Amino acid found in dietary protein.

Homocystine is a powerful risk factor for cardiovascular disease.

B-vitamins (esp. folate) help reduce serum homocystine levels.

CAD

Unmodifiable

Risk Factors

1. Age

2. Gender

3. Race

4. Genetics

CAD

Unmodifiable Risk Factors:

Gender

Men: 3x more often than women until age 65.

After 65 y/o, no gender difference although more deaths in women than men.

CAD

Unmodifiable Risk Factors:

Age

CAD

Unmodifiable Risk Factors:

Race

Increased risk in African Americans and

Native Americans.

Hispanics have a lower

death rate from CAD than non-Hispanic whites.

CAD

Unmodifiable Risk Factors:

Genetics

Congenital defects in coronary artery walls create predisposition for formation of plaques.

Familial hypercholesterolemia is strongly associated with early onset CAD.

CAD

Modifiable

Major Risk Factors

1. Elevated serum lipids

2. Hypertension

3. Tobacco use

4. Physical inactivity

5. Obesity

CAD:

Hypertension

BP of >140/90

The cause of hypertension in 90% of cases is unknown, but controllable with diet and/or drugs.

The stress of eleavted BP increases the rate of atherosclerotic development (related to the shearing stress of atherosclerotic injury).

CAD:

Tobacco Use

Risk of developing CAD is 2 to 6 times higher for tobacco users, especially smokers.  Risk is proportional to number of cigarettes smoked.

Tobacco use has been linked to lower estrogen levels, placing premenopausal women at greater risk for developing CAD.

Nicotine causes catecholamine release,

causing increased HR and peripheral vasoconstriction, increasing BP.

This increases cardiac workload, necessitaing greater myocardial O2 consumption.

Nicotine increases platelet adhesion, increasing the risk of emboli formation.

Carbon monoxide affects O2 carrying capacity of hemoglobin, increasing cardiac workload, and decreasing O2 available to the myocardium.

CAD:

Smoking Cessation

Benefits of smoking cessation are almost immediate.

CAD mortality rates drop to those of

non-smokers within 12 months.

Barriers to successful cessation include

multiple relapses, stress, weight gain,

lack of support, and depression.

CAD:

Physical Inactivity

Current recommendation is brisk walking

(or equivalent exercise causing persperation

and increase in HR by 30-50 bmp) at least 5 times per week for at least 30 minutes.

Physical activity decreases risk of CAD threefold:

more efficient lipid metabolism;

more efficient O2 utilization;

and reducing risk of obesity.

CAD

Modifiable

Contributing

Risk Factors

1. Diabetes Mellitus

2. Metabolic Syndrome

3. Phychologic State

4. Homocysteine level

The stretch of the myocardial fiber at end diastole, which is related to filling volume.

The resistance against which the ventricle must eject its volume of blood during contraction.

The resistance is produced by the volume

of blood already in the vascular system -

plus the diameter of the vessel walls. 

It is affected by the size of the ventricle, wall tension, and arterial pressure.

Left ventricular afterload

(systemic vascular resistance)

Right ventricular afterload

(pulmonary vascular resistance)

Caridac Glycosides

(and similar drugs):

Action

Actions:   Inhibits the adenosine triphosphatase (ATPase) enzyme and increases calcium into the myocardial cytoplasm).

Ø  (+) inotropic effect: increases contractility; increases renal blood flow

Ø  (-) chronotropic effect: decreases heart rate

Ø  (-) dromotropic effect: slows conduction through the AV node 

Overall effects:

1.      Increased cardiac output

2.      Decreased workload from the effect of decreased HR

3.      Mild diuretic effect

4.      Decreased heart size in cardiomyopathy patients

Uses: CHF, atrial dysrhythmias, SVT

Dig Toxicity:

1.      Monitor blood levels and signs of toxicity (Dig level .5-2 ng/ml).

2.      Monitor for factors associated with toxicity: K + <3.5 mEq/l, increased Ca+, decreased Mg (<1.8mg/dl), hypothyroidism, recent MI, vtach or heartblock, impaired renal function, dehydration, low serum albumin, rapid administration IV.

3.      Carefully monitor elderly: possible interaction with other drugs, diseases and slower absorption, which may lead to toxicity.

4.      Assess AP one full minute: hold for HR<60, or >120 unless parameters have been set by MD.

5.      Give separately from antacids (at least 1-2 hours apart).

6.      Assess renal status, monitor I & O.

7.      Assess for finding of increasing CHF.

8.      Usually requires digitalizing dose before beginning maintenance dose.

9.      Monitor electrolytes, ECG changes, BUN, Cr.

Ø      Digibind to treat toxicity if dysrhythmias are life-threatening.

Client teaching: proper dose, meds to avoid, how to count pulse rate and when to notify the MD.

Antianginals:

Drug Classes

Classifications of drugs used to treat angina:

A.    Nitrates

B.     Beta adrenergic blockers

C.     Calcium channel blockers

Nitrates:

Actions

1. decreases myocardial oxygen demand.

2. decreases preload by dilating veins.

3. higher doses dilate all major systemic arteries which decreases afterload.

Nitrates:

Indications

First line treatment for immediate and long-term prevention of angina. 

NItrates:

Nursing Implications

1.      Assess frequency and nature of angina before drug therapy and as relief is obtained.

2.      Monitor BP before any dose.

3.      (for patches and ointment application):

·         non-hairy area, rotate sites

·         remove old patch or ointment immediately before applying new dose

·         squeeze proper amount of ointment to paper and apply to skin without rubbing

·         tape paper in place with date and time applied

 4. Instructions for SL and spray: 

·         May take up to 3 SL tablets, 5 min. apart to obtain pair relief.

·         If relief is not obtained seek medical attention.

·         Tablets should be protected from light, heat, and moisture.

·         Patients taught to carry them at all times on their person.

·         Tablets should be replaced every 6 months after the bottle is opened.

·         Cotton should be removed from new bottles

·         Spray should be applied directly to oral mucosa (avoid inhaling).

Client teaching:

·         Take nitro tablets at the first sign of an anginal attack.

·         Nitrates are not habit forming but tolerances can develop.

·         Lie or sit down while taking to prevent falls from decreased preload.

·         To prevent angina, take agents before stressful physical activity (exercise, sexual activity; known to cause anginal attacks).

·         Monitor BP.

Ø      Interactions can occur with alcohol and other vasodilators.

Beta Adrenergic Blockers:

Actions

·         block beta adrenergic receptors,  which         decreases the force of contraction                     

·         slows conduction

·         decreases heart rate, which  lowers oxygen demand

• Long-term prevention of angina

• Allow chronic angina patients to increase exercise potential

• decreased BP
• decreased HR
• decreased libido
• depression
• bronchospasm
• worsening CHF\
• heart blocks
• fatigue
• constipation

 1.      Monitor BP and pulse before, during and       after therapy.

2.      Hold for pulse <60 unless other parameters are given by MD.

3.      Avoid administering at the same time as antacids, calcium channel blocker, or cardiac glycosides.

4.   Use with caution in COPD.

·         Do not abruptly withdraw med. without consulting MD (may result in angina or MI).

·         Take med. at the same time each day.

·         Report SE to MD.

·         Monitor HR every day for one full minute.

*Interactions:

• increased potential for bradycardia with concurrent use of cardiac glycosides and calcium channel blockers. 

• Increased hypotensive efect with diuretics.

Common

Beta Adrenergic Blockers

1.  metoprolol tartrate (Lopressor) *cardioselective

2.    atenolol (Tenorim)                    *cardioselective

3.      propranolol hydrochloride (Inderal)

4.      nadolol (Corgard)

5.      carvedilol (Coreg)

*Note: These drugs end in “lol”.

Calcium Channel Blockers:

Action

• Decrease myocardial contractility by preventing the influx of calcium into the cell

•  decrease oxygen demand

• dilate coronary and peripheral arterioles (decreased afterload)

• decreased HR

Calcium Channel Blockers:

Indications

Prevention of complications post-MI, angina and angina caused by vasospasm.

Calcium Channel Blockers:

Nursing Implications

Common

Calcium Channel Blockers

Diuretics:

Classifications

1. Thiazides

2. Loop Diuretics

3. Potassium Sparing Diuretics

Thiazides:

Actions

Thiazides:

Indications

Thiazides:

Major S/E

• Orthostatic hypotension
• Electrolyte imbalance: hypokalemia, lowered magnesium
•  Anorexia, nausea/vomiting
• Dry mouth, thirst

Thiazides:

Nursing Implications

1.      Check for allergies to sulfonamides

2.      Monitor glucose and potassium levels

3.      Monitor closely for renal or hepatic 

      dysfunction

1.      chlorothiazide (Diuril)

2.      hydrochlorothiazide (Esidrix, Hydrodiuril)

Loop Diuretics:

Actions

• Blocks the reabsorption of Na+ in the Loop of Henle (the ascending loop where the greatest Na+ reabsorption normally occurs)

• Reduces preload and afterload

Loop Diuretics:

Indications

• Edema: CHF, renal or hepatic dysfunction
• HTN
• whenever a more potent diuretic is needed

Loop Diuretics:

Major S/E

• Increased electrolyte depletion because of potency
• Excessive diuresis
• High doses: transient hearing loss, abdominal pain
• Leukopenia
• Thrombocytopenia
• Postural hypotension

Loop Diuretics:

Nursing Implications

1.      Give in AM to prevent nocturia

2.      Avoid if patient becomes anuric

3.      Assess for allergy to sulfonamides

Loop Diuretics:

Patient Teaching

• Consume K+ rich food
• Report muscle cramps
• Assess for signs of dehydration

Common

Loop Diuretics

1.      furosemide (Lasix)

2.      ethacrynate sodium (Edecrin)

3.      bumetanide (Bumex)

Potassium Sparing Diuretics:

Actions

• Inhibit the pump mechanism that normally exchanges potassium for sodium in the distal convoluted tubule

•  spironolacton (Aldactone) antagonizes aldosterone which mediates Na+ and K+ exchange, reducing Na+ reabsorption while retaining K+