CAD Flashcards
Risk factors for angina
Modifiable/non-modifable
x
Signs and symptoms for angina
x
Key aspects of plan of care for pt with angina
x
Key aspects and plan of care for pt with MI
x
Which drugs are considered antianginals?
x
Which drugs are used in MI?
x
What is angina pectoris?
chest pain brought about by myocardial ischemia (usually d/t sig athero)
most common CVD in adults
CAD
Most common cause of CAD?
Atherosclerosis
(causing reduced blood flow to myocardium) → atomic structure of coronary arteries makes particularly susceptible to atherosclerosis
Causes of CAD other than atheroschlerosis?
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)
If angina is severe, results in ?
MI
Consistently low CO leads to?
HF; or may even cause sudden cardiac death
What do primary and secondary prevention of CAD mean?
•Primary prev = preventing CAD; secondary prev = preventing progression of CAD
Signs and symptoms of CAD?
- Chest pain primarily
- SOB possible
- Women found to have some instead of/in addition to chest pain: dyspnea, nausea, weakness
Are prodromal symptoms usually seen in CAD?
Prodromal symptoms may occur (angine few hrs to days before acute episode), or major coronary event may be first indication
Prodromal symtoms =?
early symptom (or set of symptoms) that might indicate the start of a disease before specific symptoms occur
How are signs and symptoms of angina brought on?
•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)
Sensations felt in angina?
- 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.
Where is angina felt?
• 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.
Associated symptoms with angina?
•A feeling of weakness or numbness in the arms, wrists, and hands; SOB, pallor, diaphoresis, dizziness, nausea, vomiting and anxiety may accompany the pain
How to tell if angina is unstable? What needs to be done?
Pt’s with unstable angina are not relieved by rest or nitroglycerin; they need medical intervention.
How does angina typically differ in the elderly?
• 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)
How does onset of CAD differ in women?
• Women typically cardiac events 10 yrs later, but more chronic disease, complications + mortality
How to tell if someone has metabolic syndrome? What is this a major risk factor for?
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
Important areas of PREVENTION in CAD?
- Controlling cholesterol abnormalities
- Smoking cessation
- Managing HTN
- Controlling DM (insulin, metfomin)
Why is smokig cessation important in CAD?
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)
Management of elevated triglyceride levels:
• 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
How many doses of nitro can be given?
3
Initial nursing interventions for those with angina?
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)
Target O2 values in medical interventions?
• O2 administration: normal taget >93% (>90% in COPD)
Nitro: how does this help with angina?
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
How can nitro be given?
Given sublingual tablet or spray, oral capsule, topical agent (patch), or IV
When would an individual switch to a nitro patch (from other methods of admin?)
Once symptoms are managed
Titrated does of beta blockers given to what target HR?
Dose titrated to achieve HR of 50-60bpm
Why are beta blockers contraindicated in those with resp obstruction such as asthma?
Can cause bronchoconstriction
Effects of ca channel blockers?
o Slow HR, dec contractility (negative inotrope) → dec workload of heart
o Vasodilation → dec BP + inc coronary artery perfusion
In what condition must Ca channel blockers be taken cautiously? Why?
oBe careful with first gen Ca blockers for those with HF → dec contractility…have to use certain drugs
Worst side effect or most important thing to monitor for in those taking heparin?
Bleeding!
and Monitor for HIT (Heparin-Induced-Thrombocytopenia)
Signs of blood loss = low BP, inc HR, dec Hb + HCt
ASA in pt’s with CAD:
Why?
Typical doses?
Should it be taken with NSAIDS?
Main concern?
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 (??)
What common term is used to describe the importance of rapid response to MI?
“Time is muscle”
Signs and symptoms of MI
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)
How is a diagnosis for MI made?
Based on presenting symptoms, EGC, and lab test results
How quickly should an ECG be done when pt admitted with MI? How is monitoring with this completed after?
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
How is an NSTEMI seen in diagnostics?
NSTEMI has biomarker changes but no ECG changes
Immediate care for MI
- 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
Does CKMB rise immediately with MI?
No, takes a few hours (peaks at 24hrs or earlier)
What is myoglobin? How long does it take to peak?
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…
Phases of cardiac rehab:
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
Medical treatment guidelines for pt with MI?
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
Suspected MI given what drugs?
aspirin, nitro, morphine, B blocker if can tolerate, and others as indicated
Why might further intervention after thrombolytics be necessary to resolve source of MI?
o May dissolve thrombus, do not fix underlying athero lesion – may be referred for cardiac catheterization + other invasive interventions
Under what circumstance should thrombolytics not be used?
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
A pt on thrombolytics should be put on bleeding precautions. what does this mean?
o Put on bleeding precautions: no IM’s, minimize punctures, hold P after injection longer, prevent tissue trauma
When can troponin I and T be seen after an MI?
Enzyme detected 2-6 hrs. after
