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AGPCNP > CAD > Flashcards

CAD Flashcards

1
Q

What are some age related changes in cardiac anatomy?

A

Valves
Calcific and fatty degeneration of valve leaflets and annuli
Coronary Arteries
Dilation, tortuosity and medial calcification
Conduction system
Fibrosis and loss of special cells and fibers
Loss of 75% of pacemaker cells in SA node
Fibrosis of AV node and left anterior fascicleMyocardial relaxation decreases
Diastolic dysfunction develops
Valvular regurgitation develops
Peak exercise heart rate declines
PR, QRS, QT are prolonged

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2
Q

What are the effects of cigarette smoking on the body?

A 
increase LDL
 decrease HDL 
heart rate
Vasoconstriction
impairs oxygen transport
 myocardial oxygen demand.
Facilitates atherosclerosis
endothelium more porous= activation of the clotting cascade =   risk of thrombosis)
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3
Q

What are the hemodynamic effects of CAD?

A

Decreased lumen size (when~ 70%-angina)
reduction in the amount of blood able to pass through the narrowed area.
O2 demand >O2 supply: hemodynamically significant
(exercise& emotional stress =increased demands)
If blood flow and O2 are significantly reduced, the heart tissue has potential to become ischemic or necrotic.
Atherosclerosis=arterial stiffening=decreased compliance

Stiffening=decreased blood flow distal to plaque region.

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4
Q

WHAT IS CHEST PAIN?

A

One of the most common complaints of adult patients
Symptom- not a diagnosis
Somatic sensation of discomfort in the thoracic region
defined as that which is described by the patient
In elderly-complaint may be dyspnea or
“some type of feeling in the chest”
– not necessarily chest pain

Women-atypical symptoms

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5
Q

What is chronic stable angina?

A

Effort induced discomfort that has not changed in duration, intensity or frequency for at least two months
May be mild or debilitating
Occurs at rest or on exertion
Exertion may=increase in demand beyond supply

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6
Q

What is variant angina?

A

Angina that occurs without an increase in exercise or exertion and without warning
Believed that this pain is caused by coronary artery vasospasm
Seems to occur in cyclic fashion; same time of day
Hallmark sign on ECG

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7
Q

What is acute coronary syndrome (ACS)?

A

Occurs at rest, awakens pt at night, persists
Pt w/symptoms of ACS should not be evaluated over the telephone
Refer to a facility that allows evaluation by an NP or MD, 12-lead ECG, and biomarker determination

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8
Q

What does ischemia look like on EKG?

A

inverted T waves

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9
Q

What is ischemia?

A

T wave inversion and S-T segment depression can occur with anginal symptoms and return to baseline with relief of symptoms.
Acute decrease in blood flow and oxygen supply leads to severely ischemic tissue
may result in necrosis if interventions are not implemented within 6 hours of coronary occlusion.
Reversible if treated quickly.

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10
Q

what does injury look like on an EKG?

A

tombstones

ST elevation

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11
Q

What is injury?

A

Represented by ST segment elevation greater than .5 mm.
Represents damage to myocardium, not necessarily necrosis.
ST elevation can also be caused by pericarditis and/or ventricular aneurysm.
ST elevation is an ominous sign, it can go either way (want it to reverse!!!!!)

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12
Q

What are EKG representations of infarction?

A

Represented by pathological Q waves
Q wave width is greater than 0.04 seconds
Q wave depth is greater than 25% of the R wave

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13
Q

What are factors to consider when ordering stress testing?

A

Ability to exercise
Exercise protocol (Bruce, Modified Bruce, Naughton)
Ability to achieve target heart rate?
Asthma/Emphysema?

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14
Q

What should yo u prescribe to a patient in a low risk setting that is awaiting outpatient stress testing?

A

In low-risk patients who are referred for outpatient stress testing:
ASA, sublingual NTG, and/or beta blockers should be given while awaiting results of the stress test

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15
Q

What are indicators of a positive exercise stress test?

A

Exercise ECG or Exercise Stress Test Positive if:

new ST segment depression> 1 mm early after start of exercise

new ST segment depression> 2 mm in multiple leads

Pt unable to exercise for > 2 minutes

Pt has decreased SBP with exercise

Pt develops arrhythmias or HF w/exercise

Pt. has prolonged ECG abnormality after cessation of exercise (ST depression)

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16
Q

What are medications used in a medically induced stress test?

A

Dipyridamole
Adenosine
Dobutamine

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17
Q

What is a stress echo?

A

Ultrasound- at rest and during peak stress
Stress–exercise or pharmacologic
Ischemia defined by development of wall motion abnormalities

18
Q

What is a stress MPI?

A

Myocardial accumulation of radioactivity in proportion to blood flow

Ischemia defined by diminished perfusion during stress vs rest imagesA wide range of noninvasive nuclear studies can be performed, and these studies vary according to the characteristics of the agent used, imaging techniques, and clinical questions to be answered.
Stress MPI is one of the most commonly used procedures for the evaluation of CAD.
MPI alone measures the presence of ischemia; with simultaneous gated single-photon emission computed tomography (SPECT), wall motion and chamber function can be evaluated.
The test is based on the myocardial accumulation of a radioactive agent that is distributed in proportion to blood flow to each area of the myocardium.
Studies are interpreted by comparing distribution of the radioactivity in rest and stress images. Areas of decreased perfusion at stress that do not appear at rest are characteristic of myocardial ischemia, while defects that appear on both sets of images are characteristic of myocardial infarction.
Exercise or pharmacologic stress can be used in conjunction with nuclear studies.
An important advantage of stress MPI is the ability to perform simultaneous ECG-gated SPECT to obtain functional data.

19
Q

What are Benefits of Exercise Stress Testing over Pharmacologic?

A 
Information about functional status
Indication of threshold for ischemia
Correlation with symptoms
Evaluation of exercise induced arrhythmias
Additional prognostic information
20
Q

Discuss CT imaging role in CAD

A

CT angio-imaging coronary vessels
If images are NL, high sensitivity for excluding CAD
Risks: allergy to dye, radiation, patient with CKD

21
Q

Discuss cardiac MRI

A 
To evaluate the following and more:
Aorta and large vessels
Imaging coronary arteries
Evaluation of myocardial perfusion
No radiation exposure
“Metal unfriendly environment”
High level of technical expertise required
22
Q

What are indications for cath?

A

Angina that is not easily controlled with medication, that disrupts daily routine, occurs at rest, or recurs after heart attack
Heart failure with suspected coronary artery disease
Markedly abnormal stress test results
Recurring chest pain of unidentified cause
Recurring angina despite medical therapy
Patients at high risk of severe ischemia or sudden cardiac death
Patients who have survived sudden cardiac death or have high-risk arrhythmia

23
Q

Who is the ideal patient for cardiac cath?

A

Patients who have a high pretest probability of having stenoses
40% are negative

24
Q

What is included in management for stable angina?

A

Reduction of Risk Factors
Lifestyle changes
Medications - nitrates, beta blockers, ASA, calcium channel blockers
Control of associated illnesses which can worsen angina: anemia, hyperthyroidism, tachycardia, CHF, infection, fever

25
Q

What are lipid lowering medications?

A 
HMG Co-A Reductase Inhibitors “statins” –only agent with improved outcomes date
Goal individualized based on risk
PCSK9 Inhibitors (if statin intolerant or familial hyperlipidemia)
alirocumab Injectable
75mg-150mg every 2 weeks
evolocumab Injectable
420mg-monthly
140mg-every 2 weeks
26
Q

Discuss antiplatelet drug therapy and who should be treated

A

Antiplatelet Agents– all patients with CAD should be treated with a platelet inhibitor:
Aspirin (81 mg/day)-irreversible inhibitor of platelet cyclooxygenase activity and thereby interferes with platelet activation.
In those patients allergic to aspirin, Plavix (clopidogrel) can be used -blocks ADP receptor–mediated platelet aggregation.
Prasugrel (effient), Brillinta (ticagrelor) -newer agents
Dual Antiplatelet Therapy (DAPT) recommended:
For 1 year after acute coronary syndrome
For 3-6 months after drug-eluting stent placement (depends on patient’s risk factors for bleeding)

27
Q

What are factors used to calculate a DAPT score (dual therapy)

A 
age (want < 75, ideally < 65)
current tobacco smoker
DM
MI at presentation
prior PCI or MI
stent diameter <3 mm
paclitaxel-eluting stent
CHF or LVEF <30%
saphenous vein graft PCI

A score of ≥2 is associated with a favorable benefit/risk ratio for prolonged DAPT while a score of <2 is associated with an unfavorable benefit/risk ratio.

28
Q

What is the role of beta blocker in angina?

A

Reduce myocardial oxygen demand by decreasing heart rate, BP and contractility
All patients with recurrent episodes of exertional angina should receive a beta blocker as first line therapy unless contraindicated
If beta blockers are stopped, it should be done in a tapering fashion (or can precipitate angina)

29
Q

Which beta blockers and how dosed for angina?

A

Examples for angina:
Atenolol 50–200 mg daily
Metoprolol 50–200 mg twice daily *
Propranolol 80–120 mg twice daily *

  • sustained release formulations available
  • these are b-blockers for which the greatest amount of clinical experience exists
30
Q

How do you dose beta blockers and what are side effects?

A

Dosage:
Should be carefully titrated to achieve a resting heart rate of 50-60 bpm and an exercise heart rate that does not exceed 90-100 bpm
Side effects: bronchospasm, postural hypotension, claudication, depression, deterioration in intellectual capacity, salt retention, impotence, and potential masking of hypoglycemia

31
Q

What is the role of nitrates in angina and what are the side effects?

A

Important in the treatment of stable angina

All patients with CAD should be prescribed sublingual or aerosol nitroglycerin to abort episodes of angina [educate them about how to take, 911]

Effect of nitrates-reduction in the volume of fluid returning to the heart, improving subendocardial perfusion.

Coronary vasodilation, improvement in collateral flow and afterload reduction augment this primary effect

Side effect: headache

32
Q

What is nitrate tolerance and how do you manage it?

A

Can occur in some patients
Results in a reduced therapeutic response
A nitrate free period of at least 10-12 hours can result in enhanced efficacy
If unable to provide a drug free period, then increased doses may be required for relief

33
Q

What is the role of CCBs in angina?

A

Have antianginal effects due to direct coronary vasodilation and reduced peripheral resistance
If unable to tolerate beta blockers, then calcium channel blockers are drug of choice
Particularly effective in vasospasm

34
Q

What are the two broad classes of CCBs?

A

Dihydropyridines: (don’t effect conduction)
Amlodipine 5–10 mg daily
Felodipine 5–10 mg daily
Side Effects: Headache, edema

Non-dihydropyridines (effect conduction)
Diltiazem Immediate release: 30–80 mg 4x daily, slow release: 120–320 mg
Verapamil Immediate release: 80–160 mg tid or slow release: 120–480 mg qd
Side Effects: Hypotension, dizziness, flushing, bradycardia, edema

35
Q

What is ranolazine?

A

Decreases late sodium current
Decreases intracellular calcium overload
No effect on heart rate or BP
Dose: 500mg BID
CAUTION-can cause QT prolongation
Contraindicated in pts with prolonged QT & pts on other drugs that prolong QT (ex-sotalol)
Contraindicated in pts with liver & kidney disease

36
Q

How do you adjust anti-anginals?

A

1) Start: with 1 medication, then titrate weekly if symptoms persist
2) Next: add additional drug if necessary & titrate as needed
3) Maximal therapy-add a 3rd drug and titrate as needed

37
Q

What do you do when medications fail to relieve symptoms?

A
  1. percutaneous coronary intervention

2. CABG

38
Q

How do you identify patients at risk of UA/NSTEMI?

A

Evaluate for the presence and status of control of major risk factors for CHD for all patients at regular intervals (approx. every 3 to 5 years).
Pts with 2 or more risk factors for CHD:
Calculate ten-year risk (National Cholesterol Education Program [NCEP] global risk) of developing symptomatic CHD
to assess the need for primary prevention strategies
Identify pts with known CHD and patients with a CHD risk equivalent
PAD, DM, CKD
or 10-year Framingham risk > 20%) for secondary prevention efforts

39
Q

What is appropriate f/u for CAD?

A

Patients with CAD that is stable-see annually
After Acute MI-office visit in 1-2 weeks
After PCI-office visit in 2-6 weeks
Practitioner must be sure to receive a full report from acute care facility

40
Q

What referrals should be made for CAD?

A

Dietician referral may be necessary to make lifestyle modifications
Exercise or Cardiac rehab referral (can reduce mortality by 25%). Cardiac rehab referral after PCI is now a National Cardiovascular Data Registry (NCDR) mandate.
Home care referral may be necessary

41
Q

What should be included in patient education for CAD?

A

What CAD means
Risk factors and which one(s) the patient possesses. (write down BP, HR, lipids, Hgb A1c (<7), and weight goals)
Lifestyle modifications-how these can be achieved
Medication information
Need to call 911 if unstable symptoms (rather than be driven by family member)What side effects can occur with meds
When/what lab tests are needed
Importance of making follow up visits
Importance of adherence to medication regimen
Involve patient AND significant others in care
Importance of smoking cessation

42
Q

Smoking cessation aids

A

Bupropion:
an anxiolytic agent
weak inhibitor of neuronal uptake of neurotransmitters
has been effective when added to brief regular counseling sessions in helping patients to quit smoking.

Varenicline
first-in-class nicotine acetylcholine receptor partial agonist
designed to provide some nicotine effects (easing withdrawal symptoms)
blocks the effects of nicotine from cigarettes, discouraging smoking.
Nicotine Inhaler

Nicotine Patch

AGPCNP (30 decks)

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