Coronary Artery Disease (CAD Pathophysiology)

7/29/2019 Coronary Artery Disease (CAD Pathophysiology)

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CAD

Risk FactorsModif iable

hyperlipidemia

obesity

smoking

DM

sedentary lifestyleNon-Modif iable

age

male

race

family historyOthers

increased levels ofo homocysteineo fibrino lipoprotein

infection

inflammation

LVH (left ventricularhypertrophy)

ACS

UNSTABLE ANGINA

NON-ST SEGMENT

ELEVATION MI

MYOCARDIAL

INFARCTION

ST-SEGMENT

ELEVATION MI

ATHEROSCLEROSIS

ANGINA PECTORIS

Causes of AP

physical exertion

stress

Other Causes of AP

arterial spasm

aortic stenosis

cardiomyopathy

uncontrolled

hypertension

Non-Cardiac Causes

anemia

fever

thyrotoxicosis

Decreased oxygen due to:

Non-obstructive clot on an

atherosclerotic plaque

coronary vasospasm

atherosclerotic obstruction

without clot or vasospasm

inflammation or infection (sore

throat, gingivitis, tonsillitis)

NITRATES causes generalized vasodilation

o Can be administered orally, sublingually, transdermally,

or IV

o Provide short or long-lasting effects

o Short-acting nitrates provide immediate relief or

prophylaxis (15 MINUTES EFFECT)

o Long-acting nitrates prevent anginal episodes and/or

reduce severity and frequency of attacks

BETA-ADRENERGIC BLOCKERS inhibit SYMPATHETIC

stimulation of receptors of the heart and heart muscle

o Non-selective BAB also inhibit stimulation of the lungs.

Contraindicated for patients with COPD or ASTHMA

because it constricts the large airways in the lungs. CALCIUM CHANNEL BLOCKERSinhibit movement of

calcium within the heart muscle and coronary vessels;

promote vasodilation and prevent/control CORONARY

ARTERY SPASM

ACE INHIBITORS have therapeutic effects on the vascular

endothelium and have show to REDUCE RISK of worsening

angina

ANTILIPIDSreduce cholesterol and triglyceride levels

ANTIPLATELET AGENTS decrease platelet aggregation to

inhibit thrombus formation

FOLIC ACID AND B-COMPLEX VITAMINS treat increased

homocysteine levels

DRUG THERAPY

PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY

o A balloon tipped catheter is placed in a coronary vessel

narrowed by plaque

o The balloon is inflated and deflated to stretch the vessel

wall and flatten the plaque

INTRACORONARY ATHERECTOMY

o A blade-tipped catheter is guided into a coronary vessel

to the site of the plaque

o Plaque is either cut, shaved, or pulverized then removed

o Limited larger vessels

INTRACORONARY STENT

o A diamond mesh tubular device is placed in the

coronary vessel

o Prevents restenosis

o Drug-eluting stents contain an anti-inflammatory drug,

which decrease the inflammatory response

CABG (CORONARY ARTERY BYPASS GRAFT)

SURGERY

o A graft is surgically attached to the aorta, and the other

end of the graft is attached to a distal portion of the

coronary vessel

TRANSMYOCARDIAL REVASCULARIZATION

o laser beam, small channels are formed in the

myocardium

PERCUTANEOUS CORONARY

INTERVENTION


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CAD

CLINICAL MANIFESTATIONS

CHRONIC STABLE ANGINA

PECTORISUNSTABLE ANGINA

PECTORIS (Preinfarction)Chest pain or discomfort provoked by EXERTION or

EMOTIONAL STRESS. Relieved by REST or

NITROGLYCERIN.

Character ist ics

substernal chest pain, pressure, heaviness or

discomfort

pain may be mild or severe

gradual buildup of discomfort and subsequent

gradual fading

numbness or weakness in arms, wrists, or hands

diaphoresis

tachycardia

increased BP

Locat ion

Behind middle or upper third of sternum

+ Levine Sign

Radiat ion

Radiates to neck, jaw, shoulders, arms, hands, and

posterior intracapsular area

Durat ion

2-15 minutes (after stopping activities)

1 minute after NITROGLYCERINE

Other Precipi tat ing Factor

Exposure to hot or cold weather

Eating heavy meal

Coitus (increase workload of the heart, increase

oxygen demand)

Chest pain occurring at REST, no OXYGEN DEMAND is

placed on the heart, but an ACUTE LACK of BLOOD

FLOW to the HEART occurs because of:

Coronary artery spasm

Presence of an enlarge plaque

Hemorrhage / ulceration of a complicated lesion

Critical narrowing of the vessel lumen occurs

A change in FREQUENCY, DURATION, and

INTENSITY of stable angina symptoms

Pain lasts longer than 10 MINUTES

Pain UNRELIEVED by rest or Nitroglycerine

Mimics S&S of MI

CAN CAUSE SUDDEN DEATH OR RESULT IN MI.

SILENT ISCHEMIAAbsence of chest pain with documented evidence of an

imbalance between myocardial oxygen supply and

demand (ST DEPRESSION of 1mm or more). CIRCADIAN EVENT (occurs during the first few

hours after awakening due to an increase in

sympathetic nervous system activity)o Increase heart rate

o Increase BP

o Increase coronary vessel tone

o Increase blood viscosity

Characteristic chest pain and clinical history

Nitroglycerin test relief of pain.

Blood tests (Hemoglobin, fasting blood glucose, fasting lipid panel, coagulation studies, CRP, homocysteine, lipoprotein).

Resting ECGmay show LVH, ST-T wave changes, arrhythmias, and Q waves. ECG Stress Testing progressive increases of speed and elevation walking on a treadmill increase the workload of the heart. ST-T

wave changes occur if myocardial ischemia is induced.

Radionuclide Imaging a radioisotope, thallium 201, injected during exercise is imaged by a camera. Low uptake of the isotope by

heart muscle indicates regions of ischemia induced by exercise. Images taken during rest show a reversal of ischemia.

Radionuclide Ventriculography(gated blood pool scanning) red blood cells tagged with a radioisotope are imaged by camera

during exercise and at rest. Wall motion abnormalities of the heart can be detected and ejection fraction estimated.

Cardiac Catheterization coronary angiography performed during the procedure determines the presence, location, and extent of

coronary lesion.

PET (Positron-Emission Tomography)cardiac perfusion imaging with high resolution to detect very small perfusion differences

caused by stenotic arteries.

Electron-Beam CTdetects coronary calcium, which is found in most, but not all, atherosclerotic plaque. Low specificity.

DIAGNOSTIC EVALUATIONS


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PRIMARY PREVENTION FOR CAD

STOP SMOKING

IDEAL BODY WEIGHT


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1. Ask patient to DESCRIBE anginal attacks.

WHEN do attacks tend to occur?

WHERE is the pain located? Does it RADIATE?

Was the onset of pain SUDDEN or GRADUAL?

How LONG did it LAST?

Was the pain STEADY and UNWAVERING in quality?

Was the discomfort accompanied by other symptoms?

o SWEATING

o LIGHT-HEADEDNESS

o NAUSEA

o PALPITATIONS

o SHORTNESS OF BREATH

How is the pain RELIEVED?

2. Obtain BASELINE ECG.

3. Assess patient and familys KNOWLEDGE of disease.

4. Identify patient and familys level of anxiety and use appropriate coping mechanism.

5. Gather information about the patients cardiac risk factors.

Age

Total cholesterol level

HDL level

Systolic BP

Smoking status

10-year risk for development of CHD according to Framingham scoring method

6. Medical history

Diabetes

Heart failure

Previous MI

COPD

7. Identify factors that may contribute to NONCOMPLIANCE with prescribed drug therapy.

8. Review RENAL and HEPATIC STUDIES and CBC.

9. Discuss patient current ACTIVITY LEVELS.

10. Discuss patients BELIEFS about modification of risk factors and WILLINGNESS TO CHANGE.

Determine the 10-year risk of development of coronary heart disease (CHD) in men and women based on:

AGE CHOLESTEROL HDL BP HYPERTENSION SMOKING

NURSING ASSESSMENT


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NURSING INTERVENTIONS

Determine intensity of patients angina.o Compare pain experienced in the past.

o Observe for other signs and symptoms

(diaphoresis, sob, protective bodyposture, dusky facial color, changes in

LOC.

Position for comfort, FOWLERs

promotes ventilation.

OXYGEN (PRN)

Obtain VS (5-10 min until angina

subsides)

Obtain 12-Lead ECG

Antianginal Drug (PRN)

Monitor for relief of pain and note

duration of anginal episode

Monitor for progression from stable to

unstable angina

Identify specific activities the patientmay engage in that are below the level at

which angina pain occurs.

Notify staff when angina pain is

experienced.

RELIEVING PAIN Monitor response to therapy.

o BP and PR (provides baseline data for orthostatic hypotension) Recheck VS as indicated by ONSET of action of drug and at time of drugs PEAK

effect.

Note changes in BP of more than 10 mmHg and changes in heart rate of more

than 10 beats/min.

Note complaints of headache (esp. use of Nitrates) and dizziness.

o Analgesics for headache

o Supine position to relieve dizziness (associated with hypotension, PRELOAD is

enhanced, thereby increasing BP)

Institute continuous or PRN ECG.

o Beta-adrenergic blockers and calcium channel blockers can cause significant

bradycardia and varying degrees of heart block.

Evaluate for development of heart failure.

o Beta adrenergic blockers and calcium channel blockers DECREASE

CONTRACTILITY, increasing the likelihood of heart failure.

o Obtain daily weight and IO.

o Auscultate lung fields for CRACKLES.

o Monitor for presence of EDEMA.

Remove previous nitrate patch or paste before applying new paste or patch.

o Prevents HYPOTENSION.

o To decrease nitrate tolerance transdermal nitroglycerin may be worn only in the

daytime hours and taken off at night when physical exertion is decreased.

Be alert to ADVERSE REACTION related to ABRUPT DISCONTINUATION of beta-

adrenergic blockers and calcium channel blockers.

o Prevent rebound phenomenon.

Tachycardia

Hypertension

Chest pain

Discuss use of CHROMOTHERAPEUTIC therapy with health care provider.

o Tailoring of anginal drug therapy to the timing of circadian events.

Re ort adverse dru effects.

MAINTAINING CARDIAC OUTPUT

Rule out physiologic etiologies for

increasing anxiety before administering

PRN sedatives. Auscultate patient for signs of

HYPOPERFUSION.o Auscultate heart and lung soundso Obtain a rhythm strip

o Administer Oxygen PRN

o Notify physician immediately

Document all assessment findings,

health care provider notification and

response, and interventions and

response.

Explain reasons for hospitalization,

diagnostic tests, and therapies.

Encourage patient to verbalize fears and

concerns about illness through frequent

conversations.

Answer patients questions.

Administer anti-anxiety medication

(PRN).

Explain the importance of anxiety

reduction to assist in control of angina.

o Anxiety and fear put an increased

stress on the heart, requiring the heart

to use more oxygen.

o Teach relaxation technique.

Discuss measures to be taken when an

anginal episode occurs.

o Preparing client can decrease anxiety.

o Allow patient to accurately describe

angina.

DECREASNG ANXIETY

NITROGLCERIN

o Carry it at all times.

o Keep in original dark container.

o Should cause a slight burning or stinging sensation under the tongue when potent.

o Place under tongue at first sign of chest discomfort.

o Stop all effort or activity, sit and take tabletrelief should be after a few minutes.

o Bite tablet between front teeth and slip under tongue for quick action.

o Repeat dosage in a few minutes (3x) if relief is not obtained.

o Take prophylactically to avoid pain known to occur with certain activities.

o Remove previous paste before applying new one (same with patch).

o Do not remove patch when swimming or bathing.

VERAPAMIL (CALAN)constipation

NIFEDIPINE (PROCARDIA) ankle edema

BEETA-ADRENERGIC BLOCKERS / CALCIUM CHANNEL BLOCKERSheart

failure, shortness of breath, weight gain, REBOUND EFFECT (angina, tachycardia,

hypertension)

VASODILATORS, ANTIHYPERTENSIVES dizziness

Others: CAFFEINE increases heart rate and produce angina

DIET PILLS, NASAL DECONGESTANTS increases heart rate and stimulate high

BP

ALCOHOL increase hypotensive adverse effect of drugs

ANTI-ANGINA MEDICATIONS AND ADVERSE EFFECTS

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Coronary Artery Disease (CAD Pathophysiology)