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NUR 201 Week 5 > Acute Coronary Syndromes & Cardiac Surgery > Flashcards

Acute Coronary Syndromes & Cardiac Surgery Flashcards

1
Q

MI - Epidemiology

  • More than 1 in 3 adults lives w/1 or more types of CVD
  • Contributing risk factors for heart disease & MI include
    > cigarette smoking, hyperlipidemia, type 2 diabetes
    > elevated adrenaline (catecholamines), obesity, inactivity, HTN
A
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2
Q

Pathophysiology

  • Atherosclerosis is the gradual buildup of plaque inside the wall of the artery from CHRONIC INFLAMMATION
  • Rupture of this plaque results in thrombus formation & obstructs coronary artery flow
A
  • Ischemia & death of heart muscle are the eventual outcomes
  • Heart muscle damaged by inadequate blood supply cannot maintain normal cardiac function, which results in decreased CO & systemic sx’s assoc w/MI
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3
Q

Recognize Cues/MI Risk Factors - Non-modifiable

  • Age
  • Gender
  • Fhx
  • Ethnic background
A

Modifiable

  • Elevated serum cholesterol
  • Cigarette smoking
  • HTN
  • Impaired glucose tolerance/DM
  • Obesity
  • Excessive alcohol
  • Limited physical activity
  • Adrenaline/catecholamine increases (stress/fright)
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4
Q

Coronary Artery Disease (coronary heart disease)

  • Is a disease in which a waxy substance called plaque builds up inside the coronary arteries
  • These arteries supply O2-rich blood to the heart muscle
  • When plaque builds up in the arteries, the condition is called atherosclerosis
A
  • Hardened plaque narrows the coronary arteries & reduces the flow of O2-rich blood to the heart
  • If plaque ruptures, a blood clot can form on its surface; large blood clot can mostly or completely block blood flow through a coronary artery
  • Angina is a chest pain or discomfort; may feel like pressure or squeezing in the chest
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5
Q
  • Over time, CHD can weaken the heart muscle & lead to HF & arrhythmias
A

Plaque & clot formation

  • Lesion or inflammation in arteries
  • Body sends in cholesterol to help heal inflammation
  • Inflammation & clot formation block blood flow to the heart tissue & tissue begins to die
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6
Q

Continuum of CAD

?

Is an insufficient oxygen supply to meet requirements of myocardium

A

Ischemia

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7
Q

?

Is necrosis or cell death that occurs when severe ischemia is prolonged & decreased perfusion causes irreversible damage to tissues

A

Infarction

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8
Q

Angina

  • Stable
  • Unstable
  • Variant (Prinzmetal’s)
  • Microvascular
A
  • Typically no changes in troponin or CK levels
  • Responds to nitroglycerin (NTG) (3x every month)
  • Typically no ST changes on 12-lead EKG
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9
Q

Angina

  • Sometimes called angina pectoris
  • Happens when there’s 60-70% blockage in coronary arteries - not typically associated w/damage to heart muscle but are warning signs
A
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10
Q

?

  • Most common type
  • Happens when heart is working harder than usual; has a regular pattern
    > “Pattern” being how often the angina occurs, how severe it is & what factors trigger it
  • You could learn the pattern & when pain will occur; usually goes away a few min after rest or angina rx (likely NTG which opens up the arteries & increases blood flow)
A

Stable angina

! Isn’t an MI but suggests that & MI is more likely to happen in the future
> Make radical lifestyle changes

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11
Q

?

  • Rare; caused by a spasm in the coronary arteries
  • Occurs while @ rest; pain can be severe
  • Usually happens between midnight & early morning; rx’s can help
A

Variant (Prinzmetal’s) angina

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12
Q

?

  • Type that doesn’t follow a stable pattern
  • Can happen w/ or w/o physical exertion, & rest or rx may not relieve pain
    ! Very dangerous & needs treatment; an MI could happen
A

Unstable angina

! Can happen more often & be more severe than stable angina

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13
Q

?

  • Can be more severe & lasts longer than other types; rx may not relieve this
  • Newer studies state women have this type
A

Microvascular angina

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14
Q

! Other conditions that cause CP besides CHD include PE, a lung infection, aortic dissection, hypertrophic cardiomyopathy, pericarditis, & a panic attack

A

NTG can be taken in 5-min increments; a total of 3 doses can be given to relieve angina pain
> Usually responds to NTG but if taking 3 sublingual tablets one after another doesn’t help, an MI may be happening

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15
Q

?

Is a myocardial muscle protein released into the bloodstream w/injury to myocardial muscle

A

Troponin

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16
Q

Troponin T & and I aren’t found in healthy pts, so any rise in values indicates cardiac necrosis or acute MI

Have a wide diagnostic timeframe; are useful for pts who present several hrs after CP onset

A

! Troponin is more sensitive than myoglobin & creatine kinase

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17
Q

Troponin T < ___ ng/mL

Troponin I < ___ ng/mL

A

0.10

0.03

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18
Q
  • Cardiology sources state that the troponin is the only biomarker that’s recommended to be used for dx of acute MI @ this time b/c of its superior sensitivity & accuracy
A
  • Pts w/elevated troponin lvls but negative creatinine-kinase-MB (CK-MB) values who were formerly dx’d w/unstable angina or minor myocardial injury are now reclassified as non-ST segment elevated MI (NSTEMI), even in absence of diagnostic ECG changes
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19
Q

?

Is an enzyme specific to cells of the brain, myocardium, & skeletal muscle

  • Appearance in the blood indicates tissue necrosis or injury, w/lvls following a predictable rise & fall during a specified period
A

Creatinine kinase (CK)

20
Q

3 isoenzymes of CK

CK-MM - found in ___

CK-MB - found in ___
> Is most specific for MI & shows a predictable rise & fall during 3 days; peak lvl occurs ~24 hrs >CP onset

CK-BB - found in ___

A

skeletal muscle

myocardial muscle

brain

21
Q

?

Is a low-molecular-weight heme protein found in cardiac & skeletal muscle; is earliest marker detected - as early as 2 hrs >MI w/rapid decline >7 hrs

  • Is not cardiac specific so usefulness is more limited than troponin
A

Myoglobin

22
Q

?

Has been the most studied marker of inflammation

  • Any inflammatory process can produce this in the blood
  • Elevations also seen w/HTN, infection, & smoking
A

hsCRP (highly sensitive C-reactive protein)

23
Q

hsCRP

Low risk = < ___ mg/dL; over ___ mg/dL puts pt @ risk for heart disease

A

1; 3

! CRP is very helpful in determining treatment outcomes in pts @ risk for coronary dz & in managing statin therapy >an acute MI
> Most useful time to measure appears to be for risk assessment in middle-age or older

24
Q

hsCRP

Lower risk: <2.0 mg/L

Higher risk: > or = 3.0 mg/L

A

Acute inflammation: >10.0 mg/L

25
Q

?

Means that there’s still some flow in the cardiac arteries

A

NSTEMI

26
Q
  • Infarction is a dynamic process that takes time
  • Cardiac cells can withstand ischemic conditions for approx 20 min before cell death begins
  • Earliest tissue to become ischemic is the ___ (innermost layer of tissue in cardiac muscle)
    > Is b/c it’s too far away from the blood in the ventricular cavity & the O2 from the carotid artery
A

subendocardium

27
Q
  • Doesn’t usually progress to a Q wave & is sometimes called a non Q wave MI
A

Cardiac markers of NSTEMI vs STEMI

  • CK-MB, troponin I and T all elevate in both cases
    > Elevation mild in NSTEMI compared w/STEMI

! Needs intervention to enhance perfusion - usually PCI w/stents

28
Q

NSTEMI or NSTE-ACS

  • NON ST elevation MI aka Non ST elevation Acute Coronary Syndrome
  • ST and T wave ___, typically indicating ischemia
  • Cardiac enzymes initial WNL, then ELEV over 3 to 12 hrs (slower process than STEMI)
  • Causes: PARTIAL OCCLUSION of blood flow to coronary arteries
A

depression

29
Q

?

Represents complete blockage of the coronary artery usually from thrombus formation; causes transmural damage meaning that necrosis goes through all levels of the muscle

A

STEMI

30
Q
  • STEMI shows ST segment elevation in ECG d/t full thickness injury of heart muscle & later progresses to a Q-wave
    > Also called a Q wave MI
  • Ultimate ECG findings of STEMI are ST-segment elevation & elevated troponin levels
A
  • If ischemia persists, it takes approx 4-6 hrs for entire thickness of heart muscle to become necrotic
31
Q

! Thrombus causes can abrupt 100% occlusion to the coronary artery, is a medical emergency, & requires immediate revascularization of the blocked coronary artery

! Intervention needed = PCI within 120 min of sx onset; also undergo clot busting and/or CABG

A

! After 48 hrs infarcted area turns gray w/yellow streaks as neutrophils invade tissue & begin to remove necrotic cells

> By 8-10 days >infarction, granulation tissue forms at edges of necrotic tissue
Over 2-3 month period, necrotic area eventually develops into a shrunken, thin, firm scar

32
Q
  • Scar tissue permanently changes the size & shape of the entire left ventricle, called ventricular remodeling
  • Remodeling may decrease left ventricular function, cause HF, and increase morbidity & mortality
A
  • Scarred tissue doesn’t contract or conduct electrically, thus is why this area is often the cause of chronic ventricular dysrhythmias surrounding the infarcted zone
33
Q

Sx’s of Complete Occlusion MI

Right Coronary Artery
> ___
> ___
> ___

A

JVD

Hypotension

Bradycardia

34
Q

LCA or Left Ventricle Infarct

  • Worse prognosis; highest risk of sudden cardiac death; CHF
    > Dyspnea
    > Tachypnea
    > HTN
A
35
Q

Analysis: Analyze Cues & Prioritize Hypotheses

  • Acute pain d/t an imbalance between myocardial oxygen supply & demand
  • Decreased myocardial tissue perfusion d/t interruption of arterial blood flow
A
  • Potential for dysrhythmias d/t ischemia & ventricular irritability
  • Potential for HF d/t left ventricular dysfunction
36
Q

ACS: Planning & Implementation: Generate Solutions & Take Action

  • Managing acute pain
  • Increasing myocardial tissue perfusion
  • Identifying & managing dysrhythmias
  • Monitoring for & managing HF
A
  • Before giving NTG, ensure that the pt hasn’t taken any phosphodiesterase inhibitors (PI’s) for ED, like sildenafil, tadalafil, avanafil, or vardenafil, within past 24-48 hrs
    > Concomitant use of NTG w/these inhibitors can cause profound hypotension

> Some PI’s are used in the treatment of PAH & pts w/PAH can’t stop taking the PI (! NTG contraindicated)

37
Q

NTG

  • Increases collateral blood flow
  • Redistributes blood flow toward the subendocardium
  • Dilates coronary arteries
  • Decreases myocardial O2 demand by peripheral vasodilation which decreases preload & afterload
A
  • Morphine may also be given to pain unresponsive to NTG
38
Q

! Re: O2 Use

  • Oxygen use in the ABSENCE of hypoxemia has been shown to INCREASE coronary vascular resistance, DECREASE coronary blood flow, & INCREASE mortality
A
39
Q

CAD: Older Adult Considerations

  • Recognize that CP may not be evident in the older pt. Examples of assoc sx’s are unexplained dyspnea, confusion, or GI sx’s
  • Although older adults have a greater reduction in mortality rate from MI w/the use of fibrinolytic therapy, they also have the most severe side effects
  • Dysrhythmia may be a normal age-related change rather than a complication of MI. Determine whether the dysrhythmia is causing significant sx’s. Then notify the HCP.
A
  • If beta blockers are used, assess the pt carefully for the development of side effects. Exacerbation of the depression some older adults have is a sig problem w/beta blockade.
  • Plan slow, steady increases in activity. Older adults w/minimal previous exercise show particular benefit from a gradual increase in activity.
  • Older adults should plan longer warm-up & cool-down periods when participating in an exercise program. Their pulse rates may not return to baseline until 30 min or longer >exercise.
40
Q

Expected outcomes are that patient will:

  • State that pain is alleviated
  • Have adequate myocardial perfusion
  • Be free of complications such as dysrhythmias & HF
A

Sx’s

! Ask about radiating pain also; jaw/mouth/throat, arm/back

! Pts w/diabetes may not present w/CP (may have damage to nerve conduction)

41
Q

Nursing Process: Assessment

  • Restlessness
  • Pain characteristics
  • Focused cardiac assessment
  • ECG changes
    > ST segment changes indicative of ischemia or injury
    > Presence of Q wave diagnostic for MI
A
  • Troponin levels
    > Elevates within 4 hrs & can stay elevated for days
  • VS/oximetry
    > Tachycardia w/a borderline low BP & dec O2 sat is a sign of inadequate cardiac output & O2 delivery
  • Skin/peripheral pulses
    > Dec pulses & cold, clammy, pale skin are signs of inadequate tissue perfusion & inadequate CO; activation of SNS w/low CO will stimulate diaphoresis
  • Urine output
    > Decreased or absent urine output is a sign of dec renal perfusion r/t dec cardiac output
42
Q

Assess, Take Action, Evaluate Outcomes, Repeat

  • Monitor ABCs, VS, LOC, heart & breath sounds, cardiac rhythm, & O2 sat
  • Assess & record response to rx’s (e.g., decrease in CP), & re-medicate or titrate rx’s (e.g., NTG) as needed
  • Provide reassurance & emotional support to pt & caregiver
  • Explain all interventions & procedures to pt & caregiver in simple terms
A
  • Anticipate need for intubation if respiratory distress is evident
  • Prepare for CPR & defibrillation if indicated
  • Anticipate the need for transcutaneous pacing if indicated
43
Q
A
44
Q

MI - Potential Complications

  • Dysrhythmias
  • HF
  • Cardiogenic shock
  • Embolism
  • Papillary muscle dysfunction
A
  • Ventricular aneurysm
  • Pericarditis
  • Dressler syndrome - a pericarditis following MI, trauma, or surgery
45
Q

Cardiac Rehab

  • 2-8 wks up to 6 mos
  • Specific to the type & degree of injury & type & degree of treatment
  • Assess educational needs of pt & family & readiness to learn
A
  • Risk modification
  • Diet, exercise, complementary, drug therapies, sexual activity
  • Community resources

NUR 201 Week 5 (5 decks)

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