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Nursing 232 > CAD > Flashcards

CAD Flashcards

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1
Q

Risk factors for angina

Modifiable/non-modifable

A

x

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2
Q

Signs and symptoms for angina

A

x

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3
Q

Key aspects of plan of care for pt with angina

A

x

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4
Q

Key aspects and plan of care for pt with MI

A

x

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5
Q

Which drugs are considered antianginals?

A

x

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6
Q

Which drugs are used in MI?

A

x

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7
Q

What is angina pectoris?

A

chest pain brought about by myocardial ischemia (usually d/t sig athero)

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8
Q

most common CVD in adults

A

CAD

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9
Q

Most common cause of CAD?

A

Atherosclerosis
(causing reduced blood flow to myocardium) → atomic structure of coronary arteries makes particularly susceptible to atherosclerosis

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10
Q

Causes of CAD other than atheroschlerosis?

A

vasospasm of coronary arteries, myocardial trauma from internal or external forces, structural disease, congenital abnormalities, dec O2 supply (d/t acute blood loss, anemia, low BP) and inc O2 demand (rapid HR, thyrotoxicosis, or use of cocaine)

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11
Q

If angina is severe, results in ?

A

MI

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12
Q

Consistently low CO leads to?

A

HF; or may even cause sudden cardiac death

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13
Q

What do primary and secondary prevention of CAD mean?

A

•Primary prev = preventing CAD; secondary prev = preventing progression of CAD

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14
Q

Signs and symptoms of CAD?

A
  • Chest pain primarily
  • SOB possible
  • Women found to have some instead of/in addition to chest pain: dyspnea, nausea, weakness
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15
Q

Are prodromal symptoms usually seen in CAD?

A

Prodromal symptoms may occur (angine few hrs to days before acute episode), or major coronary event may be first indication

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16
Q

Prodromal symtoms =?

A

early symptom (or set of symptoms) that might indicate the start of a disease before specific symptoms occur

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17
Q

How are signs and symptoms of angina brought on?

A 
•Brought on by physical exertion, cold, eating heavy meal (less blood + O2 available for heart as goes to mesenteries)
and stress (release catecholamines, inc BP, HR, myocardial workload)
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18
Q

Sensations felt in angina?

A
  • May feel mild indigestion up to a choking or heavy sensation in the upper chest - ranges from discomfort to agonizing pain, severe apprehension, feeling of impending death.
  • The pt often feels tightness or a heavy, choking, or strangling sensation.
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19
Q

Where is angina felt?

A

• The pain is deep in the chest behind the sternum; it can also radiate to the neck, jaw, shoulders, and inner aspects of upper arms, usually the left arm.

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20
Q

Associated symptoms with angina?

A

•A feeling of weakness or numbness in the arms, wrists, and hands; SOB, pallor, diaphoresis, dizziness, nausea, vomiting and anxiety may accompany the pain

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21
Q

How to tell if angina is unstable? What needs to be done?

A

Pt’s with unstable angina are not relieved by rest or nitroglycerin; they need medical intervention.

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22
Q

How does angina typically differ in the elderly?

A

• In elderly: dimished responses of neurotransmitters means may not experience typical → dyspnea + diaphoresis more often presenting symptom; pain usually in arms not chest, can have “silent” CAD (no symptoms)

23
Q

How does onset of CAD differ in women?

A

• Women typically cardiac events 10 yrs later, but more chronic disease, complications + mortality

24
Q

How to tell if someone has metabolic syndrome? What is this a major risk factor for?

A

For CVD

o Exists if have 3 of the following:

  • abdominal obesity (waist >102cm in men, >88cm in women)
  • Elevated triglycerides (> or equal to 150mg/dL)
  • Diminished HDL cholesterol
  • Systemic HTN
  • Elevated fasting glucose
25
Q

Important areas of PREVENTION in CAD?

A
  • Controlling cholesterol abnormalities
  • Smoking cessation
  • Managing HTN
  • Controlling DM (insulin, metfomin)
26
Q

Why is smokig cessation important in CAD?

A

inc CO in blood, which binds Hg (dec O2 available to heart); inc HR + BP; detrimental vascular response & inc platelet adhesion; esp not recommended in use of contraceptive use (inc risk of CAD and SCD)

27
Q

Management of elevated triglyceride levels:

A

• weight reduction, limiting fats, sugar, alcohol, smoking, and inc physical activity
•Inc soluble fibre intake (fresh fruit, cereal grains, beggies legumes) → inc excretion of cholesterol
•Physical activity: for av person, 30 mins moderate exercise on most days
- Lipid lowering drugs

28
Q

How many doses of nitro can be given?

A

3

29
Q

Initial nursing interventions for those with angina?

A

o Looking for signs of ischemia (get pt hx of these signs)
o PQRST assessment – how often? Etc…does nitro help? How many doses required? Does it last?
o Get to rest, sit semi-fowler position, vitals, look for resp distress
o Nitro – up to 3 doses (each time monitor BP, HR, and ECG
o O2 admin (usually 2-4L nc)
o Anxiety + stress reducing technqiues; discuss condition and tx to reduce fear
o Pain prevention + teaching self-care (p. 804 med surg)

30
Q

Target O2 values in medical interventions?

A

• O2 administration: normal taget >93% (>90% in COPD)

31
Q

Nitro: how does this help with angina?

A

o Dilates veins: Less blood back to heart → dec preload
o High dose dilates arteries: reduces afterload → less work → less O2 requirements of myocardium –> less ischemia –> less pain

32
Q

How can nitro be given?

A

Given sublingual tablet or spray, oral capsule, topical agent (patch), or IV

33
Q

When would an individual switch to a nitro patch (from other methods of admin?)

A

Once symptoms are managed

34
Q

Titrated does of beta blockers given to what target HR?

A

Dose titrated to achieve HR of 50-60bpm

35
Q

Why are beta blockers contraindicated in those with resp obstruction such as asthma?

A

Can cause bronchoconstriction

36
Q

Effects of ca channel blockers?

A

o Slow HR, dec contractility (negative inotrope) → dec workload of heart
o Vasodilation → dec BP + inc coronary artery perfusion

37
Q

In what condition must Ca channel blockers be taken cautiously? Why?

A

oBe careful with first gen Ca blockers for those with HF → dec contractility…have to use certain drugs

38
Q

Worst side effect or most important thing to monitor for in those taking heparin?

A

Bleeding!
and Monitor for HIT (Heparin-Induced-Thrombocytopenia)

Signs of blood loss = low BP, inc HR, dec Hb + HCt

39
Q

ASA in pt’s with CAD:

Why?
Typical doses?
Should it be taken with NSAIDS?
Main concern?

A

Prevents platelet activation and reduces incidence of MI and death in those with CAD

  • 160-325mg given as soon as angina diagnosis made, then 81-325mg continuous
  • Ensure continue to take even if also taking NSAIDS
  • Main concern: GI upset (??)
40
Q

What common term is used to describe the importance of rapid response to MI?

A

“Time is muscle”

41
Q

Signs and symptoms of MI

A

chest pain, ½ report no prior symptoms; SOB, indigestion, nausea, anxiety, cool, pale moist skin, inc HR and RR (from SS activation, may be short lived or perisist)

42
Q

How is a diagnosis for MI made?

A

Based on presenting symptoms, EGC, and lab test results

43
Q

How quickly should an ECG be done when pt admitted with MI? How is monitoring with this completed after?

A

should be done w/in 10 minutes of pain or pt arriving

oSerial ECGs done to monitor changes in location, evolution, and resolution of MI

44
Q

How is an NSTEMI seen in diagnostics?

A

NSTEMI has biomarker changes but no ECG changes

45
Q

Immediate care for MI

A
  • Physical rest in bed with backrest elevated or cardiac chair to min discomfort + dyspnea (improves tidal volume with less pressure from abdomen, drainage of upper lung improves, venous return decreases)
  • Reg vitals + resp assessment – encourage deep breathing + frequent position change to prevent fluid buildup
46
Q

Does CKMB rise immediately with MI?

A

No, takes a few hours (peaks at 24hrs or earlier)

47
Q

What is myoglobin? How long does it take to peak?

A

heme protein in muscle (not specific to heart)

inc levels w/in 1-3hrs, peaks 12 hrs after onset of symptoms
**sooner than cardiac-specific CKMB and troponin but not specific…

48
Q

Phases of cardiac rehab:

A

1) Phase I: Occurs at time of diagnosis of atherosclerisos (may be when admitted for first ACS event) → low level activites + initial education for pt and family → assume can largely resume normal life after MI
2) Phase II: after pt discharged; lasts 4-6wks; supervised exercise program, support and guidance for lifestyle modifications, set short and long term goals, outpatient cardiac rehab classes, etc.
3) Phase III: community-based phase; pt self-directed and no longer supervised

49
Q

Medical treatment guidelines for pt with MI?

A

1) obtain 12 lead ECG w/in 10 minutes
2) Obtain lab data for cardiac biomarkers
3) Obtain other diagnostics to clarify diagnosis
4) Begin routine medical interventions: supplemental O2, nitro, morphine, aspirin (162-325mg), beta-blocker, ACEI (within 24 hrs)
5) Evaluate for indications for reperfusion tx: PCI or fibrinolytic therapy
6) Continuous therapy as indicated: IV heparin or LMWH, clopidogrel (plavix) or ticlopidine (Ticlid), glycoprotein IIb/IIa inhibitor, best rest for min of 12-24hrs

50
Q

Suspected MI given what drugs?

A

aspirin, nitro, morphine, B blocker if can tolerate, and others as indicated

51
Q

Why might further intervention after thrombolytics be necessary to resolve source of MI?

A

o May dissolve thrombus, do not fix underlying athero lesion – may be referred for cardiac catheterization + other invasive interventions

52
Q

Under what circumstance should thrombolytics not be used?

A

o Dissolve ALL clots: should not be used if going to dissolve protective clots (such as those after major sx or hemorrhagic stroke); not used if has bleeding disorder

53
Q

A pt on thrombolytics should be put on bleeding precautions. what does this mean?

A

o Put on bleeding precautions: no IM’s, minimize punctures, hold P after injection longer, prevent tissue trauma

54
Q

When can troponin I and T be seen after an MI?

A

Enzyme detected 2-6 hrs. after

Nursing 232 (12 decks)

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