Week 3: Coronary Artery Disease Flashcards
1
Q
what is coronary artery disease
A
progressive atherosclerotic disorder of coronary arteries that results in narrowing or complete occlusion of one or more arteries
2
Q
what is atherosclerosis
A
progressive build up of plaque impacting medium-sized arteries that perfuse the heart and major organs
- this causes narrowing which can stop/decrease blood flow leading to heart attacks
3
Q
what are the common hints of a heart attack
A
- chest pain - midsternal
- sweating (diaphoretic)
- shortness of breath
4
Q
give the 3 aspects of coronary artery disease (presentations, syndrome)
A
- asymptomatic
- stable angina
- acute coronary syndrome: unstable angina, myocardial infarction, sudden coronary death
5
Q
why is there angina with coronary artery disease
A
lack of balance of O2 supply and demand
- decreased supply of blood due to the artery size leading to anemia and hypoxia
6
Q
what are the 12 things that decrease O2 supply
A
- anemia
- CAD
- hypoxia
- COPD, asthma, pneumonia
- arrhythmias
- CHF
- coronary spasm
- thrombosis
- valve disorders
7
Q
what are the 9 things that increase O2 demand / consumption
A
- anxiety
- cocaine use
- hyperthermia
- hyperthyroidism
- physical exertion
- aortic stenosis
- arrhythmias - ↑ rates/work of heart
- cardiomyopathy
- hypertension
8
Q
how do we decrease the risk of developing atherosclerosis
A
- diet
- statin medications
- exercise
- education
- stress management
- treat comorbidities
9
Q
what does the endothelium regulate
A
- dilation and constriction of vessels
- thrombosis: formation of blood clots
- transport of substances to and from the vascular space
- growth and ‘apoptosis’ of vascular wall
10
Q
what can cause endothelial dysfunction
A
- inadequate vasodilation (hypertension)
- prothrombotic
- altered permeability (electrolyte imbalances)
- increased secretion of growth factors (hypertrophy)
- increased oxidation of LDL (fatty plaques)
11
Q
what is collateral circulation
A
body is creating collateral capillaries to adapt to the narrowing of arteries in order to have a different route of blood flow
12
Q
which population develops CAD fast
A
- CAD is #1 killer of women due to hormonal changes
- women post menopausal due to low estrogen levels (decreased cardio protectiveness)
- low estrogen causes no collateral circulation development
13
Q
what are some signs of a cardiac event for women
A
- absence or vagueness of cp
- no radiation of pain
- heaviness of arms
- lightheadedness
- epigastric burning
- nausea and vomiting
- diaphoresis
- feeling flushed
- prodromal symptoms: sleep disturbances, unusual fatigue, shortness of breath, indigestion, anxiety
14
Q
what are some signs of a cardiac event for men?
A
- chest pain / aching / tightness / pressure / jaw pain
- shortness of breath
- pain between shoulder blades
- shoulder/arm/neck pain
- headache
- inndigestion
- palpitations
- cough
- diaphoresis
- fatigue
- nausea and vomiting
15
Q
what are the challenges of care for CAD?
A
- failure to recognize & difficulty interpreting symptoms
- failure of HCP to recognize prodromal symptoms
- ECG & stress test less sensitive
- plaque tends to be distributed diffusely (plenty of occluded arteries)
- less likely to be evaluated for risk factors or treated aggressively
16
Q
what are the atypical presentations in the elderly? (most frequent symptoms of acute MI, the pre-existing conditions, treatment)
A
Most common symptoms of acute MI:
- shortness of breath
- fatigue and weakness
- abdominal or epigastric discomfort
Pre-existing conditions:
- hypertension
- CHF
- previous AMI
Treatment:
- likely to delay seeking treatment
17
Q
what are the atypical presentations in patients with diabetes?
A
- acute presentation due to autonomic dysfunction (neuropathic symptoms, do not present the same with pain)
common signs / symptoms:
- generalized weakness
- generalized feeling of not being well
- syncope
- lightheadedness
- change in mental status
18
Q
what are some non-modifiable risk factors for CAD
A
- age
- male > female until 65
- genetics
- ethnicity
19
Q
what are some modifiable risk factors for CAD? (major and contributing)
A
Major:
- tobacco use
- abdominal obesity
- hypertension > 140/90 mmHg
- hyperlipidemia
- physical inactivity
Contributing:
- psychosocial risk factors depression, hostility, anger, stress)
- elevated homocysteine levels
- diabetes mellitus
- metabolic syndrome
20
Q
among non-smokers without diabetes what are the low risk factors (BP, Cholesterol)
A
BP: untreated pressure <120 / <80
Cholesterol: 4.7 mmol/L
21
Q
among non-smokers without diabetes what are the moderate risk factors (BP, Cholesterol)
A
BP: systolic 120-130 mmHg or diastolic 80-89 mmHg
Cholesterol: 4.8 - 5.1 mmol/L
22
Q
among non-smokers without diabetes what are the elevated risk factors (BP, Cholesterol)
A
BP: untreated systolic 140-159 mmHg or diastolic 90-99 mmHg
Cholesterol: 5.2 - 6.1 mmol/L
23
Q
how often should low risk factor people be assessed? how often should high risk people be assessed?
A
low risk: every 3-5 years
high risk: every year
24
Q
what are some major risk factors for CAD?
A
- treated hyperlipidemia or total cholesterol 6.2 mmol/L
- treated hypertension or untreated systolic pressure ≥160 mmHg or diastolic ≥100 mmHg
25
who are some people we should screen?
- men ≥ 40
- women ≥ 50 or post-menopausal
- anyone with: smoker, hypertension, elevated cholesterol, diabetic, family history, erectile dysfunction, obesity, inflammatory disease, COPD, HIV
26
what does an initial assessment for a CAD patient include?
1. baseline VS and 12 lead ECG within 10 min (high concern)
2. assessment of chest pain and associated symptoms (high concern)
3. physical assessment (high concern)
4. medications (high concern)
5. personal and family history (low concern)
6. environmental factors (low concern)
7. psychosocial history (low concern)
8. patient's attitudes and beliefs about health and illness (level of motivation) (low concern)
27
what is the point of a ECG for a CAD patient
- goal is to complete it 10 mins of presentation to ER
- it is a primary diagnostic tool
- shows changes in QRS complex, ST segment, and T wave
- dynamic process and can show if condition evolves overtime
- need to repeat every 15-30 min to 2-4 hours (depends on patient condition)
28
what type of ECG do we use for CAD?
12 lead in order to see different areas of the heart
29
what sites does the 12 lead ECG monitor?
Anterior, Lateral, Inferior, Posterior
Side note: review where the areas are on the ECG paper bc i cannot insert images
30
who would have ST depression?
someone with ischemia, no heart attack
- decrease O2 = lack of oxygenation
- no damage yet, can avoid damage if we respond appropriately
31
what does a ST elevation indicate? what do we do?
represents prolonged ischemia with damage present
- more significant condition, need aggressive interventions
32
what are some locations of chest pain patients may experience?
use OPQRST mnemonic
- upper chest
- substernal radiating to neck/jaw
- substernal radiating down left arm
- epigastric
- epigastric radiating to neck, jaw, arms
- neck and jaw
- left shoulder and down both arms
- intrascapular
33
what are some additional patient complaints or presentations regarding STEMI?
- difficulty breathing
- excessive sweating
- unexplained nausea or vomiting
- generalized weakness
- dizziness
- syncope or near-syncope
- palpitations
- isolated arm/jaw pain
- fatigue
- dysrhythmias
34
what are the diagnostic studies of CAD/ Heart attacks?
- 12 lead EKG
- cardiac monitor
- chest x-ray (helps identify any issues with lungs)
- coronary angiography (gold standard)
- exercise stress test (done if not acute unstable state)
- echocardiogram (done if not acute unstable state)
35
what is a cardiac angiography? what does it assess?
thread catheter into coronary arteries and inject dye which reveals image of arteries - helps determine blockage location
assesses:
- coronary arteries
- pressures in cardiac chambers
- valve function
- ventricular function
36
what is a stress tested used for?
- detect ischemia, ST segment changes, Arrhythmias
- determines functional capacity
- identifies efficacy of medical or surgical intervention
37
what is echocardiography? what does it assess?
ultrasound of heart to see what the atria and ventricles look like
assesses:
- myocardial structures
- ventricular function: ejection fraction, heart motion abnormalities
- effusions
- thrombus formations
- ischemia
38
what are the laboratory studies for CAD?
serum cardiac markers:
- muscle damage releases enzymes into blood
- troponin: gold standard enzyme suggesting muscle cell death
- serum creatinine kinase (CK, CK-MB): CK-MB looks specifically at cardiac muscle
- myoglobin
c-reactive protein: indicates inflammation
lipid profile: indicates cholesterol levels
blood glucose, electrolytes, kidney function
39
what are some considerations for serum creatinine kinase (CK)? (time for rise & peak, when it returns to normal?)
- fractionated into bands: CK-MB
- Rises 3-12h
- peaks in 24h
- returns to normal 2-3 days
40
what are some considerations for troponin? (time for rise & peak, when it returns to normal?)
- 2 subsets cTnT and cTn1
- greater specificity than CK-MB
- levels rise within 3-12h
- peak at 24-48h
- returns to normal 5-14 days
41
why are serum cardiac marker considerations important?
they take awhile to elevate therefore we need to trend the values overtime, cannot only look at them once
42
which patient population is most commonly to have a missed diagnosis of heart attack?
- women < 55
- person of colour
- shortness oof breath as major presenting symptom
- normal / non diagnostic ECG (misread)
43
what is the assessment of chronic stable angina?
- how long does pain last for?
- what does it respond well to?
- what makes it subside?
- ECG reading
- when does pain occur?
- what can it be controlled with?
- pain lasts for 3-5 min
- responds well to nitroglycerin
- subsides when precipitating factor is relieved (physical exertion, temp extremes, smoking, strong emotions, heavy meal)
- ST segment depression
- pain occurs intermittently over long period with same pattern of onset, duration, and intensity of symptoms
- can control with medications - meds can be timed due to predictable nature of angina
44
what is silent ischemia? what is it associated with?
- asymptomatic ischemia
- associated with diabetes mellitus
45
what is nocturnal angina?
- occurs only at night but not necessarily during sleep
46
what is angina decubitus? what is it relieved by
- chest pain that only occurs while lying down
- relieved by standing/sitting
47
what is Prinzmetal's (variant) angina? who is likely to have it? how can it be relieved?
- occurs at rest usually in response to aspam of major coronary artery
- seen in clients with a history of migraine headaches and Raynaud's phenomenon
- spasm may occur in absence of CAD
- may be relieved by moderate exercise
48
what is the assessment of unstable angina?
- when is it considered angina?
- frequency
- what is it associated with
- what can it progress to?
- symptoms
- chest pain that is new in onset, occurs at rest or has a worsening pattern
- unpredictable, not relieved by rest
- when chronic stable angina increases in frequency, duration, severity
- pain refractory to nitroglycerin (does not work)
- associated with deteriooration of once stabel atherosclerotic pllaque
- unstable lesion may progress to MI or return to stable
- symptoms: fatigue, shortness of breath, indigestion, anxiety
49
what is a myocardial infarction? (MI)
- what is it associated with?
- transmural vs subendocardial
severe prolonged decrease in O2 supply (ischemia) resulting in necrosis
- associated with acute coronary thrombosis
- presence of Q wave: area of necrosis, permanent
- transmural: full thickness necrosis
- subendocardial: portions of heart
NOTE: review the ECG graphs for inferior, anterior, lateral and STEMI
50
what is zone of infarction? zone of injury? zone of ischemia?
zone of infarction: necrosis and damage
zone of injury: injury but we can improve if we intervene
zone of ischemia: no injury but can lead to injury if not intervened
51
Symptoms of myocardial infarctions (9 points)
- severe, immobilizing chest pain not relieved by rest, position change, nitrate administration (diabetics may not experience pain)
- epigastric pain - indigestion
- shortness of breath, diaphoresis, N/V
- SNS stimulation: ↑ glucose, vasoconstriction (cool, ashen, clammy skin), ↑ BP/HR initially - its the body's defense system kicking in bc no oxygen/not pumping well
- CO falls: ↓BP, crackles, JVD, peripheral edema, hepatic engorgement
- pulmonary edema (crackles in lung)
- dizziness
- extra heart sounds (S3,S4, Ventricular dysfunction) - more turbulent blood flow
- fever (inflammation due to myocardial cell death)
52
what is the MI diagnosis?
need 2/3 criteria:
1. chest pain > 30 min
2. ECG - Q waves / ST segment elevation / T inversion
3. serum cardiac markers are positive (Troponin T, creatine kinase (CK))
53
STEMI vs NSTEMI
Both heart attacks but differ in severity, ECG findings, and treatments
- STEMI
○ Complete blockage of coronary artery due to thrombus
○ ST-segment elevation in 2+ continuous leads
○ Most severe bc full-thickness myocardial damage (transmural)
○ Treatment: immediate reperfusion therapy, antiplatelets, anticoagulants, beta-blockers, statins, pain managements
- NSTEMI
○ Partial block of coronary artery resulting in reduced blood flow
○ No ST segment elevation, may have ST depression, T wave inversion
○ Less severe but still dangerous as it causes partial thickness myocardial damage (subendocardial)
Treatment: antiplatelets, anticoagulants, beta-blockers, statins
54
NSTEMI vs Unstable Angina
NSTEMI
- Cause: Partial blockage of coronary artery
- No ST segment elevation, may have ST depression or T way inversion
- Elevated cardiac markers
- More severe bc permanent damage present
- Chest pain at rest or worsening with less exertion
- Treatment: antiplatelets, anticoagulants, beta-blockers, statins, possible percutaneous coronary intervention (PCI)
Unstable Angina
- Cause: Partial blockage of a coronary artery
- No ST segment elevation, may have ST depression or T way inversion
- Normal cardiac markers
- Less severe bc no permanent damage
- Chest pain at rest or worsening with less exertion
Treatment: similar to NSTEMI but no urgent PCI
55
goals for acute coronary syndrome patient management
1. relief of ischemic pain
2. preservation of myocardium (decrease O2 demand or increase O2 supply)
3. Immediate and appropriate ischemia treatment (drug therapy, interventions)
4. effective coping with illness-associated anxiety
5. participating in rehab plan
6. reduction of risk factors
56
7 Acute interventions for acute coronary syndrome
1. prompt sign and symptom recognition (airway, breathing, circulation, hemodynamic stability, preliminary history)
2. 12 lead and continuous ECG monitoring
3. blood work (routine, Trop, CK-MB)
4. Oxygenation +/- (to keep SaO2 > 90%)
5. IV access
6. Initial medications
7. immediate reperfusion therapy (PCI - angiography/Fibrinolytic therapy - meds that blow up clots to re-establish perfusion)
57
what are the 4 initial medications given for acute coronary syndrome?
name, dose, indication
ASA: 160-325 mg, chewed & Plavix: 600 mg OR Ticagrelor: 180 mg
- prevents additional platelet activation and interferes with platelet adhesion
Oxygen
- given only for hypoxic patients, respiratory distress where SaO2 < 90%
- do not give more then 8L/min bc it can worsen size of infarct w high flow rates
- titrate to SaO2
Nitro
- S/L (3x if needed) followed with IV for persistent pain, hypertension, or heart failure
Morphine
- if nitro uneffective
- if↓myocardial O2 consumption, ↓BP/HR, ↓ contractility
- can counteract asprin's job
58
what are some additional medications that can be considered for acute coronary syndrome? (7)
name, indication
1. b-adrenergic blockers (within 24h with no contraindications)
- lowers BP and HR
2. LMWH or IV heparin (minimally 48h after MI)
- prevents re-thrombosis or acute stent thrombosis
3. angiotensin converting enzyme inhibitors
- lower BP and reduce vasoconstriction and fluid retention
4. P2Y12 inhibitors (Ticagrelor, Plavix)
5. antidysrhythmic meds
6. cholesterol lowering medications (Statins)
7. stool softeners
59
what is reperfusion therapy?
(2 types)
Mechanical reperfusion
- primary percutaneous coronary intervention (PCI)
- catheter via angiogram, inject dye, determine if stent is needed
- GOLD STANDARD
Fibrinolytic therapy (pharmacological)
- streptokinase, Alteplase (tPA), Reteplase (rPA), Tenecteplase (TNK-tPA)
- ONLY FOR STEMI bc if not there are more complications for NSTEMI
- med goes and blows up the clots
60
what are the indications of PCI
primary percutaneous coronary intervention
- electively for chronic stable angina
- urgently for unstable angina
- emergently for myocardial infarction
- 1 or 2 vessel disease
- performed within 120 min of first medical contact (ideally within 90 min)
61
complications of PCI
- Restenosis: renarrowing for artery
- coronary artery spasm
- arterial wall damage
- heart irritation (dysrhythmias)
- bleeding
62
what meds are given for delayed PCI (4)
ASA - 160 mg po chew STAT
Fibrinolytic IV (STEMI only)
Plavix 300 mg po STAT
Unfractionated heparin bolus - 60 units/kg followed by continuous heparin drip at 12 units/kg/hr
63
what meds are given for immediate PCI
ASA - 160 mg po chew STAT
Plavix - 300 mg po STAT
Unfractionated Heparin bolus 70 units/kg
Standing for transfer to Cath lab
64
what are the 4 nursing managements for percutaneous coronary intervention?
1. Angina: may be caused by coronary vasospasm or signal more serious complication
2. vascular site care: assess for bleeding and swelling at sheath site
3. peripheral ischemia: secondary to cannulation of vessel, assess for circulation
4. renal protection: hydration, fluids, D/C of some meds
65
Fibrinolytic therapy: target time, complications, eligibility criteria
- target within first 30 min, ideally within 1st hour after symptom onset, less than 6h = improved results
- complications: bleeding!!
- eligibility: recent onset (<12h, usually <6h) of chest pain and persistent ST elevation, patients presenting with bundle branch blocks (BBBs), chest pain unresponsive to nitro, no conditions that predisposition to hemorrhage
66
why do we not give Fibrinolytic therapy after 6h?
significant risks for bleeding - we do more damage
67
what are the absolute contraindications for Fibrinolytic therapy (7)
1. active internal bleeding / bleeding diathesis
2. known history for cerebral aneurysm or arteriovenous malformation
3. known intracranial neoplasm (primary or metastatic)
4. previous cerebral hemorrhage
5. ischemic stroke within last 3 months
6. significant closed head/facial trauma within past 3 months
7. suspected aortic dissection
68
what are the relative contraindications of Fibrinolytic therapy (9)
1. active peptic ulcer disease
2. current use of anticoagulants
3. pregnancy
4. prior ischemic stroke not within past 3 months; dementia; known intracranial disease
5. surgery/puncture of noncompressible vessel within past 3 weeks
6. internal bleeding within 2-4 weeks
7. serious systemic disease
8. severe uncontrolled hypertension (BP> 180/110 mmHg)
9. traumatic or prolonged cardiopulmonary resuscitation (>10 min)
69
What is coronary artery bypass graft?
option when stent cannot be put in
- take saphenous vein and attach it in order for it to bypass the blockage in the coronary artery
70
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
- lifestyle limiting angina unresponsive to medical therapy or PCI
71
what is the POST MI ongoing assessment and care for a patient?
1. pain
2. bleeding/surgical site care, chest tubes, pacer wire care
3. catheter site, assessment of extremities
4. evaluate left ventricular function
5. monitor cardiac, respiratory, VS, O2
6. rest and sleep
7. anxiety
8. effectiveness of interventions
9. emotional and behavioural reactions
72
what would you teach a patient post MI?
- pain management - identify precipitating factors
- identify personal risk
- sexual activity
- drug therapy
73
what are the long term interventions for post MI
- BP control
- cholesterol management
- smoking cessation
- physical activity
- decrease stress (lifestyle)
- heart healthy diet
- reduce obesity
- management of diabetes
- drug therapy
74
what are the 6 long term drugs used post MI
antiplatelet therapy
statins
beta blockers
ACE inhibitors or ARBS
nitrates
calcium channel blockers
75
why do we use long term antiplatelet therapy? provide med examples
- can use Plavix if allergic to ASA
- use ASA + ticagrelor/plavix for dual antiplatelet therapy
- used by patients recovering from acute coronary syndrome (for ~1 year)
- patients who underwent coronary artery stent placement
76
why do we use long term statin therapy? provide med examples
- all patients with acute coronary syndrome use high-intensity statin therapy
- Atorvastatin 80 mg or Rosuvastatin 20/40mg daily
77
why do we use long term beta blocker therapy? provide med examples
- decrease contractility
- decrease heart rate
- decrease afterload
- lower O2 demand and increase supply
- metoprolol, atenolol
78
why do we use long term ACE/ARB therapy?
- BP management
- prevent remodelling of left ventricle
- patients with heart failure or less than normal left ventricular ejection fraction, diabetes, and kidney failure
- ramipril, captopril
79
why do we use long term nitrate therapy?
- promotes peripheral vasodilation: decreases preload and afterload
- enhanced collateral blood flow
- dilate large coronary arteries: increase perfusion to ischemic zones
80
why do we use long term calcium channel blocker therapy?
- coronary and peripheral vasodilation
- reduces contractility
- used in combo with beta blockers
- Diltiazem, Verapamil, Nifedipine
81
what are possible complications post MI (she said to know these)
- arrhythmias: ventricular tachycardia/fibrillation, atrial fibrillation, bradycardia and heart blocks
- congestive heart failure
- cardiogenic shock
- papillary muscle dysfunction
- ventricular aneurysm
- pericarditis
- pulmonary embolism
