue is s2ll weak

•  Heart muscle vulnerable to stress

•  Monitor pa2ent carefully as ac2vity level increases

•  By 6 weeks aQer MI, scar 2ssue has replaced necro2c 2ssue –  Area is said to be healed, but

less compliant •  Ventricular remodeling

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

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Complica2ons of Myocardial Infarc2on

•  Dysrhythmias –  Most common complica2on –  Can be caused by ischemia,

electrolyte imbalances, or SNS sDmulaDon

–  VT and VF are most common cause of death in prehospitaliza2on period

•  Heart failure –  Pumping power of heart has

diminished –  LeQ-‐sided HF –  Right-‐sided HF

•  Cardiogenic shock –  Severe LV failure, papillary

muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarc2on

–  Requires aggressive management

•  Associated with a high death rate

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Complica2ons of Myocardial Infarc2on

•  Acute pericardiDs –  Inflamma2on of pericardium

–  Mild to severe chest pain •  Increases with inspira2on, coughing, movement of upper body

•  Relieved by sixng in forward posi2on

–  Pericardial fric2on rub •  Papillary muscle

dysfuncDon or rupture –  Causes mitral valve regurgita2on

•  LeX ventricular aneurysm –  Myocardial wall becomes thinned and bulges out during contrac2on

–  Leads to HF, dysrhythmias, and angina

•  Ventricular septal wall rupture and leX ventricular free wall rupture –  HF and cardiogenic shock –  Emergency repair

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Unstable Angina and MI Diagnos2c Studies

•  Cardiac Biomarkers – Troponin

•  Rises within 4-‐6 hours, peaks 10-‐24 hours, detected for up to 10-‐14 days

– Creatine kinase (CK) •  CK-‐MB cardiac specific •  Rises in 3-‐6 hours, peaks in 12-‐24 hours, returns to baseline within 12-‐48 hours

–  Serial Cardiac Biomarkers + ECG (i.e. Q8 hrs)

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Interprofessional Care Acute Coronary Syndrome

•  Ini2al interven2ons – 12-‐lead ECG – Upright posi2on – Oxygen – keep O2 sat > 93% –  IV access – Nitroglycerin (SL) and ASA (PO/PR) – Sta2n – Morphine

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•  Ongoing monitoring –admission to hospital – Treat dysrhythmias – Frequent vital sign monitoring – Bed rest/limited ac2vity for 12–24 hours

•  UA or NSTEMI – Dual an2platelet therapy –aspirin, clopidogrel (Plavix) , and heparin

– Cardiac catheteriza2on with PCI once stable – Reperfusion therapy

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•  Emergent PCI – Treatment of choice for confirmed STEMI – Goal: 90 minutes from door to catheter laboratory – Balloon angioplasty + stent(s) – Many advantages over Coronary Artery Bypass GraQ (CABG) –surgical interven2on

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•  Thromboly2c therapy –  Only for paDents with a STEMI

•  Agencies that do not have cardiac catheteriza2on resources

–  Given IV within 30 minutes of arrival to the ED

–  Pa2ent selec2on cri2cal due to bleeding complica2ons

–  Draw blood and start 2–3 IV sites: what blood studies will you draw?

–  Administer according to protocol

–  Monitor closely for signs of bleeding

–  Assess for signs of reperfusion

•  Cardiac rhythm –return of ST segment to baseline best sign, VS, cardio/pulmonary and neurological assessment

•  IV heparin to prevent reocclusion –  Heparin gZ (25,000 units/500ml NS or D5W)

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•  Surgical revasculariza2on if: – Failed medical management – Presence of leQ 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 dysfunc2on, chronic kidney disease

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A pa2ent is admiZed to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscita2on. When reviewing the health care provider’s admission orders, which order should the nurse ques2on? a.  Oxygen at 4 L/min per nasal cannula b.  Morphine sulfate 2 mg IV every 10 minutes un2l the

pain is relieved c.  Tissue plasminogen ac2vator (tPA) 100 mg IV infused

over 3 hours d.  IV nitroglycerin at 5 mcg/minute and increase 5 mcg/

minute every 3 to 5 minutes


Audience Response QuesDon

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Interprofessional Care Acute Coronary Syndrome –Tradi2onal coronary

artery bypass graQ (CABG) surgery

–  Requires sternotomy and

cardiopulmonary bypass (CPB) –  Uses arteries and veins for graQs

•  The internal mammary artery (IMA) is most common artery used for bypass graQ

•  Radial artery is another poten2al graQ

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Nursing Management Acute Coronary Syndrome

•  Complica2ons 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

–  Infec2ons

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•  CABG: postopera2ve nursing care –  ICU for first 24–36 hours –  Pulmonary artery catheter –  Intraarterial line –  Pleural/medias2nal chest

tubes –  Con2nuous ECG –  ET tube with mechanical

ven2la2on –  Epicardial pacing wires –  Urinary catheter –  NG tube

–  Assess pa2ent for bleeding –  Monitor hemodynamic status –  Assess fluid status (I&Os) –  Replace blood and

electrolytes PRN –  Restore temperature –  Monitor for atrial fibrilla2on

(which is common) –  Surgical site care

•  Radial artery harvest site •  Leg incisions •  Chest incision

–  Pain management –  DVT preven2on –  Pulmonary hygiene –  Cogni2ve dysfunc2on

•  Begin cardiac rehabilita2on

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•  This is a postopera2ve pa2ent –basic individualized care on its own despite the type of surgical interven2on done. What else will you an2cipate as far the progression of this pa2ent with regards to other body systems (i.e. diet, ac2vity, elimina2on, etc.)?

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•  Drug therapy –postopera2ve: –  IV nitroglycerin (NTG) – Analgesics –morphine – β-‐adrenergic blockers – ACE inhibitors – An2dysrhythmic drugs – Lipid-‐lowering drugs – Stool soQeners – Maintenance IVF – Electrolyte replacement – Blood products

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•  Acute Care -‐Psychosocial – Anxiety reduc2on

•  Iden2fy source and alleviate •  Pa2ent teaching important

– Emo2onal and behavioral reac2on •  Maximize pa2ent’s social support systems •  Consider open visita2on

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Nursing Management Chronic Stable Angina and ACS

•  Planning: Overall goals –  Relief of pain –  Preserva2on of heart muscle

–  Immediate and appropriate treatment

–  Effec2ve coping with illness-‐associated anxiety

–  Par2cipa2on in a rehabilita2on plan

–  Reduc2on of risk factors

•  Evalua2on –  Stable vital signs –  Relief of pain –  Decreased anxiety –  Realis2c program of ac2vity

–  Effec2ve management of therapeu2c regimen

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•  Ambulatory Care –  Cardiac rehabilita2on –  Pa2ent and caregiver teaching

–  Physical ac2vity •  Gradually increased •  Monitor heart rate •  Low-‐level stress test before discharge

•  Isometric vs isotonic ac2vi2es

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•  Ambulatory Care – Resump2on of sexual ac2vity –moderate energy ac2vity equivalent to climbing 2 flights of stairs

•  Teach when discuss other physical ac2vity •  Erec2le dysfunc2on drugs contraindicated with nitrates

•  Prophylac2c nitrates before sexual ac2vity • When to avoid sex •  Typically 7–10 days post MI or when pa2ent can climb two flights of stairs

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Documents

Chapter 33- Coronary Artery Disease and Acute Coronary