Acute Coronary Syndromes & Cardiac Surgery Flashcards
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
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
- 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
Recognize Cues/MI Risk Factors - Non-modifiable
- Age
- Gender
- Fhx
- Ethnic background
Modifiable
- Elevated serum cholesterol
- Cigarette smoking
- HTN
- Impaired glucose tolerance/DM
- Obesity
- Excessive alcohol
- Limited physical activity
- Adrenaline/catecholamine increases (stress/fright)
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
- 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
- Over time, CHD can weaken the heart muscle & lead to HF & arrhythmias
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
Continuum of CAD
?
Is an insufficient oxygen supply to meet requirements of myocardium
Ischemia
?
Is necrosis or cell death that occurs when severe ischemia is prolonged & decreased perfusion causes irreversible damage to tissues
Infarction
Angina
- Stable
- Unstable
- Variant (Prinzmetal’s)
- Microvascular
- Typically no changes in troponin or CK levels
- Responds to nitroglycerin (NTG) (3x every month)
- Typically no ST changes on 12-lead EKG
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
?
- 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)
Stable angina
! Isn’t an MI but suggests that & MI is more likely to happen in the future
> Make radical lifestyle changes
?
- 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
Variant (Prinzmetal’s) angina
?
- 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
Unstable angina
! Can happen more often & be more severe than stable angina
?
- Can be more severe & lasts longer than other types; rx may not relieve this
- Newer studies state women have this type
Microvascular angina
! Other conditions that cause CP besides CHD include PE, a lung infection, aortic dissection, hypertrophic cardiomyopathy, pericarditis, & a panic attack
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
?
Is a myocardial muscle protein released into the bloodstream w/injury to myocardial muscle
Troponin
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
! Troponin is more sensitive than myoglobin & creatine kinase
Troponin T < ___ ng/mL
Troponin I < ___ ng/mL
0.10
0.03
- 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
- 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
?
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
Creatinine kinase (CK)
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 ___
skeletal muscle
myocardial muscle
brain
?
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
Myoglobin
?
Has been the most studied marker of inflammation
- Any inflammatory process can produce this in the blood
- Elevations also seen w/HTN, infection, & smoking
hsCRP (highly sensitive C-reactive protein)
hsCRP
Low risk = < ___ mg/dL; over ___ mg/dL puts pt @ risk for heart disease
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
hsCRP
Lower risk: <2.0 mg/L
Higher risk: > or = 3.0 mg/L
Acute inflammation: >10.0 mg/L
?
Means that there’s still some flow in the cardiac arteries
NSTEMI
- 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
subendocardium
- Doesn’t usually progress to a Q wave & is sometimes called a non Q wave MI
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
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
depression
?
Represents complete blockage of the coronary artery usually from thrombus formation; causes transmural damage meaning that necrosis goes through all levels of the muscle
STEMI
- 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
- If ischemia persists, it takes approx 4-6 hrs for entire thickness of heart muscle to become necrotic
! 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
! 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
- 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
- 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
Sx’s of Complete Occlusion MI
Right Coronary Artery
> ___
> ___
> ___
JVD
Hypotension
Bradycardia
LCA or Left Ventricle Infarct
- Worse prognosis; highest risk of sudden cardiac death; CHF
> Dyspnea
> Tachypnea
> HTN
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
- Potential for dysrhythmias d/t ischemia & ventricular irritability
- Potential for HF d/t left ventricular dysfunction
ACS: Planning & Implementation: Generate Solutions & Take Action
- Managing acute pain
- Increasing myocardial tissue perfusion
- Identifying & managing dysrhythmias
- Monitoring for & managing HF
- 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)
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
- Morphine may also be given to pain unresponsive to NTG
! Re: O2 Use
- Oxygen use in the ABSENCE of hypoxemia has been shown to INCREASE coronary vascular resistance, DECREASE coronary blood flow, & INCREASE mortality
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.
- 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.
Expected outcomes are that patient will:
- State that pain is alleviated
- Have adequate myocardial perfusion
- Be free of complications such as dysrhythmias & HF
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)
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
- 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
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
- Anticipate need for intubation if respiratory distress is evident
- Prepare for CPR & defibrillation if indicated
- Anticipate the need for transcutaneous pacing if indicated
MI - Potential Complications
- Dysrhythmias
- HF
- Cardiogenic shock
- Embolism
- Papillary muscle dysfunction
- Ventricular aneurysm
- Pericarditis
- Dressler syndrome - a pericarditis following MI, trauma, or surgery
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
- Risk modification
- Diet, exercise, complementary, drug therapies, sexual activity
- Community resources
