CAD and Acute Coronary Syndrome Flashcards
CAD
coronary artery disease
a progressive atherosclerotic disorder of the coronary arteries that results in narrowing or complete occlusion of one or more arteries
What does atherosclerosis affect?
medium-sized arteries that perfuse the heart and other major organs
progressive build up of plaque in a person’s arteries
What happens when blood flow is stopped?
MI
CAD spectrum (3)
1) Asymptomatic
2) Stable Angina
3) Acute Coronary Syndrome
Types of Acute Coronary Syndrome (3)
1) Unstable Angina
2) Myocardial Infarction
3) Sudden Coronary Death
Ischemic occurs when arteries are about ___% occluded
70
Common signs of a heart attack
1) midsternal chest pain
2) sweating
3) SOB
Factors that DECREASE O2 supply (many)
Anemia
CAD
Hypoxia
COPD, asthma, pneumonia
Arrhythmias
CHF
Coronary spasm
Thrombosis
Valve disorders
T or F: Someone with extreme anemia can get a heart attack.
TRUE
hemoglobin carries oxygen
someone with a low vs high hemoglobin - can have the same O2 sat but not indicator of how much oxygen is being delivered
T or F: Someone with healthy arteries cannot get a heart attack.
FALSE
Arteries can be fine! But can still get heart attack
Factors that INCREASE O2 demand (many)
Anxiety
Cocaine use
Hyperthermia
Hyperthyroidism
Physical exertion
Aortic stenosis
Arrhythmias- ↑ rates
Cardiomyopathy
Hypertension
Stages of development in atherosclerosis (4)
1) Damaged endothelium & response to injury
2) Fatty streak
3) Fibrous plaque
4) Complicated lesion
atherosclerosis progression prevention (many)
pharmaceuticals - statins
diet - low salt, Mediterranean
exercise
stress management
treat co-morbidities - hypertension, diabetes
Endothelium regulates…
dilation and constriction of vessels
thrombosis – the formation of blood clots
transport of substances to and from the vascular space
growth and ‘apoptosis’ of vascular wall
Endothelial dysfunction leads to… (many)
inadequate vasodilation
prothrombotic
altered permeability
increased secretion of growth factors (hypertrophy - decreases contraction)
increased oxidation of LDL
Collateral Circulation
a protective adaptation
narrowing of arteries starts
capillaries join so there is route to go around the narrowing
so with an occlusion, there is not necessarily no oxygen
Who has more collateral circulation
a) men
b) women
a) men
when women in menopause lose estrogen and cardioprotectiveness, don’t have collateral circulation developed
Signs of CAD in women (many)
absence of cp/ or vague
NO radiation of pain
heaviness of arms
light-headedness
epigastric burning
N/V
diaphoresis
feeling flushed
prodromal symptoms (months before)
-sleep disturbances
-unusual fatigue
-SOB
-indigestion
-anxiety
Signs of CAD in men (many)
chest pain / aching / tightness / pressure / jaw pain
SOB
pain b/w shoulder blades
shoulder/Arm/Neck pain
headache
indigestion
palpitations
cough
diaphoresis
fatigue
N/V
T or F: The treadmill/stress test is less sensitive for women compared to men.
TRUE
Challenges of care - sex differences
failure to recognize & difficulty interpreting symptoms
failure of HCP to recognize prodromal symptoms
ECG & stress test less sensitive
plaque tends to be distributed diffusely (women - many smaller arteries with dif levels of occlusion vs 1 big artery that is majorly occluded)
less likely to be evaluated for risk factors or treated aggressively
Most frequent symptoms of acute MI in the elderly (3)
atypical presentation!
1) SOB
2) fatigue and weakness (“I just don’t feel well”)
3) abdominal or epigastric discomfort
Common pre-existing conditions in the elderly (3)
1) hypertension
2) CHF
3) Previous AMI (acute myocardial infarction)
T or F: Elderly are more likely to delay seeking treatment.
TRUE
transportation, financial costs/risks, think its part of aging
Atypical presentation in the patient with diabetes - common signs and symptoms (many)
why: due to autonomic dysfunction
1) generalized weakness
2) generalized feeling of not being well
3) syncope
4) lightheadedness
5) change in mental status
Non-modifiable risk factors for CAD (4)
1) age
2) male> female until 65
3) genetics
4) ethnicity
Modifiable risk factors for CAD (many)
tobacco use
abdominal obesity
hypertension >140/90mm Hg
hyperlipidemia
physical inactivity
Contributing factors to CAD
psychosocial risk factors (depression, hostility, anger, stress)
elevated homocysteine levels
diabetes Mellitus
metabolic Syndrome
Those with low-risk factors should be assessed every __ years and those with high-risk factors should be assessed every __
3 to 5
every year
Low risk factors
untreated
non-smokers without diabetes
total cholesterol: 4.7 mmol/L
BP: <120/<80
Moderate risk factors
untreated
non-smokers without diabetes
total cholesterol: 4.8 - 5.1 mmol/L
Systolic BP: 120 - 139
Diastolic BP: 80 - 89
Elevated risk factors
untreated
non-smokers without diabetes
total cholesterol: 5.2 - 6.1 mmol/L
Systolic BP: 140 - 159
Diastolic BP: 99 - 99
Major risk factors
TREATED
current smoker
diabetes
cholesterol: 6.2 mmol/L
systolic BP: ≥ 160
diastolic BP: ≥100
Who should we screen?
men ≥ 40 years
women: ≥ 50 years of age OR post-menopausal
smoker
hypertension
elevated cholesterol
diabetic
family history
erectile dysfunction
obesity
inflammatory disease
COPD
HIV
Priority assessments if heart attack is suspected (5)
1) baseline VS and 12-lead ECG
-within 10 minutes****
2) assessment of chest pain
-OPQRST
3) associated symptoms
4) physical assessment
5) meds
To reiterate, what should you do immediately if heart attack is suspected?
Baseline VS and 12-lead ECG!!!
within 10 minutes
Other things to assess, when the patient is stable (4)
1) personal and fam history
2) environmental factors
3) psychosocial history
4) patient’s attitudes and beliefs about health and illness, level of motivation
ECG findings
primary DIAGNOSTIC tool
changes in QRS complex, ST segment & T wave
dynamic process & evolves over time
Repeat every 15-30 minute to 2-4 hours
How often should ECGs be repeated?
every 15-30 minute to 2-4 hours
What does an ST depression indicate?
ischemia
lack of oxygenation
permanent damage can be avoided if we respond appropriately
What does an ST elevation indicate?
infarction
more than just ischemia
damage! permanent death of heart tissue
Assessment - Diagnostic Studies
1) 12 lead EKG
2) cardiac monitor
3) chest X-ray [lungs]
4) coronary angiography
-GOLD STANDARD
other:
5) exercise stress test
6) echocardiogram
Cardiac angiography used to assess (4)
1) coronary arteries
2) pressures in cardiac chambers
3) valve function
4) ventricular function
Which arteries are used for access during cardiac angiography?
femoral or radial
Stress test used to assess…
ischemia
ST segment changes
arrhythmia
functional capacity
efficacy of medical or surgical intervention
Which populations can you not do a stress test with?
elderly
patients with mobility issues
Echocardiography used to assess…
myocardial structures
ventricular function
ejection fraction
heart motion abnormalities
effusions
thrombus
ischemia
Assessment - labs (6)
1) serum cardiac markers
2) C-reactive protein
-marker that indicates inflammation
3) lipid profile
-won’t tell if MI occurred, but will tell if elevated cholesterol for follow-up
4) blood glucose
-regardless of diabetic status
5) electrolytes
-increases risk of cardiac events
6) kidney function
-hopefully no damage
Serum cardiac monitors (3)
1) troponin
-GOLD STANDARD
2) Serum creatinine kinase (CK) – CK-MB
-do MB specifically which looks at cardiac muscle
-death to tissue - releases enzymes
3) myoglobin
-rarely used
T or F: Serum cardiac markers are done once, upon initial assessment
FALSE
take a while to elevate in your system
not a one time thing - trend these
every 6 to 8 hours over 24 hours
What has greater specificity?
a) CK-MB
b) Troponin
b) Troponin
Serum creatinine kinase (CK)
fractionated into bands- CK-MB
rises: 3 - 12 hours
peaks: 24 hours
returns to normal: 2-3 days
Troponin
2 subsets: cTnT and cTn1
rises: 3 - 12 hours
peak: 24 - 48 hours
returns to normal: 5-14 days
Main diagnoses for chest pain (3)
1) Stable angina
2) Unstable angina
3) MI
Patient population most commonly with missed Dx (4)
1) women < 55
2) POC
3) SOB as main presenting symptom
4) normal or nondiagnostic ECG (misread)
Characteristics of chronic stable angina (many)
pain usually lasts 3-5 minutes
responds WELL to nitroglycerin (lessening O2 demand)
subsides when the precipitating factor is relieved
pain at rest is unusual
ECG reveals ST segment depression
chest pain occurs intermittently over a long period with the SAME PATTERN of symptoms
can be controlled with medications on an outpatient basis
predictable - medications can be timed
Variants of stable angina (4)
1) silent ischemia
2) nocturnal angina
3) angina decubitus
4) Prinzmetal’s (variant) angina
Silent ischemia
ischemia that is asymptomatic
associated with diabetes mellitus
Nocturnal angina
occurs only at night but not necessarily during sleep
can wear nitro patches at night
Angina decubitus
chest pain that occurs only while LYING DOWN
relieved by standing or sitting
Prinzmetal’s (variant) angina
occurs at rest usually in response to spasm of major coronary artery
seen in clients with a history of migraine headaches and Raynaud’s phenomenon
spasm may occur in the absence of CAD
may be relieved by moderate exercise
Characteristics of unstable angina (many)
chest pain that is new in onset, occurs at rest or has a worsening pattern
chronic stable angina that increases in frequency, duration or severity
unpredictable
NOT relieved by rest
pain refractory to nitroglycerin
associated with deterioration of once stable atherosclerotic plaque
unstable lesion can progress to MI or return to stable lesion
Symptoms of unstable angina (4)
1) fatigue
2) SOB
3) indigestion
4) anxiety
Myocardial Infarction
severe, prolonged ↓ O2 supply (ischemia) resulting in necrosis
90% associated with acute coronary thrombosis
presence of Q wave- area of necrosis, permanent
transmural (full thickness) versus subendocardial (partial)
Should you give nitro before or after an ECG?
AFTER
give info on what heart look like without intervention
How to differentiate between non-ST elevation STEMI and unstable angina?
troponin!!
eventually their troponin will rise - someone with unstable angina will not
What is worse - an occlusion higher up on the artery or lower?
higher up
feeds more muscle
Zones (3)
1) zone of infarction
2) zone of injury
3) zone of ischemia
Zone of infarction
necrosis and damage
want to prevent this zone from spreading
Zone of injury
compromise of oxygen delivery
still salvageable
Zone of ischemia
deprived of oxygen
also salvageable
Characteristics of an MI (many)
severe, immobilizing chest pain
not relieved by rest, position change, or nitrate administration
epigastric pain – indigestion
SOB, diaphoresis, N&V, dizziness
SNS stimulation:
-elevated glucose
-vasoconstriction (skin ashen, cool or clammy)
-increased BP & HR (initially)
if CO falls:
-decreassed BP
-crackles
-JVD
-peripheral edema
-hepatic engorgement
pulmonary edema (crackles on lung auscultation)
extra heart sounds (S3 & S4)- ventricular dysfunction
fever (inflammatory process)
T or F: Diabetic patients may not experience any pain with an MI
TRUE
Diagnostic criteria for MI (3)
2 out of 3
1) Chest pain > 30 minutes
2) ECG – Q waves / ST segment elevation / T wave inversion
3) Serum cardiac markers:
Troponin T
Creatine kinase (CK)
Goal for patient with ACS
relief of ischemic pain
preservation of the myocardium
(decrease O2 demand or increase O2 supply)
immediate and appropriate treatment of ischemia
-drug therapy
-interventions
effective coping with illness-associated anxiety
participation in a rehabilitation plan
reduction of RF
Acute interventions for ACS
prompt recognition of S&S
-assessment of CAB
-hemodynamic stability
preliminary history
12 lead and continuous ECG monitoring
bloodwork (Routine, Trop, CK-MB)
oxygenation +/- (to keep O2>90%)
IV access
initial medications
immediate reperfusion therapy
-PCI or fibrinolytic therapy
Initial meds (4)
1) ASA (160-325mg, chewed) and
Plavix (600mg)/Ticagrelor (180mg)
-prevent additional platelet activation and interferes with platelet adhesion
2) Oxygen
-given to hypoxic patients, respiratory distress
-SaO2<90%
-can worsen size of infarct with high flow rates 8L/min
-titrate to SaO2
3) Nitro
-S/L (x3 if needed) followed by IV for persistent pain, hypertension or heart failure
4) Morphine
-when nitro ineffective
-decreases myocardial O2 consumption, BP & HR, contractility
Other meds (7)
1) beta-blockers
-initiated within 24 hours/no contraindications (super bradycardic or hypotensive)
2) LMWH or IV heparin
-minimally 48 hours after MI
-to prevent re-thrombosis or acute stent thrombosis
3) ACE inhibitors
-lowers BP
-reduce vasoconstriction and fluid retention
4) P2Y12 inhibitors (Ticagrelor, Plavix)
5) Antidysrhythmic medications (ami)
6) Cholesterol lowering medications (statin)
7) Stool softeners
-from narcotics
Reperfusion therapy types (2)
trying to salvage as much of the heart as you can
1) Mechanical Reperfusion
2) Pharmacologic Reperfusion
Mechanical Reperfusion
Primary Percutaneous Coronary Intervention (Primary PCI)
angiogram then insert stent to reestablish perfusion distal to where occlusion is - localized
stable angina, unstable angina, MI
1 or 2 vessel disease
PCI should be performed within _____ minutes of first medical contact
120 minutes
ideally 90 minutes
not great if you live in a rural area :/
Goal of PCI
trying to perfuse to stop pain***
PCI Nursing Management
Angina
-ay be caused by transient coronary vasospasm, or it may signal a more serious complication
Vascular site care
-assessing for bleeding and swelling at sheath site
Peripheral Ischemia
-secondary to cannulation of vessel, assess for adequate circulation
Renal protection
-hydration
-fluids
-D/C of some meds - dye and Metformin hard on the kidneys
Pharmacologic Reperfusion
fibrinolytic therapy
-streptokinase, Alteplase (tPA), Reteplase (rPA), Tenecteplase (TNK-tPA))
STEMI only**
systemic, risk for bleeding, risk for stroke
Fibrinolytic therapy target (time)
first 30 minutes!
ideally within 1st hour after onset of symptoms
less than 6 hrs improved results
after 6 hours - risk for bleeding
Major complication of fibrinolytic therapy
BLEEDING
differentiate between surface and internal bleeding
surface bleeding e.g. IV site –> continue
internal bleeding e.g. stroke –> STOP
Eligibility criteria for fibrinolytic therapy
patients with recent onset (less than 12 hours) of chest pain and persistent ST elevation
patients who present with bundle branch blocks (BBBs) that may obscure ST segment analysis and a history suggesting an acute MI
chest pain unresponsive to S/L nitro
no conditions that might cause a predisposition to hemorrhage
Absolute contraindications for fibrinolytic therapy (many)
active internal bleeding or bleeding diathesis (except for menstruation)
known history of brain aneurysm
known brain cancer
previous cerebral hemorrhage
oschemic stroke within past 3 mo
significant closed head or facial trauma within past 3 mo
suspected aortic dissection
Relative contraindications for fibrinolytic therapy
active peptic ulcer disease
current use of anticoagulants
pregnancy
prior ischemic stroke not within past 3 mo; dementia; or known intracranial disease not covered under absolute contraindications
surgery (including laser eye surgery) or puncture of noncompressible vessel within past 3 wk
internal bleeding within past 2–4 wk
serious systemic disease (e.g., advanced or terminal cancer, severe liver or kidney disease)
severe uncontrolled hypertension (BP >180/110 mm Hg)
traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Coronary Artery Bypass Graft
when you have blockages but stent isn’t appropriate
not usually an emergency surgery
take from breast or leg
put into heart to bypass area where there is an occlusion
reestablish perfusion distal
Who is considered for Coronary Artery Bypass Graft Surgery (CABG)?
left main disease
multivessel disease
satisfactory improvement is not reached with medical management
patient is not a candidate for PCI (e.g., lesions are long or difficult to access)
lifestyle limiting angina unresponsive to medical therapy or PCI
Post MI Ongoing Assessment and Care (many)
ARE THEY STILL HAVING PROBLEMS
pain
site care
PCI - assessment of extremities
monitoring
-cardiac
-respiratory
-VS, O2
ultrasound
-left ventricular function
rest and sleep - activity gradually increased
anxiety - give info**
driving - 1 week
effectiveness of interventions
patient teaching
emotional and behavioural reactions
Long-term drug therapy (6)
1) Antiplatelet therapy
-aspirin
-Clopidogrel (Plavix)
-ASA plus Ticagrelor or Plavix
2) Statins
-atorvastatin 80 mg daily or Rosuvastatin 20 or 40 mg daily
3) Beta-blockers
4) ACE inhibitors or ARB’s (“pril”
5) Nitrates
6) Ca+ channel blockers (e.g. Diltiazem, Verapamil, Nifedipine)
Complications post MI (many)
arrhythmias
-ventricular Tachycardia/Fibrillation
-atrial Fibrillation
-bradycardia and heart blocks
congestive heart failure
cardiogenic shock
-not pumping effectively, not enough perfusion leading to cariogenic shock
papillary muscle dysfunction
ventricular aneurysm
pericarditis
pulmonary embolism
