MED SURG UNIT 3 EXAM REVIEW (CH35,36,37) CHAPTER 35 1.

Hypertension preload versus after load

Three factors affect stroke volume: preload, contractility, and afterload. Preload. Preload is the amount of blood remaining in a ventricle at the end of diastole or the pressure generated at the end of diastole. Increased preload results in increased stroke volume and, therefore, increased cardiac output. Factors that increase preload include increased venous return to the heart and overhydration. Factors that decrease preload include dehydration, hemorrhage, and venous vasodilation. Contractility. Contractility is the ability of cardiac muscle fibers to shorten and produce a muscle contraction. Inotropy is a term used to refer to the contractile state of the cell. Factors that increase contractility are said to have a positive inotropic effect, and factors that decrease contractility create a negative inotropic effect. Afterload. Afterload is the amount of pressure the ventricles must overcome to eject the blood volume. It is determined primarily by the pressure in the arterial system. Afterload is decreased by vasodilation and increased by vasoconstriction.

2. KNOW WHAT IS MODIFIABLE AGE P631

Risk Factors. Factors that increase the risk of atherosclerosis include increased serum lipids, high blood pressure, cigarette smoking (nicotine), diabetes mellitus with elevated blood glucose, obesity, sedentary lifestyle, age, gender, race, and heredity. These risk factors are divided into two categories: risk factors that can be modified and those that cannot be modified. Risk factors that cannot be modified are age, gender, heredity, and race. The focus of patient education is on reducing the risk factors that can be modified. Other factors that may also contribute to the development of coronary heart disease are stress, sex hormones, birth control pills, excessive alcohol intake, and high homocysteine levels. Healthy People 2010 has set several goals related to serum lipid levels. One of these is to reduce the mean total blood cholesterol in adults from 206 mg/dL to 199 mg/dL. In addition, efforts will be made to reduce the proportion of adults with high blood cholesterol, increase the proportion of adults who have had their blood cholesterol checked within the past 5 years, and increase the proportion of individuals with CAD who have LDL levels treated to the goal of equal to or less than 100 mg/dL

3. TEE DIAGNOSTIC TEST

TRANSESOPHAGEAL ECHOCARDIOGRAM At times, the echocardiogram is not diagnostic and a transesophageal echocardiogram (TEE) is used. A flexible endoscopic probe with an ultrasound transducer is passed down the back of the throat into the esophagus. A local anesthetic to the throat decreases the gag reflex. Occasionally, an intravenous sedative is needed to reduce patient anxiety. Images are obtained from behind the heart as the probe moves down into the stomach. The probe is down for approximately 15 to 20
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minutes. The TEE provides information useful in the evaluation of ventricular wall motion and function and possible heart valve disorders. 4. NURSING INTERVENTION WILL BE IMPORTANT WITH THE TEE TEST FOR PT SAFETY Used when conventional echocardiogram not diagnostic. Probe inserted through esophagus into stomach (behind heart). Same purpose as echocardiogram Tell patient what to expect: throat will be anesthetized, may have IV. Signed consent required. Monitor vital signs, gag reflex, and, if sedated, level of consciousness 5. FIVE CHARACTERISTICS OF A NORMAL SINUS RHYTHM The normal finding is called a normal sinus rhythm, which is characterized by the following: 1.A rate of 60 to 100 bpm 2.A regular rhythm 3.A P wave preceding each QRS complex o 4.A PR interval that is within 0.12 to 0.20 second 5.A QRS complex that is 0.10 second or less 6. WHAT MEDS ARE ACE INHIBITORS AND HOW IT AFFECTS THE ARTERIAL SYSTEM ON PATIENTS ACE inhibitors may be prescribed for some patients to minimize the abnormal shaping or remodeling that can occur in the damaged ventricular muscle. ACE inhibitors decrease preload and afterload by blocking the RAA system, resulting in vasodilation, decreased blood volume, and lower blood pressure. In addition, ACE inhibitors are thought to limit the progression of ventricular remodeling. Angiotensin-converting enzyme (ACE) inhibitors (ACEI) work against the renin-angiotensinaldosterone system to dilate arteries and decrease the resistance to blood flow in the arteries (reduced afterload). In addition, less fluid is retained because aldosterone release is blocked. ACE inhibitors are prescribed for patients with heart failure, some cases of hypertension, and in some cases after myocardial infarction Examples of these medications are captopril (Capoten), enalapril (Vasotec), and quinapril (Accupril). 7. ATHEROSCLEROSIS :KNOW THE CONDITION Atherosclerosis, a form of arteriosclerosis, is an inflammatory disease that begins with endothelial injury and progresses to the complicated lesion seen in advanced stages of the disease process. Atherosclerosis begins with injury to the endothelial cells that line the wall of the arteries. Endothelial injury, which leads to inflammation and dysfunction of the endothelial cells, results in the deposit of LDLs along the intima of arteries. These deposits are called foam cells. When enough foam cells accumulate, they progress to the lesions associated with atherosclerosis: fatty streaks, fibrous plaque, and complicated (advanced) lesions.
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Progression of Lesions. Fatty Streak. The fatty streak is the earliest lesion to develop in atherosclerosis. Yellow-colored lipids (fat) fill smooth muscle cells, producing streaks of fat that cause no obstruction to the affected vessel. It is commonly found in the aorta by age 10 and in coronary arteries by age 15 regardless of race, gender, or environmental factors. The fatty streak is thought to be reversible. There are no symptoms associated with these lesions. Fibrous Plaque. The fibrous plaque is the characteristic lesion of progressing atherosclerosis, which develops over time. Smooth muscle cells, chronically stimulated by LDLs and platelet activated growth factors, proliferate, produce collagen, and migrate over the fatty streak. This forms a fibrous plaque that protrudes out from the wall of the artery into the lumen. Other substances (WBCs, platelets, lipids, calcium) adhere to and collect within the plaque. The fibrous plaque is whitish or grayish appearing, may develop in one portion of the artery or circle the entire lumen, and may have smooth or rough edges. Fibrous plaque contributes to the loss of arterial elasticity and impairs the vessel's ability to vasodilate to meet increased oxygen needs. Complicated Lesions. Complicated lesions develop as ulceration or rupture of the plaque occurs and platelets adhere to the lesion. Platelet adherence can trigger the coagulation cascade with the development of a thrombus that obstructs (occludes) the artery. Collateral Circulation. If plaque formation occurs slowly, collateral circulation may develop. Collateral blood vessels are new branches that grow from existing arteries to provide increased blood flow. Risk Factors. Factors that increase the risk of atherosclerosis include increased serum lipids, high blood pressure, cigarette smoking (nicotine), diabetes mellitus with elevated blood glucose, obesity, sedentary lifestyle, age, gender, race, and heredity. These risk factors are divided into two categories: risk factors that can be modified and those that cannot be modified. Risk factors that cannot be modified are age, gender, heredity, and race. The focus of patient education is on reducing the risk factors that can be modified. Other factors that may also contribute to the development of coronary heart disease are stress, sex hormones, birth control pills, excessive alcohol intake, and high homocysteine levels. Healthy People 2010 has set several goals related to serum lipid levels. One of these is to reduce the mean total blood cholesterol in adults from 206 mg/dL to 199 mg/dL. In addition, efforts will be made to reduce the proportion of adults with high blood cholesterol, increase the proportion of adults who have had their blood cholesterol checked within the past 5 years, and increase the proportion of individuals with CAD who have LDL levels treated to the goal of equal to or less than 100 mg/dL (Centers for Disease Control and Prevention/National Institutes of Health, 2005). 8. EXPLAIN UNSTABLE ANGINA ; DIFFERENCE BETWEEN STABLE AND UNSTABLE Angina pectoris (shortened to angina), or chest pain, the most common symptom of CAD, results when the demand for oxygen by the myocardial cells exceeds the supply of oxygen delivered. There are different types of angina: stable, unstable, and variant. Stable angina (also called chronic angina or exertional angina) occurs most often with exercise or activity and
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usually subsides with rest. Other precipitating factors are smoking, physical exertion, emotional stress, and heavy meals. The pain is usually substernal and described by the patient as viselike, burning, squeezing, or smothering. The pain may radiate to either arm, the shoulder, the jaw, the neck, or the epigastrium. Accompanying symptoms are diaphoresis, dyspnea, nausea, and vomiting. Stable angina occurs intermittently and is often predictable. Usually, stable angina lasts only a few minutes and is relieved by rest or with nitroglycerine (NTG). Unstable angina (categorized and treated as an acute coronary syndrome) is also called crescendo angina or preinfarction angina. The pain of unstable angina is more severe, occurs at rest or with minimal exertion, is often not relieved by NTG or requires more frequent NTG administration, and is not predictable. Unstable angina may occur in a patient with a history of stable angina. The patient may describe a change in the pain pattern or in the severity of the pain. Or, unstable angina may be the first clinical manifestation of CAD that a patient experiences. In either case, unstable angina is considered more serious than stable angina and will be treated differently. Patients with unstable angina are at higher risk for acute myocardial infarction (AMI) and are often hospitalized for diagnostic workup and treatment. 9. HEART MURMURS CAUSED BY VALVES THAT DO NOT CLOSE WELL. READ ABT THE CONDITION AGE-RELATED CHANGES It is difficult to separate the normal age-related changes in the heart and blood vessels from the changes caused by disease. In general, age-related changes progress slowly, whereas pathogenic changes are more likely to be sudden. HEART Changes in the heart muscle include increased density of connective tissue and decreased elasticity. Cardiac contractility may decline, making the heart less able to adapt to changes in circulating blood volume. The valves may thicken and stiffen. If they do not close properly, the patient may have a murmur. The valves may also partially block the path of blood flow, causing incomplete emptying of the chambers. The number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in the ventricles. The aging heart takes longer to respond to stress and then responds less dramatically. It also takes longer to return to normal after exercise or stress. Cardiac dysrhythmias are more common in older people but should still be evaluated because they can be dangerous. Health Promotion Considerations Long-Term Conditioning Long-term conditioning with an exercise program may help decrease arterial stiffening and improve the function of the left ventricle in older individuals. Physical exercise does not have to be strenuous to be helpful. Activity should become a part of an individual's regular routine. Table 35-2 Grading of Heart Murmurs GRADE DESCRIPTION I Very faint II Faint, but recognizable III Loud, but moderate in intensity IV Loud and accompanied by a palpable thrill
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GRADE V VI

DESCRIPTION Very loud, accompanied by a palpable thrill, and audible with the stethoscope partially off the client's chest Extremely loud, may be heard with the stethoscope slightly above the client's chest

Heart Murmurs. A heart murmur is the sound produced by turbulent blood flow across the valves. Murmurs are recorded as having high, low, or medium pitch, and they are located using the anatomic landmarks where they are heard best. The timing of a murmur relates to when it is heard in the cardiac cycle: systole or diastole. Murmurs are graded according to intensity or loudness (Table 35-2).
10. & 11 .WHY IS IT IMPORTANT TO CK FOR BLEEDING AT THE PUNCTURE

SITE WITH CARDIAC CATHERIZATION PTS? A catheter is passed through a vein or artery and dye is injected. Radiographs are taken to visualize heart structures and blood vessels. The procedure is done in a special room. Blood pressure, pulse, and ECG are monitored throughout test. Tell patient what to expect. Assess allergies to seafood or iodine and inform radiologist. NPO for specified time before procedure. Tell patient to expect flushing sensation when dye is injected. Give sedative if ordered. Signed consent required. Check puncture site; maintain pressure per protocol if a vascular sealing device is not used. Monitor vital signs and peripheral pulses on affected extremity. Enforce bed rest as ordered. CARDIAC CATHETERIZATION (CARDIAC ANGIOGRAPHY, CORONARY ARTERIOGRAPHY) Cardiac catheterization is a procedure in which a catheter is inserted into a vein or artery and is threaded into the heart chambers, coronary arteries, or both, under fluoroscopy (Fig. 35-6). A contrast dye is injected through the catheter, and films are made of the visualized heart structures. Vital signs and ECG are monitored during the procedure. In a catheterization of the right side of the heart, the catheter is inserted into a vein and threaded into the vena cava, RA, RV, and pulmonary artery. Pressures in the RA, RV, and pulmonary artery may be determined. The function of the pulmonic and tricuspid valves may be assessed. In a catheterization of the left side of the heart, the catheter is inserted into an artery and threaded against the flow of blood into the coronary arteries or the LV. The femoral vein and artery are the preferred insertion sites. The function of the coronary arteries and the aortic and mitral valves may be assessed. Blood samples may be drawn, and pressures in the various structures are measured. Complications of cardiac catheterization include bleeding, hematoma formation, infection, and embolus or thrombus formation. Nursing care before and after the procedure is very important. 11. SEE #10 WHAT DO U CK BEFORE GOING TO HAVE THIS PROCEDURE AND WHAT ALLERGIES?
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12. TESTS TO DETECT MYOCARDIAL INFARCTIONS ALSO LDH 3-6 DAYS

Troponin Troponin is a protein involved in the contraction of muscles. Two subtypes, troponin T (cTnT) and troponin I (cTnI) are specific to cardiac muscle and are released into the circulation after an acute myocardial infarction. Troponin levels, generally not detectable in healthy individuals, will elevate significantly after an acute myocardial infarction. Levels may elevate slightly as a result of lesser insults, such as an episode of angina. Troponin levels rise in 3 to 6 hours from onset of symptoms, peak in 24 hours, and remain in the circulation for up to 2 weeks. This test is done in the emergency department because the results are available more quickly than the cardiac enzymes. Troponin T (cTnT) and troponin I (cTnI) are proteins released from cardiac muscle when the muscle is damaged. Troponin levels elevate in 3 hours after myocardial injury, peak in 24 hours, and remain in the circulation for up to 2 weeks (cTnI remains elevated for 5 to 7 days; cTnT for 10 to 14 days). Troponin levels may be drawn in the emergency room Creatine Phosphokinase The creatine phosphokinase enzyme is found in high concentration in three tissues: the brain, the heart, and the skeletal muscle. The type of creatine phosphokinase (CPK) specific to heart tissue is CPK-MB. Elevation of the CPK-MB level indicates damage to the myocardial cells. The CPK-MB can be expected to rise 4 to 6 hours after an AMI, peak in 12 to 24 hours at more than 6 times the normal value, and return to normal within 2 to 3 days if no new damage occurs. Serial trends should be observed. The nurse can plot these trends. Musculo-skeletal injuries (especially fractures and surgery) and recent excessive athletic activity can also elevate the total CPK level. Lipid Profile A lipid profile is a battery of tests that measure the most common serum lipids: cholesterol, triglycerides, and lipoproteins. Cholesterol is a blood lipid produced by the liver. It is used to form bile salts for the digestion of fat and for the production of adrenal, ovarian, and testicular hormones. The normal adult serum cholesterol level is less than 200 mg/dL. Elevated cholesterol levels (hypercholesterolemia) are associated with increased risk of CAD, hypertension, and AMI. The cholesterol accumulates in the arterial lumen and in time results in decreased blood flow and occlusion. 13. LDL(LETHAL) VS HDL( HEALTHY) LEVELS Several forms of cholesterol are identified; however, the high-density lipoproteins (HDLs) and the low-density lipoproteins (LDLs) are the two that most closely correlate with coronary artery disease. The HDLs are desirable because they promote the excretion of cholesterol; therefore higher levels of HDLs are encouraged. On the other hand, elevated LDL levels are associated with a higher risk of CAD; therefore lower LDL levels are encouraged. A good way to remember the difference is that HDLs are healthy and LDLs are lethal. Currently, the recommendations are for HDL levels greater than 40 mg/dL and for LDL levels less than 100 mg/dL (American Heart Association, 2007). Triglycerides are a major contributor to CAD. They are produced in the liver. Triglyceride levels increase when LDL levels increase. The normal triglyceride level is less than 150 mg/dL.
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Low HDL levels can be raised by being physically active at least 30 minutes every day, by not smoking, and by losing weight (or maintaining a healthy weight). 14. KNOW THAT ATROPINE INCREASES THE HEART RATE AND MONITOR PT FOR TACHYCARDIA AND URINE RETENTION ATROPINE SULFATE Usage: Vagal blocker. Increases HR and CO in heart blocks and severe bradycardia. Used in symptomatic bradycardia and bradydysrhythmias. Nursing interventions: Assess HR and rhythm and BP. 15. KNOW THE THERAPEUTIC LIPID LEVELS Lipid-Lowering Agents Lipid-lowering medications are frequently part of the overall treatment plan, along with diet and exercise, for many patients with heart disease. The goal of therapy is for the patient to have decreased serum triglyceride and LDL levels and an improved HDL level. Patients on this group of medications need to be encouraged to adhere to diet restrictions, exercise, and quit smoking. Serial laboratory tests (lipid profile and liver function) will be closely monitored. Selected lipid-lowering medications are included in the Drug Therapy table on p. 645. LIPID-LOWERING AGENTS Cholestyramine (Questran) Prescribed when diet, exercise, and weight loss fail to bring cholesterol levels under control. Lowers LDL cholesterol. Increases HDL cholesterol. Interferes with absorption of some other drugs, so check drug-drug interactions before giving. To get the best effect, teach patients: Continue diet and exercise. Increase fluid intake to counter constipating effects Gemfibrozil (Lopid) Decreases synthesis and secretion of VLDL by liver. Decreases triglyceride levels. For best effect, teach patient: Continue diet and exercise. Take with meals. Nicotinic acid (niacin) Decreases synthesis/secretion of VLDL and LDL by liver. Increases HDL. For best effect, teach patient: Continue diet and exercise. Take with meals to decrease GI side effects. Pravastatin (Pravachol);Simvastatin (Zocor);Lovastatin (Mevacor),Atorvastatin (Lipitor) Increases rate of removal of LDL from plasma. Decreases synthesis of LDL. Monitor liver function tests. For best effect, teach patient: Continue diet and exercise. Report muscle tenderness. Take as single dose in the evening Have routine eye examinations
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16. KNOW THE S/S OF FUILD VOLUME EXCESS AND CHF Monitor for jugular venous distention Fluid Volume Excess The patient will have normal and peripheral edema. Auscultate heart related to decreased fluid balance as evidenced and lung sounds q 4 hr. Measure weight glomerular filtration rate, by weight of 145 lbs, daily and intake and output accurately. increased aldosterone, absence of edema, absence Maintain intravenous lines and correct sodium and water of crackles and wheezes in fluid infusion rate. Administer diuretics retention, and increased lungs, and ability to as ordered. Teach about sodium antidiuretic hormone participate in activities of restriction and rationale. Protect release daily living without dyspnea. edematous extremities from pressure or injury. Fluid Volume Excess Fluid retention is a response to HF, an attempt to maintain normal cardiac output. Unfortunately, it compounds the problem by increasing the workload on the heart. Therefore measures are taken to reduce the fluid volume to normal while improving the function of the heart. Administer diuretics as ordered, and monitor the patient for adverse effects. The most common adverse effects of diuretic therapy are fluid and electrolyte disturbances. Signs and symptoms that may indicate fluid or electrolyte disturbances include cardiac dysrhythmias, muscle weakness or twitching, cramps, changes in mental status, and abdominal distention. Frequent serum electrolyte measurements are usually ordered. Note the results and notify the physician of abnormal findings. If hourly urine output is being measured, report an output of less than 30 mL/hr to the physician as well. The patient should be weighed daily. An intravenous catheter is usually placed to provide a line for drug administration. If intravenous fluids are administered, monitor the rate of administration very carefully. If fluid retention is not relieved by other means, fluid restriction may be instituted. All staff should know the exact amount of fluid allowed and must record all intake. Fluid restriction can be very uncomfortable for the patient. Even with fluid volume excess, the patient may feel thirsty because of electrolyte imbalances. Present oral fluids in small containers, and offer them at reasonable intervals. Frequently provide mouth care. The patient and family must understand why fluids are restricted so that the patient does not exceed the prescribed intake. CHF The most common therapeutic dietary measure for CHF is sodium restriction. The patient may be limited to 2 g of sodium/day. In severe cases, a limitation of 500 to 1000 mg/day may be prescribed. Reduced sodium intake decreases fluid retention, thereby reducing the cardiac workload. For a 2-g sodium diet, advise the patient to avoid foods high in sodium (a list should be provided), not to add salt before or after cooking, and to use no more than 2 cups of milk products daily. Patients often have difficulty changing their use of seasonings. Acknowledge the difficulty, and explain how sodium limitation contributes to improvement of cardiac function. It is best to identify the type of diet to be prescribed on discharge as early as possible. This allows time for a dietary consultation to be arranged, which should be followed by reinforcement by the nurse. The person who prepares the patient's meals at home must be included in the teaching sessions. 17. WHAT DO U DO BEFORE DIGOXIN?
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CARDIAC GLYCOSIDES Obtain baseline vital signs, ECG, and electrolytes before administering first dose. Assess apical pulse for 1 min; hold and notify physician if <60. Cannot be Delays impulse conduction through administered intramuscularly. Monitor K+ AV node to slow heart rate (negative levels; administer K+ supplements as chronotropic effect). Increases strength ordered. Decreased renal function may Digoxin or force of myocardial contraction delay excretion and lead to toxicity. Toxic (Lanoxin) (positive inotropic effect). Increases effects may be indicated by dysrhythmias, stroke volume and CO. Used for HF, pulse <60, anorexia, nausea, syncope, visual atrial fibrillation and flutter, and disturbances, and abdominal pain. paroxysmal atrial tachycardia. Therapeutic level: 0.82.0 ng/mL. Toxic level: >2.0 ng/mL. Teach the patient: Take radial pulse for 1 min at the same time each day. Cardiac Glycosides The cardiac glycosides are also called cardiotonics or digitalis glycosides. Examples are digoxin (Lanoxin) and digitoxin. These drugs have several important pharmacologic actions on the heart. They slow the heart rate (negative chronotropic effect) and increase the force of myocardial contraction (positive inotropic effect), causing increased stroke volume and cardiac output. Cardiac glycosides are widely used in the treatment of heart failure (HF). They are also used to treat some cardiac dysrhythmias. When rapid effects are needed, a patient can be given a loading dose (called a digitalizing dose) of cardiac glycosides. Once therapeutic blood levels are obtained, a maintenance dose is prescribed to maintain the therapeutic effects. These drugs have high potential for toxicity and require close monitoring. Common practice is to count the apical pulse before giving each dose. If the rate is below 60 bpm in adults, withhold the dose and contact the physician. Because patients are often on cardiac glycosides for long-term therapy, they must be taught to monitor their own pulse and to report symptoms of toxicity (anorexia, nausea, visual disturbances). 18. WHY DO U STOP A BETA BLOCKER AND WHY OR WHY NOT? Propranolol (Inderal) Nonselective beta-adrenergic blocker. Decreases HR, myocardial irritability, and contractibility. Decreases BP in hypertension. Decreases CO. Used in dysrhythmia, myocardial infarction, hypertension, migraines, and chronic stable angina. Monitor vital signs. May be administered with diuretic to decrease Na+ and water retention. May cause bronchial constriction. Use with caution in all patients with obstructive lung disease. Auscultate lungs for crackles and heart for S3 and S4. Monitor weight daily; check for peripheral edema. Monitor blood glucose with diabetes. Teach the patient:
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 Do not discontinue this drug abruptly; taper over 2 weeks. Take at the same time(s) each day. While on this drug, use alcohol only in moderation; no smoking; decrease sodium intake. There is not the normal increase in heart rate with exercise and stress; increase activity slowly. Weigh daily; check for edema. 19. KNOW HOW TO ASSESS FOR ORTHOSTATIC HYPOTENSION (SEE BP) Orthostatic hypotension, also known as postural hypotension, refers to a condition where the blood pressure falls rapidly after a change in body position. Patients with orthostatic hypotension usually experience symptoms of low blood pressure when they stand up after sitting or lying for a period of time. The problem is relatively common, and tends to affect primarily older adults, though younger patients sometimes experience the condition as well. The diagnosis of orthostatic hypotension requires a blood pressure decline of 20mmHg in the systolic pressure or 10mmHg in the diastolic pressure within five minutes of rising from a seated or lying position. Blood Pressure. The correct-size blood pressure cuff must be used. Position the arm at the heart level, and check the blood pressure in both arms. Note the pulse pressure (difference between the systolic and diastolic pressures) because it is a noninvasive measure of cardiac output. Next, measure blood pressures and pulse rates in the lying, sitting, and standing positions. A blood pressure decrease of 20 mm Hg or more with a position change indicates decreased blood volume or an autonomic response. As blood pressure decreases, the pulse should increase as a compensatory mechanism.

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