Coronary Artery Disease- Sowinski Flashcards
What is the difference between Stable Ischemic Heart Disease (SIHD) and Acute Coronary Syndrome?
SIHD is manageable at home, while CAD should be treated in the hospital. CAD includes UNSTABLE angina, NSTEMI, and STEMI.
What causes myocardial ischemia?
Imbalance between oxygen supply and demand. This is a disturbance in myocardial function WITHOUT necrosis.
What is angina?
Symptom of ischemia
What percent reduction of flow is usually needed for angina to be present?
<70%
Do drugs usually help to improve oxygen supply or oxygen demand in the heart?
Drugs reduce oxygen demand
What is cardiac syndrome x?
Microvascular angina
How does microvascular angina differ from regular stable angina?
It is not caused by disease of the large vessels, but instead of the small vessels. We still treat it the same way.
What is a typical clinical presentation of angina pectoris?
PPQRST
P1 and P2
Precipitating factors: exertion (anything that increases the demand on the heart)
Palliative measures: rest and/or sublingual nitroglycerin
Q
Quality of pain: squeezing, heaviness, tightness, elephant sitting on chest, NOT usually a piercing pain, SOB, gradual increase in intensity and gradually fades away
R
Region and radiation: substernal and down left arm
S
Severity of the pain: subjective, but usually greater than a 5/10
T
Timing and temporal pattern: lasts less than 20 minutes and usually is relieved within 5-10 minutes
What are some symptoms of a heart attack in women?
Discomfort in the back, shoulders, arms, stomach, jaw, neck, or throat Can't sleep SOB lightheadedness nausea/vomiting cold sweat
What is seen on an EKG when someone is having stable angina?
ST-segment depression during exertion
What is seen on an EKG when someone has VARIANT angina?
ST segment elevation
How do we diagnose IHD?
Cardiac imaging: stress testing, nuclear imaging, electron beam computerized tomography
Echocardiography
Cardiac catheterization- but this is invasive
What are our desired outcomes from treatment of ischemic heart disease?
Prevent ACS and death: we use statins, antihypertensives, and antiplatelets, beta blockers
Alleviate acute symptoms and prevent recurring symptoms: nitroglycerin and CCBs
What does ABCDE stand for?
A: asprin/antiplatelet/anti-anginal B: beta blockers/blood pressure C: Cholesterol/cigarettes D: Diet/diabetes E: Education/exercise
Risk factor treatment: dyslipidemia
50% reduction in LDL, <7% saturated fat, Total cholesterol<200
Lifestyle modifications, statins (moderate-high), plant sterols, omega 3 fatty acids
Risk factor treatment: hypertension
BP <140/90
Beta blockers for all post-MI, angina with no contraindications
ACEis in all pts, especially DM and CKD
Risk factor treatment: weight management
BMI: 18.5-24.9
Waist circumference 40 men, 35 women
Lose 5-10% of weight initially
Diet counseling
Risk factor treatment: physical activity
30-60 minutes for 5-7 days/week
Cardiac rehab supervised
What is a common side effect seen with ticagrelor?
dyspnea
What drug therapy is recommended for people who have stable ischemic heart disease without a stent?
ASA 75-162mg/day indefinitely
OR clopidogrel 75mg if ASA intolerant
What drug therapy is recommended for people who have stable ischemic heart disease with a stent?
- ASA 81mg indefinitely
- clopidogrel 75mg- 6 months minimum for drug-eluting or 1 month minimum for bare metal stent
If no high risk of bleeding is present, continue for about 12 months
What drug therapy is recommended for people who have a CABG?
ASA 81mg/day indefinitely + Clopidogrel 75mg/day for 12 months
Why is it important to look at concurrent PPI therapy in a person who will be put on an antiplatelet?
Some PPIs inhibit 2C19, so clopidogrel and prasugrel are unable to be activated.
What are the benefits to using an ACEi in a person with IHD?
Prevents acute coronary syndrome (ACS) and death
stabilizes plaque
improves endothelial function
Inhibits vascular smooth muscle (VSM) growth
Decrease macrophage migration
DOES NOT IMPROVE SYMPTOMS
How do we prevent ACS and death?
Antiplatelet therapy
Statins
ACEi/ARB
Beta blockers
What drugs increase myocardial oxygen supply, and how do they do this?
nitrates and beta blockers
They do this by dilating coronary arteries, increasing collateral blood flow (by making blood go AROUND the diseased vessel), and by prolonging diastole.
What drugs decrease myocardial oxygen demand, and how do they do this?
Beta blockers, non-DHP CCBs
They do this by decreasing heart rate, decreasing myocardial contractility, and by decreasing left ventricular wall tension (beta blockers may increase this due to increased preload).
How do nitrates affect the acute symptoms of IHD? Long term?
The reduce preload by way of venous dilation, which decreases oxygen demand and increases supply.
They do not have a long-term effect on the progression of the disease.
What do nitrates do to heart rate?
Increase (reflex tachycardia)
What do beta blockers do to heart rate?
Decrease (antagonize beta 1/2 in cardiac myocytes and prevents phosphorylation of Ca channels, so not as much calcium comes into the cell for it to contract)
What does nifedipine (DHP) do to heart rate?
Increase (reflex tachycardia)
What does verapamil do to heart rate?
Decrease (decreases Ca in nodal cells, so less signals sent out to contract)
What does diltiazem do to heart rate?
Decrease (no clue how :))
How do beta blockers affect myocardial contractility?
Decrease (blocks formation of calcium channels, so less contraction)
How does verapamil affect myocardial contractility?
Decrease (decreases Ca in nodal cells, so less signals sent out to contract)
How do beta blockers affect systolic pressure? Left ventricular volume?
Decrease systolic pressure by relaxing arteries and decreasing afterload, but increases left ventricular volume (preload)
How should you instruct someone to take their nitroglycerin tablets?
Take 1 at onset of symptoms, sit down, wait 5 minutes. If still in pain, call 911 and take 1 more. Wait 5 minutes. Take a 3rd tablet and wait for ambulance.
Which beta blockers are cardioselective?
Acebutolol, metoprolol, and atenolol
What is the usual dose for atenolol?
50-100mg qd
What is the usual dose for carvedilol?
25-50mg bid
What is the usual dose for metoprolol tartrate?
50-100mg bid
What is the usual dose for metoprolol succinate?
100-200mg qd
What is the usual dose for propranolol?
80-160mg qd
What is the receptor selectivity for atenolol?
beta-1 (only in doses below 100mg/day)
What is the receptor selectivity for carvedilol?
Beta-1, beta-2, and alpha-1
What is the receptor selectivity for metoprolol?
Beta-1 (only in doses of 200mg/day)
What is the receptor selectivity for propranolol?
Beta-1, beta-2
How is atenolol eliminated?
renally
How is carvedilol eliminated?
hepatic
How is metoprolol eliminated?
hepatic
How is propranolol eliminated?
hepatic
What does intrinsic sympathomimetic activity (ISA) mean?
The beta blocker may increase heart rate at rest, however it does not increase it during exercise. We do not use beta blockers with ISA (ex. acebutolol, carteolol, pindolol) because this defeats the purpose of using them in someone at risk for a MI
What is the goal heart rate for beta blockers?
Rest: 50-60bpm
Exercise: <100bpm (because if their heart rate gets too high, they will have chest pain)
What are some adverse effects for beta blockers?
Sinus bradycardia, sinus arrest, AV block, reduced LVEF (reduced systolic function)
Watch out for beta blocker withdrawal syndrome, must taper over 4-5 days
How do DHPs differ from non-DHPs?
DHPs act on the vasculature more often. Verapamil and diltiazem act more on the heart, sort of like beta blockers
How do the side effects for verapamil and diltiazem differ?
Reduced myocardial contractility V>D
Bradycardia V>D
Hypotension, flushing, headache, constipation, etc. V>D
