2013 103 notes 7.docx

8/22/2019 2013 103 notes 7.docx

1/18

Page 1 of18

Ms. April Anne D. Balanon GreywolfRed

IDTER

The Re

i a o and

Ca dio

a cula em

HA DOUT 7 OXY E ATIO :

Coronary Artery Disease ( CAD ) or Ischemic Heart Disease

Stages of Development

Atherosclerosis- myocardial injury Angina Pectoris- myocardial ischemia Myocardial Infarction- myocardial necrosis

Atherosclerosis- Narrowing of an artery r/t lipid/fat deposits at tunica intima an abnormal accumulation of lipid, orfatty,substances and fibrous tissue in the vessel wall. These substances create blockages or narrow the vessel in a way

that reduces blood flow to the myocardium.

Atherosclerosis involves a normally patent artery (A) and an inflammatory response whereby smooth muscle cellsproliferate within the blood vessel to form a fibrous cap (B). The proliferation results in deposits, called atheromas orplaques, which protrude into the lumen of the vessel, narrowing it and obstructing blood flow. If the cap ruptures andhemorrhages into the plaque (C), a thrombus (D) may develop and obstruct blood flow further.

CLINICAL MANIFESTATIONS: Coronary atherosclerosis produces symptoms and complications according to the location and degree of narrowing of the

arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium.

This impediment to blood flow is usually progressive, causing an inadequate blood supply that deprives the muscle cells ofoxygen needed for their survival.

The condition is known as ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. Angina pectoris usually is caused by significant coronary atherosclerosis. If the decrease in blood supply is great enough, of

long enough duration, or both, irreversible damage and death of myocardial cells, or MI, may result. Over time, irreversiblydamaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardialdysfunction.

Significant myocardial damage may cause inadequate cardiac output, and the heart cannot support the bodys needs forblood, which is called heart failure (HF). A decrease in blood supply from CAD may even cause the heart to stop abruptly, anevent that is called sudden cardiac death.

RISK FACTORS:Nonmodifiable Risk FactorsFamily history of coronary heart diseaseIncreasing ageGenderRace (higher incidence of heart disease in AfricanAmericans thanin Caucasians)

Modifiable Risk FactorsHigh blood cholesterol levelCigarette smoking, tobacco useHypertensionDiabetes mellitusLack of estrogen in womenPhysical inactivity

Obesity

Arteriosclerosis- Hardening of an artery r/t Ca+2 & CHON deposits at tunica media

Predisposing Factors Diet saturated fats, Obesity Hyperlipidemia Prolonged use of OCP Type A personality

Treatment PTCA (Percutaneous Transluminal Coronary Angioplasty)

TO: Revascularize myocardium, Prevent Angina Pectoris, and survival rate

8/22/2019 2013 103 notes 7.docx

2/18

Page 2 of18


IDTER

The Re

i a o and

Ca dio

a cula em


After PTCA, a portion of the plaque that was not removed may block the artery. The coronary artery may recoil(constrict) and the tissue remodels, increasing the risk for restenosis. A coronary artery stent is placed toovercome these risks.

Astent is a woven mesh that provides structural support to a vessel at risk of acute closure. The stent is placed over the angioplasty balloon. When the balloon is inflated, the mesh expands and presses

against the vessel wall, holding the artery open. The balloon is withdrawn, but the stent is left permanently inplace within the artery.

ANGINA PECTORIS

Clinical syndrome characterized by paroxysmal chest pain, usually relieved by REST or by taking NTG resultingfrom temporary myocardial ischemia

Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in theanterior chest.

The cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in

response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply.

Precipitating Factors (4 Es) Excessive physical exertion Extreme emotional response Exposure to cold environment-vasoconstriction Excessive intake of foods saturated fats

Types

Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest Unstable angina (also called preinfarction angina or crescendo angina): symptoms occur more frequently and

last longer than stable angina. The threshold for pain is lower, and pain may occur at rest. Intractable or refractory angina: severe incapacitating chest pain Variant angina (also called Prinzmetals angina): pain at rest with reversible ST-segment elevation; thought to

be caused by coronary artery vasospasm

8/22/2019 2013 103 notes 7.docx

3/18

Page 3 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), butpatient reports no symptoms

Signs and Symptoms Initial Levines sign (hand clutching of the chest) Chest Pain crushing, stabbing, heaviness, located substernally, radiates to back, shoulder, arm, axilla and jaw

muscles, usually relieved by rest or NTG If radiating cardiac in origin otherwise, it is pulmonary in origin

Dyspnea, tachycardia, palpitations, diaphoresisDiagnostic Procedures

Stress Test- abnormal ECG ECG- ST depression Serum cholesterol and uric acid

Nursing Management CBR Administer meds as ordered:

A. Nitroglycerine (NTG) Smaller dose (venodilator)- dilates veins to LE venous pooling venous return Nitrates remain the mainstay for treatment of angina pectoris. A vasoactive agent, nitroglycerin (Nitrostat, Nitrol, Nitrobid IV) is administered to reduce myocardial oxygen

consumption, which decreases ischemia and relieves pain. Nitroglycerin dilates primarily the veins and, in higher doses, also dilates the arteries. It helps to increase

coronary blood flow by preventing vasospasm and increasing perfusion through the collateral vessels.

Max. dose given- 3, q 3-5 min. interval If S/Sx not relieved give Morphine and O2 MI

Nursing Management with NTG Monitor S/E Orthostatic hypoTN transient headache and dizziness Assist in ambulation; instruct pt to rise slowly from lying to sitting position

B. Beta- blockers- Propanolol (Inderal) Beta-blockers such as propranolol (Inderal), metoprolol (Lopressor, Toprol), and

atenolol (Tenormin) appear to reduce myocardial oxygen consumption by blockingthe beta-adrenergic sympathetic stimulation to the heart.

The result is a reduction in heart rate, slowed conduction of an impulse through the heart,decreased blood pressure, and reduced myocardial contractility (force of contraction) thatestablishes a more favorable balance between myocardial oxygen needs (demands) and the

amount of oxygen available (supply). This helps to control chest pain and delays the onset of ischemia during work or exercise.

C. Ca+2 antagonist- Nifedipine (Calcibloc) Calcium channel blockers (calcium ion antagonists) have different effects. Some decrease sinoatrial node automaticity and atrioventricular node conduction,

resulting in a slower heart rate and a decrease in the strength of the heart musclecontraction (negative inotropic effect). These effects decrease the workload of theheart.

Calcium channel blockers also relax the blood vessels, causing a decrease in blood pressure andan increase in coronary artery perfusion.

Calcium channel blockers increase myocardial oxygen supply by dilating the smooth muscle wallof the coronary arterioles; they decrease myocardial oxygen demand by reducing systemicarterial pressure and the workload of the left ventricle.

The calcium channel blockers most commonly used are amlodipine (Norvasc), verapamil (Calan,Isoptin, Verelan), and diltiazem (Cardizem, Dilacor, Tiazac).

They may be used by patients who cannot take beta-blockers, who develop significant sideeffects from beta-blockers or nitrates, or who still have pain despite beta blocker andnitroglycerin therapy.

8/22/2019 2013 103 notes 7.docx

4/18

Page 4 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Calcium channel blockers are used to prevent and treat vasospasm, which commonly occursafter an invasive interventional procedure.

MYOCARDIAL INFARCTION

MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed. Like unstableangina, MI is

usually caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by anembolus or thrombus.

Terminal stage of CAD, due to permanent malocclusion, necrosis and scarring2 Types

Subendocardial- malocclusion of either R and L coronary arteries Transmural- more dangerous type, malocclusion of both arteries

Most critical period 48-72 hrs majority of arrythmias occur (esp. PVC)Signs and Symptoms Chest pain- excruciating, visceral pain in substernal/precordial area radiating to back, shoulder, arm, axilla, jaw

and abdominal muscles NOT RELIEVED BY REST OR NTG Dyspnea Initial BP and T mild apprehension/ restlessness Occasional findings:

Rales, crackles Split S1 and S2 Pericardial friction rub S4 atrial gallop

ADDITIONAL READING ASSIGNMENT:

Cardiovascular Chest pain or discomfort, palpitations. Heart sounds may include S3, S4, and new onset of a murmur. Increased jugular venous distention may be seen if the MI has caused heart failure. Blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased

contractility, impending cardiogenic shock, or medications. Pulse deficit may indicate atrial fibrillation. In addition to ST-segment and T-wave changes, ECG may show tachycardia, bradycardia, and

dysrhythmias.

Respiratory Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion. Pulmonary edema may be present.

Gastrointestinal Nausea and vomiting.

Genitourinary Decreased urinary output may indicate cardiogenic shock.

Skin Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation from loss of

contractility may indicate cardiogenic shock. Dependent edema may also be present due to poor contractility.

Neurologic

Anxiety, restlessness, light-headedness may indicate increased sympathetic stimulation or a decreasein contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock. Headache, visual disturbances, altered speech, altered motor function, and further changes in level of

consciousness may indicate cerebral bleeding if patient is receiving thrombolytics.

Psychological Fear with feeling of impending doom, or patient may deny that anything is wrong.

Diagnostic Procedures

8/22/2019 2013 103 notes 7.docx

5/18

Page 5 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Cardiac EnzymesElevate peak period of elevation

CPK II MB 4-8h 12-36h 72hLDH 12-24h 24-96h 8-14dSGOT (ALT) 6-12h 36-48h 4-6d

Troponin test- levels Initial BP and T ECG- ST elevation, widened QRS

CBC- WBC Serum cholesterol and uric acid

Nursing Management

CBR without bathroom privileges, bedside commode to myocardial workload Avoid Valsalva maneuver Place pt in semi-fowlers position Monitor VS, I/O, breath sounds, ECG tracings Diet: gen. liquid to soft, no caffeine, fat, Na+, may drink 20-30 cc of red wine, brandy or whiskey/week

vasodilation Administer O2 as ordered (2nd immediate intervention during acute attack) Administer meds as ordered:

Narcotic analgesic: Morphine SO4 vasodilation, anxiety (1st nursing intervention during acuteattack)

S/E: respiratory depression, antidote: Narcan Thrombolytics/Fibrinolytics (monitor bleeding time)

U-rokinase S-treptokinase- S/E- urticaria, allergic reaction T-issue Plasminogen Activator

Anti-coagulants Heparin- PTT: N- 30-45 sec, antidote: Protamine SO4 Coumadin- PT: N- 10-14 sec, antidote: Vit. K

Anti-platelet: ASA (Aspirin)HEART FAILURE

Heart failure is a clinical syndrome that results from the progressive process of remodeling, in which mechanicaland biochemical forces alter the size, shape, and function of the ventricle's ability to pump enough oxygenatedblood to meet the metabolic demands of the body.

Pathophysiology and Etiology Cardiac compensatory mechanisms (increases in heart rate, vasoconstriction, heart enlargement) occur to assist

the struggling heart.o These mechanisms are able to compensate for the heart's inability to pump effectively and maintain

sufficient blood flow to organs and tissue at rest.o Physiologic stressors that increase the workload of the heart (exercise, infection) may cause these

mechanisms to fail and precipitate the clinical syndrome associated with a failing heart (elevatedventricular/atrial pressures, sodium and water retention, decreased CO, circulatory and pulmonary

congestion).o The compensatory mechanisms may hasten the onset of failure because they increase afterload and

cardiac work. Two types of dysfunction may exist with heart failure

o Systolic failure: poor contractility of the myocardium resulting in decreased CO and a resulting increasein the systemic vascular resistance. The increased SVR causes an increase in the afterload (the force theleft ventricle must overcome in order to eject the volume of blood).

8/22/2019 2013 103 notes 7.docx

6/18

Page 6 of18


IDTER

The Re

i a o and

Ca dio

a cula em


o Diastolic failure: stiff myocardium, which impairs the ability of the left ventricle to fill up with blood.This causes an increase in pressure in the left atrium and pulmonary vasculature causing the pulmonarysigns of heart failure.

Caused by disorders of heart muscle resulting in decreased contractile properties of the heart; CHD leading to MI;hypertension; valvular heart disease; congenital heart disease; cardiomyopathies; dysrhythmias.

Clinical Manifestations Initially, there may be isolated left-sided heart failure, but eventually the right ventricle fails because of the

additional workload. Combined left- and right-sided heart failure is common.

1. Left-Sided Heart Failure (Forward Failure) Congestion occurs mainly in the lungs from blood backing up into pulmonary veins and capillaries.

o Shortness of breath, dyspnea on exertion, paroxysmal nocturnal dyspnea (due to reabsorption ofdependent edema that has developed during day), orthopnea, pulmonary edema

o Cough: may be dry, unproductive; usually occurs at night Fatigability: from low CO, nocturia, insomnia, dyspnea, catabolic effect of chronic failure. Insomnia, restlessness. Tachycardia: S3 ventricular gallop.

2. Right-Sided Heart Failure (Backward Failure) Edema of ankles; unexplained weight gain Liver congestion: may produce upper abdominal pain Distended jugular veins Abnormal fluid in body cavities (pleural space, abdominal cavity) Anorexia and nausea: from hepatic and visceral engorgement Weakness

Cardiovascular Findings in Both Types Cardiomegaly (enlargement of the heart) detected by physical examination and chest X-ray Ventricular gallop: evident on auscultation Rapid heart rate Development of pulsus alternans (alternation in strength of beat)

Diagnostic Evaluation Echocardiography: may show ventricular hypertrophy, dilation of chambers, and abnormal wall motion. ECG (resting and exercise): may show ventricular hypertrophy and ischemia. Chest X-ray may show cardiomegaly, pleural effusion, and vascular congestion. ABG studies may show hypoxemia due to pulmonary vascular congestion.

Drug Classesa. Diuretics

Eliminate excess body water and decrease ventricular pressures. A low-sodium diet and fluid restriction complement this therapy. Some diuretics may have slight venodilator properties.

b. Positive inotropic agents: increase the heart's ability to pump more effectively by improving the contractileforce of the muscle.

Digoxin (Lanoxin) may only be effective in severe cases of failure. Dopamine (Intropin) improves renal blood flow in low dose range. Dobutamine (Dobutrex). Milrinone (Primacor) and amrinone (Inocor) are potent vasodilators.

c. Vasodilator therapy: decreases the workload of the heart by dilating peripheral vessels Nitrates, such as nitroglycerin (Tridil), isosorbide (Isordil), nitroglycerin ointment (Nitro-Bid):

predominantly dilate systemic veins

Hydralazine (Apresoline): predominantly affects arterioles Prazosin (Minipress): balanced effects on both arterial and venous circulation Morphine (Duramorph): decreases venous return, decreases pain and anxiety and thus cardiac work

d. Angiotensin-converting enzyme (ACE) inhibitors: inhibit the adverse effects of angiotensin II (potentvasoconstriction/sodium retention). Decreases left ventricular afterload with a subsequent decrease in heart rateassociated with heart failure, thereby reducing the workload of the heart and increasing CO. May decreaseremodeling of the ventricle.

Captopril (Capoten) and enalapril (Vasotec) are commonly used.

8/22/2019 2013 103 notes 7.docx

7/18

Page 7 of18


IDTER

The Re

i a o and

Ca dio

a cula em


e. Beta-adrenergic blockersdecrease myocardial workload and protect against fatal dysrhythmias by blockingnorepi-nephrine effects of the sympathetic nervous system.

Metoprolol (Lopressor) or metoprolol CR or XL (Toprol XL) are commonly used. Carvedilol (Coreg) is a nonselective beta- and alpha-adrenergic blocker.

f. Aldosterone antagonists: decrease sodium retention, sympathetic nervous system activation and cardiacremodeling.

Spironolactone (Aldactone) is most commonly used.Diet Therapy

Restricted sodium and Restricted fluidsComplications

Cardiac dysrhythmias. Myocardial failure and cardiac arrest. Digoxin toxicity: from decreased renal function and potassium depletion.

Nursing Assessment Obtain history of symptoms, limits of activity, response to rest, and history of response to drug therapy. Assess peripheral arterial pulses; note quality, character; assess heart rhythm and rate and BP; assess edema. Assess weight and ask about baseline weight. Note results of serum electrolyte levels and other laboratory tests.

Nursing Diagnoses Decreased Cardiac Output related to impaired contractility and increased preload and afterload Impaired Gas Exchange related to alveolar edema due to elevated ventricular pressures Excess Fluid Volume related to sodium and water retention Activity Intolerance related to oxygen supply and demand imbalance

ADDITIONAL READING ASSIGNMENT:Nursing Interventions

1. Maintaining Adequate Cardiac Output Place patient at physical and emotional rest to reduce work of heart.

o Provide rest in semi-recumbent position or in a chair: reduces work of heart, increases heart reserve,reduces BP, decreases work of respiratory muscles and oxygen utilization, improves efficiency of heartcontraction; recumbency promotes diuresis by improving renal perfusion.

o Provide bedside commode: to reduce work of getting to bathroom and for defecation. Evaluate frequently for progression of left-sided heart failure. Take frequent BP readings.

o Observe for lowering of systolic pressure.o Note narrowing of pulse pressure.o Note alternating strong and weak pulsations (pulsus alternans).

Auscultate heart sounds frequently and monitor cardiac rhythm.o Note presence of S3 or S4 gallop (S3 gallop is a significant indicator of heart failure).o Monitor for premature ventricular beats.

Observe for signs and symptoms of reduced peripheral tissue perfusion: cool temperature of skin, facial pallor,poor capillary refill of nail beds.

Administer pharmacotherapy as directed. Monitor clinical response of patient with respect to relief of symptoms (lessening dyspnea and orthopnea,

decrease in crackles, relief of peripheral edema).

2. Improving Oxygenation Raise head of bed 8 to 10 inches (20 to 30 cm): reduces venous return to heart and lungs; alleviates pulmonary

congestion.o Support lower arms with pillows: to eliminate pull of their weight on shoulder muscles.o Sit orthopneic patient on side of bed with feet supported by a chair, head and arms resting on an over-the-bed table, and lumbosacral area supported with pillows.

Observe for increased rate of respirations (could be indicative of falling arterial pH). Observe for Cheyne-Stokes respirations (may occur in elderly patients because of a decrease in cerebral

perfusion). Position the patient every 2 hours (or encourage the patient to change position frequently): to help prevent

atelectasis and pneumonia. Encourage deep-breathing exercises every 1 to 2 hours: to avoid atelectasis.

8/22/2019 2013 103 notes 7.docx

8/18

Page 8 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Offer small, frequent feedings: to avoid excessive gastric filling and abdominal distention with subsequentelevation of diaphragm that causes decrease in lung capacity.

Administer oxygen as directed.3. Restoring Fluid Balance Administer prescribed diuretic as ordered. Give diuretic early in the morning: nighttime diuresis disturbs sleep. Keep input and output record: patient may lose large volume of fluid after a single dose of diuretic. Weigh patient daily: to determine if edema is being controlled: weight loss should not exceed 1 to 2 lb (0.5 to 1

kg)/day. Assess for signs of hypovolemia caused by diuretic therapy: thirst, decreased urine output, orthostatic

hypotension, weak, thready pulse, increased serum osmolality, and increased urine specific gravity. Administer I.V. fluids carefully to prevent fluid overload. Caution patients to avoid added salt in food and foods with high sodium content.

4. Improving Activity Tolerance Increase patient's activities gradually. Alter or modify patient's activities: to keep within the limits of hiscardiac reserve.

o Assist patient with self-care activities early in the day (fatigue sets in as day progresses).o Be alert to complaints of chest pain or skeletal pain during or after activities.

Observe the pulse, symptoms, and behavioral response to increased activity.o Monitor patient's heart rate during self-care activities.o Allow heart rate to decrease to preactivity level before initiating a new activity.

Patient Education and Health Maintenance

a. Teach the signs and symptoms of recurrence. Watch for:o Gain in weight: report weight gain of more than 2 to 3 lb (0.9 to 1.4 kg) in a few days. Weigh at same time daily to

detect any tendency toward fluid retention.o

Swelling of ankles, feet, or abdomen.o Persistent cough.o Tiredness, loss of appetite.o Frequent urination at night.

b. Review medication regimen.o Label all medications.o Give written instructions.o Inform the patient of adverse drug effects.

c. Review activity program. Instruct the patient as follows:o Increase walking and other activities gradually, provided they do not cause fatigue and dyspnea.o In general, continue at whatever activity level can be maintained without the appearance of symptoms.o Avoid excesses in eating and drinking.o Avoid extremes in heat and cold, which increase the work of the heart; air conditioning may be essential in a hot,

humid environment.

d.Restrict sodium as directed.

o Teach restricted sodium diet and the DASH dieto Give patient a written diet plan with lists of permitted and restricted foods.

ANEURYSM An aneurysm is a distention of an artery brought about by a weakening/destruction of the arterial wall They are lined with intraluminal debris, such as plaque and thrombi Because of the high pressure in the arterial system, aneurysms can enlarge, producing complications by

compressing surrounding structures; left untreated, they may rupture, causing a fatal hemorrhage The aorta is the most common site for aneurysms

Pathophysiology and Etiology Aneurysms may form as the result of:

o Atherosclerosis.o Infection.o Trauma.

False aneurysms (pseudoaneurysm) are associated with trauma to the arterial wall, as in blunt trauma or traumaassociated with arterial punctures for angiography and/or cardiac catheterization.

Contributing factors include:o Hypertension.o Arteriosclerosis.o Congenital weakness of vessels.

8/22/2019 2013 103 notes 7.docx

9/18

Page 9 of18


IDTER

The Re

i a o and

Ca dio

a cula em


o Trauma. Morphologically, aneurysms may be classified as follows:

o Saccular: distention of a vessel projecting from one sideo Fusiform: distention of the whole artery (ie, entire circumference is involved)o Dissecting: hemorrhagic or intramural hematoma, separating the medial layers of the aortic wall

GERONTOLOGIC ALERT Because of vascular changes that occur as a natural process of aging, all patients over age 65 are

assessed for the potential for aneurysms.

Clinical Manifestations

1. Aneurysm of the Thoracoabdominal Aorta From the aortic arch to the level of the diaphragm. At first, no symptoms; later, symptoms may come from

heart failure or a pulsating tumor mass in the chest

Pulse and BP difference in upper extremities if aneurysm interferes with circulation in left subclavian artery Pain and pressure symptoms Constant, boring pain because of pressure Dilated superficial veins on chest Cyanosis because of vein compression of chest vessels

2. Abdominal Aneurysm Many of these patients are asymptomatic Abdominal pain is most common, either persistent or intermittent: often localized in middle or lower

abdomen to the left of midline

Lower back pain Feeling of an abdominal pulsating mass, palpated as a thrill, auscultated as a bruit Hypertension Distal variability of BP, pressure in arm greater than thigh If rupture, will present with hypotension and/or hypovolemic shock

GERONTOLOGIC ALERT Most abdominal aneurysms occur between ages 60 and 90. Rupture of the aneurysm is likely if there is

coexistent hypertension or if the aneurysm is larger than 6 cm.

Diagnostic Evaluation Abdominal or chest X-ray may show calcification that outlines aneurysm. CT scanning and ultrasonography are used to detect and monitor size of aneurysm. Arteriography allows visualization of aneurysm and vessel.

Management

Surgery:o Resection of the aneurysm via abdominal incision and placement of a prosthetic graft to restore vascular

continuity.

Complications Fatal hemorrhage Myocardial ischemia Stroke

Paraplegia due to interruption of anterior spinalartery

Abdominal ischemiaNursing Assessment

In patient with thoracoabdominal aortic aneurysm, be alert for sudden onset of sharp, ripping, or tearing painlocated in anterior chest, epigastric area, shoulders, or back, indicating acute dissection or rupture.

In patients with abdominal aortic aneurysm, assess for abdominal (particularly left lower quadrant) pain andintense lower back pain caused by rapid expansion. Be alert for syncope, tachycardia, and hypotension, whichmay be followed by fatal hemorrhage due to rupture.

Nursing Diagnoses Ineffective Tissue Perfusion (vital organs) related to aneurysm or aneurysm rupture or dissection Risk for Infection related to surgery Acute Pain related to pressure of aneurysm on nerves and postoperatively

8/22/2019 2013 103 notes 7.docx

10/18

Page 10 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Nursing Interventions1. Maintaining Perfusion of Vital Organs

a. Preoperatively: Assess for chest pain and abdominal pain. Prepare patient for diagnostic studies or surgery as indicated. Monitor for signs and symptoms of hypovolemic shock. Perform neurovascular checks to distal extremities.

b. Postoperatively: Monitor vital signs frequently. Assess for signs and symptoms of bleeding:

o Hypotensiono Tachycardiao Tachypneao Diaphoresis

Monitor laboratory values as ordered Monitor urine output hourly. Assess abdomen for bowel sounds and distention. Observe for diarrhea, which occurs sooner than one

would expect bowel function. Perform neurovascular checks to distal extremities. Assess feet for signs and symptoms of embolization:

o Cold feeto Cyanotic toes or patchy blue areas on plantar surface of feeto Pain in feet

Maintain I.V. infusion to administer medications to control BP and provide fluids postoperatively. If thoracoabdominal aneurysm repair has been performed, monitor for signs and symptoms of spinal

cord ischemia:o Paino Numbnesso Paresthesiao Weakness

2. Preventing Infection Monitor temperature. Monitor changes in WBC count. Monitor incision for signs of infection. Administer antibiotics, if ordered.

3. Relieving Pain Administer pain medication as ordered or monitor patient-controlled analgesia. Keep head of bed elevated no more than 45 degrees for the first 3 days postoperatively to prevent

pressure on incision site.

Patient Education and Health Maintenance Instruct patient about medications to control BP and the importance of taking them. Discuss disease process and signs and symptoms of expanding aneurysm or impending rupture, or rupture, to be

reported. For postsurgical patients, discuss warning signs of postoperative complications (fever, inflammation of operative

site, bleeding, and swelling). Encourage adequate balanced intake for wound healing. Encourage patient to maintain an exercise schedule postoperatively.

HYPERTENSION

Hypertension (high BP) is a disease of vascular regulation in which the mechanisms that control arterial pressurewithin the normal range are altered

Predominant mechanisms of control are the central nervous system (CNS), the renal pressor system (renin-angiotensin-aldosterone system), and extracellular fluid volume. BP is elevated when there is increased cardiac output plus increased peripheral vascular resistance

Pathophysiology and Etiology

a. Primary or Essential Hypertension (Approximately 95% of patients with hypertension) When the diastolic pressure is 90 mm Hg and/or the systolic pressure is 140 mm Hg or higher and other causes

of hypertension are absent, the condition is said to be primary hypertension

8/22/2019 2013 103 notes 7.docx

11/18

Page 11 of18


IDTER

The Re

i a o and

Ca dio

a cula em


an individual is considered hypertensive when the average of three or more BP readings taken at rest severaldays apart exceeds the upper limits shown in Table 14-3.

TABLE 14-3 Classification of Blood Pressure for Adults

BP CLASSIFICATION SBP* (MM HG) DBP* (MM HG)

Normal < 120 < 80

Prehypertension 120-139 80-89

Stage 1 hypertension 140-159 90-99

Stage 2 hypertension 160 100

DBP:diastolic blood pressure SBP:systolic blood pressure. Treatment determined by highest BP category. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.

b. Secondary Hypertension Occurs in approximately 5% of patients with hypertension secondary to other pathology.

Renal pathology:o Congenital anomalies, pyelonephritis, renal artery obstruction, acute and chronic glomerulonephritiso Reduced blood flow to kidney causes release of renin. Renin reacts with serum protein in liver

angiotensin I; this plus angiotensin-converting enzyme angiotensin II leads to increased BP.

Endocrine disturbances:o Pheochromocytoma: a tumor of the adrenal gland that causes release of epinephrine and norepinephrine

and a rise in BP (extremely rare).o Adrenal cortex tumors lead to an increase in aldosterone secretion (hyperaldosteronism) and an elevated

BP (rare).

oCushing's syndrome leads to an increase in adrenocortical steroids (causing sodium and fluid retention)and hypertension.

o Hyperthyroidism: causes increased cardiac output. Medications, such as estrogens, sympathomimetics, antidepressants, NSAIDs, steroids.

Consequences of Hypertension1. Prolonged hypertension damages blood vessels in the brain, eyes, heart, and kidneys and increases the risk of

stroke, angina, MI, blindness, and heart and kidney failure.2. Blood vessel damage occurs.3. Damage to heart, brain, eyes, and kidneys is termed target organ disease; this is the major object of prevention

in patients with high BP.

Prevalence and Risk Factors

Hypertension is one of the most prevalent chronic diseases for which treatment is available; however, mostpatients with hypertension are untreated.

There are no symptoms; thus, it is termed silent killer Increase in incidence is associated with the following risk factors:

o Age: between 30and 70

o Race: Blacko Family historyo Smokingo Sedentary lifestyle

o Diabetes mellituso overweight

Clinical Manifestations Usually asymptomatic May cause headache, dizziness, blurred vision when greatly elevated BP readings as shown in Table 14-3

Diagnostic Evaluation ECG: to determine effects of hypertension on the heart (left ventricular hypertrophy, ischemia) or presence of

underlying heart disease

Chest X-ray: may show cardiomegaly Proteinuria, elevated serum blood urea nitrogen (BUN), and creatinine levels: indicate kidney disease as a cause

or effect of hypertension

Serum potassium: decreased in primary hyperaldosteronism; elevated in Cushing's syndrome, both causes ofsecondary hypertension

8/22/2019 2013 103 notes 7.docx

12/18

Page 12 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Urine (24-hour) for catecholamines: increased in pheochromocytomaManagement

1. Lifestyle Modifications Lose weight if body mass index is greater than or equal to 25. Limit alcohol-no more than 1 oz ethanol daily for men, 0.5 oz for women. Get regular aerobic exercise equivalent to 30 to 45 minutes of brisk walking most days. Cut sodium intake to 2.4 g or less per day. Smoking cessation. Reduce dietary saturated fat and cholesterol. Consider reducing coffee intake (5 cups per day has been shown to increase BP in hypertensive men). If, despite lifestyle changes, the BP remains at or above 140/90 mm Hg (or is not at optimal level in the presence

of other cardiovascular risk factors) over 3 to 6 months, drug therapy should be initiated.

Nursing Assessment Nursing History: Query the patient about the following: Family history of high BP Previous episodes of high BP Dietary habits and salt intake Target organ disease or other disease processes

that may place the patient in a high-risk grouplike diabetes, CAD, kidney disease

Cigarette smoking

Episodes of headache, weakness, muscle cramp,tingling, palpitations, sweating, visiondisturbances

Medication that could elevate BP:o Hormonal contraceptives, steroidso NSAIDs

Physical Examination Auscultate heart rate and palpate peripheral pulses; determine respirations. Examine the heart for a shift of the point of maximal impulse to the left, which occurs in heart enlargement. Auscultate for bruits over peripheral arteries to determine the presence of atherosclerosis, which may be

manifested as obstructed blood flow. Determine mentation status by asking patient about memory, ability to concentrate, and ability to perform simple

mathematical calculations.

Blood Pressure Determination Measure the BP of the patient under the same conditions each time. Avoid taking BP readings immediately after stressful or taxing situations. Wait 30 minutes after patient has

smoked. Place the patient in a position of comfort and have him or her remain silent. Make sure feet are on the floor or

otherwise supported.

Nursing Diagnoses Deficient Knowledge regarding the relationship between the treatment regimen and control of the disease

process Ineffective Therapeutic Regimen Management related to medication adverse effects and difficult lifestyle

adjustments

Nursing Interventions1. Providing Basic Education

Explain the meaning of high BP, risk factors, and their influences on the cardiovascular, cerebral, and renalsystems.

Stress that there can never be total cure, only control, of essential hypertension; emphasize theconsequences of uncontrolled hypertension.

Explain the pharmacologic control of hypertension.o Explain that the drugs used for effective control of elevated BP will likely produce adverse effects.o Warn the patient of the possibility that orthostatic hypotension may occur initially with some drug

therapy. Instruct the patient to get up slowly to offset the feeling of dizziness. Encourage the patient to sit or lie down immediately if he feels faint.

o Alert the patient to expect initial effects, such as anorexia, light-headedness, and fatigue, withmany medications.

Educate the patient to be aware of serious adverse effects and report them immediately so thatadjustments can be made in individual pharmacotherapy.

8/22/2019 2013 103 notes 7.docx

13/18

Page 13 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Note that dosages are individualized; therefore, they may need to be adjusted because it is oftenimpossible to predict reactions.

2. Encouraging Self-Management Enlist the patient's cooperation in redirecting lifestyle in keeping with the guidelines of therapy,

acknowledge the difficulty, and provide support and encouragement Develop a plan of instruction for medication self-management.

o Plan the patient's medication schedule so that the many medications are given at proper andconvenient times; set up a daily checklist on which the patient can record the medication taken.

Determine recommended dietary plans and provide dietary education as appropriateADDITIONAL READING ASSIGNMENT:

INFECTIVE ENDOCARDITIS Infective endocarditis (IE; bacterial endocarditis) is an infection of the inner lining of the heart caused by direct

invasion of bacteria or other organisms leading to deformity of the valve leaflets.

Pathophysiology and Etiology When the inner lining of the heart (endocardium) becomes inflamed, a fibrin clot (vegetation) forms. The fibrin clot may become colonized by pathogens during transient episodes of bacteremia resulting from

invasive procedures (venous and arterial cannulation, dental work causing gingival bleeding, GI tract surgery,liver biopsy, sigmoidoscopy), indwelling catheters, urinary tract infections, and wound and skin infections.

Platelets and fibrin surround the invading microorganisms, forming a protective covering and causing the infectedvegetation to enlarge.

o The enlarged vegetation (the basic lesion of endocarditis) can deform, thicken, stiffen, and scar the freemargins of valve leaflets as well as the fibrous ring (annulus) supporting the valve.

o The vegetations may also travel to various organs and tissues (spleen, kidney, coronary artery, brain, andlungs) and obstruct blood flow.

o The protective covering surrounding the vegetation makes it difficult for WBCs and antimicrobial agentsto infiltrate and destroy the infected lesion.

IE may develop on a heart valve already injured by rheumatic fever, congenital defects, on abnormallyvascularized valves, normal heart valves, and mechanical and biological heart valves.

IE may be acute or subacute, depending on the microorganisms involved. Acute IE manifests rapidly with danger of intractable heart failure and occurs more commonly on

normal heart valves. Subacute IE manifests a prolonged chronic course with a lesser risk of complications and occurs

more commonly on damaged or defective valves.Clinical Manifestations

Severity of manifestations depends on invading microorganism.

General Manifestations Fever, chills, sweats (fever may be absent in elderly patients or those with uremia) Anorexia, weight loss, weakness Cough, back and joint pain (especially in patients over age 60) Splenomegaly

Skin and Nail Manifestations Petechiae in conjunctiva, mucous membranes Splinter hemorrhages in nail beds Osler's nodes or painful red nodes on pads of fingers and toes; usually late sign of infection and found with a

subacute infection

Heart Manifestations New pathologic or changing murmur:no murmur with other signs and symptoms may indicate right heart

infection Tachycardia:related to decreased CO

Central Nervous System Manifestations Localized headaches Transient cerebral ischemia Altered mental status, aphasia Hemiplegia

8/22/2019 2013 103 notes 7.docx

14/18

Page 14 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Cortical sensory loss Roth's spots on fundi (retinal hemorrhages)

Pulmonary Manifestations Usually occur with right-sided heart involvement Pneumonitis, pleuritis, pulmonary edema, infiltrates

Management I.V. antimicrobial therapy, based on sensitivity of causative agent, for 4 to 6 weeks

o Bactericidal serum levels of selected antibiotics are monitored by serial titers; if serum lacks adequatebactericidal activity, more antibiotics or a different antibiotic is given.

Close follow-up by cardiologist Supplemental nutrition

Nursing Assessment Identify factors that may predispose to endocarditis, such as rheumatic heart disease, congenital heart defects,

idiopathic hypertrophic subaortic stenosis (IHSS), I.V. drug abuse, prosthetic heart valves, aortic or mitral

stenosis, previous history of endocarditis. Determine onset of signs and symptoms of endocarditis (early treatment of infection improves prognosis) Identify potential incidents that may have precipitated a transient bacteremia capable of causing endocarditis Obtain blood cultures, CBC, renal and hepatic studies, and a baseline 12-lead ECG Assess patient for allergies, with special emphasis on adverse reactions to antibiotic therapy Identify patient's and family's level of anxiety and use of appropriate coping mechanisms.

Nursing Diagnoses Decreased Cardiac Output related to structural factors (incompetent valves) Ineffective Tissue Perfusion (renal, cerebral, cardiopulmonary, GI, and peripheral) related to interruption of blood

flow Hyperthermia related to illness, potential dehydration, and aggressive antibiotic therapy Imbalanced Nutrition: Less Than Body Requirements related to anorexia Anxiety related to acute illness and hospitalization

Nursing Interventions1. Maintaining Adequate Cardiac Output

Auscultate heart to detect new murmur or change in existing murmur; presence of gallop. Monitor BP and pulse.

o Note presence of pulsus alternans (indicative of left-sided heart failure).o Evaluate pulse pressure (30 to 40 mm Hg is normal; indicates adequate CO).

Evaluate jugular vein distention. Record intake and output. Record daily weight. Auscultate lung fields for evidence of crackles (rales).

2. Maintaining Tissue Perfusion Observe patient for altered mentation, hemoptysis, hematuria, aphasia, loss of muscle strength, complaints

of pain. Notify health care provider of observed changes in the patient's status. Reposition patient frequently to prevent skin breakdown and pulmonary complications associated with bed

rest.3. Maintaining Normothermia

Observe basic principles of asepsis, good handwashing techniques, and continuity of patient care byprimary nurse.

Administer parenteral antibiotic therapy as directed.o Develop chart for rotation of sites for I.M. administration of antibiotic therapy.o Observe for adverse reactions to antibiotic therapy (severe respiratory distress, rash, itching,

fever).o Observe for adverse effects of long-term antibiotic therapy- ototoxicity, renal failure.

Monitor temperature every 2 to 4 hours.o Provide blankets and temperature-controlled comfortable environment if patient has shaking chills;

change bed linens as necessary.o Administer analgesic medications as directed.

8/22/2019 2013 103 notes 7.docx

15/18

Page 15 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Monitor laboratory values: HCT, BUN, creatinine, WBC, antibiotic levels, blood cultures. Promote adequate hydration, because diaphoresis and increased metabolic rate may cause dehydration.

o Encourage oral fluid intake.o Administer I.V. fluids as directed.o Observe skin turgor and mucous membranes.

4. Improving Nutritional Status Consult with a dietitian about nutritional needs of patient and food preferences. Encourage small meals and snacks throughout the day. Record daily caloric intake and weight. Educate family about the patient's caloric needs. Encourage family to assist the patient with meals and bring in patient's favorite foods.

5. Reducing Anxiety Explain to patient and family reasons for hospitalization, diagnostic tests, and therapies administered. Encourage patient to verbalize fears about illness and hospitalization. Explain procedures to patient before initiation. Offer patient literature, if available, about the disease. Encourage diversional activities for patient, such as television, reading, and interaction with other patients. Encourage family to interact with patient as frequently as possible.

RHEUMATIC ENDOCARDITIS (RHEUMATIC HEART DISEASE)

Rheumatic endocarditis is an acute, recurrent inflammatory disease that causes damage to the heart as a sequelato group A beta-hemolytic streptococcal infection, particularly the valves, resulting in valve leakage (insufficiency)and/or obstruction (narrowing or stenosis)

Pathophysiology and Etiology Rheumatic fever is a sequela to group A streptococcal infection that occurs in about 3% of untreated infections. It

is a preventable disease through the detection and adequate treatment of streptococcal pharyngitis.

Connective tissue of the heart, blood vessels, joints, and subcutaneous tissues can be affected. Lesions in connective tissue are known as Aschoff bodies, which are localized areas of tissue necrosis surrounded

by immune cells. Heart valves are affected, resulting in valve leakage and narrowing. Compensatory changes in the chamber sizes and thickness of chamber walls occur. Heart involvement (carditis) also includes pericarditis, myocarditis, and endocarditis.

Clinical Manifestations Symptoms of streptococcal pharyngitis may precede rheumatic symptoms

o Sudden onset of sore throat; throat reddened with exudateo Swollen, tender lymph nodes at angle of jawo Headache and fever

Warm and swollen joints (polyarthritis) Chorea (irregular, jerky, involuntary, unpredictable muscular movements) Erythema marginatum (transient meshlike macular rash on trunk and extremities) Subcutaneous nodules (hard, painless nodules over extensor surfaces of extremities; rare) Prolonged PR interval demonstrated by ECG Heart murmurs; pleural and pericardial rubs

Diagnostic Evaluation Throat culture:to determine presence of streptococcal organisms Sedimentation rate, WBC count and differential, and CRP:increased during acute phase of infection ECG-prolonged PR interval or heart block

Management Antimicrobial therapy: penicillin is the drug of choice Rest: to maintain optimal cardiac function Salicylates or NSAIDs: to control fever and pain

Nursing Assessment Ask patient about symptoms of fever or throat or joint pain. Ask patient about chest pain, dyspnea, fatigue. Observe for skin lesions or rash on trunk and extremities. Palpate for firm, nontender movable nodules near tendons or joints. Auscultate heart sounds for murmurs and/or rubs.

8/22/2019 2013 103 notes 7.docx

16/18

Page 16 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Nursing Diagnoses

Hyperthermia related to disease process Decreased Cardiac Output related to decreased cardiac contractility Activity Intolerance related to joint pain and easy fatigability

Nursing Interventions1. Reducing Fever

Administer penicillin therapy as prescribed to eradicate hemolytic streptococcus; an alternative drugmay be prescribed if patient is allergic to penicillin, or sensitivity testing and desensitization may bedone.

Give salicylates or NSAIDs as prescribed to suppress rheumatic activity by controlling toxicmanifestations, to reduce fever, and to relieve joint pain.

Assess for effectiveness of drug therapy.2. Maintaining Adequate Cardiac Output Assess for signs and symptoms of acute rheumatic carditis.

o Monitor for tachycardia (usually persistent when patient sleeps) or bradycardia.o Be alert to development of second-degree heart block or Wenckebach's disease (acute

rheumatic carditis causes PR interval prolongation). Auscultate heart sounds every 4 hours.

o Document presence of murmur or pericardial friction rub.o Document extra heart sounds (S3 gallop, S4 gallop).

Monitor for development of chronic rheumatic endocarditis, which may include valvular disease andheart failure.

3. Maintaining Activity Maintain bed rest for duration of fever or if signs of active carditis are present. Provide ROM exercise program. Provide diversional activities that prevent exertion.

MYOCARDITIS Myocarditis is an inflammatory process involving the myocardium.

Pathophysiology and Etiology Focal or diffuse inflammation of the myocardium; may be acute or chronic.

Clinical Manifestations Symptoms depend on type of infection, degree of myocardial damage, capacity of myocardium to recover, and

host resistance Can be acute or chronic and can occur at any age Symptoms may be minor and go unnoticed.

o Fatigue and dyspneao Palpitationso Occasional precordial discomfort

Cardiac enlargement. Abnormal heart sounds: murmur, S3 or S4, or friction rubs. Signs of heart failure (eg, pulsus alternans, dyspnea, crackles). Fever with tachycardia.

Diagnostic Evaluation

Transient ECG changes: ST segment flattened, Twave inversion, conduction defects, Elevated WBC count and sedimentation rate

Chest X-ray: may show heart enlargement and lungcongestion

Stool and throat cultures isolating bacteria or a virus

Endomyocardial biopsy for definitive diagnosis

Echocardiogram: defines size, structure, and functionof heart

Magnetic resonance imaging: may be helpful todetermine structural alterations

ManagementTreatment objectives are targeted toward management of complications.

Diuretic and digoxin (Lanoxin) therapy for heart failure and atrial fibrillation

8/22/2019 2013 103 notes 7.docx

17/18

Page 17 of18


IDTER

The Re

i a o and

Ca dio

a cula em


Antidysrhythmic therapy (usually quinidine [Quinaglute] or procainamide [Pronestyl]) Strict bed rest to promote healing of damaged myocardium Antimicrobial therapy if causative bacteria is isolated Anticoagulation therapy

Complications Heart failure Cardiomyopathy

Nursing Assessment Assess for fatigue, palpitations, fever, dyspnea, and chest pain. Auscultate heart sounds. Evaluate history for precipitating factors.

Nursing Diagnoses Hyperthermia related to inflammatory/infectious process Decreased Cardiac Output related to decreased cardiac contractility and dysrhythmias Activity Intolerance related to impaired cardiac performance and febrile illness

Nursing Interventions

1. Reducing Fever Administer antipyretics as directed. Check temperature every 4 hours. Administer antibiotics as directed.

2. Maintaining Cardiac Output Evaluate for clinical evidence that disease is subsiding; monitor pulse, auscultate for abnormal heart sounds

(murmur or change in existing murmur), check temperature, auscultate lung fields, monitor respirations.

Record daily intake and output.Record daily weight. Check for peripheral edema. Elevate head of bed, if necessary, to enhance respiration. Evaluate patient's pulse and apical rate for signs of tachycardia and gallop rhythm: indications that heart

failure is recurring. Evaluate for evidence of dysrhythmias: patients with myocarditis are prone to develop dysrhythmias.

o Institute continuous cardiac monitoring if evidence of a dysrhythmia develops. DRUG ALERT

Patients with myocarditis may be sensitive to digoxin. Assess for toxic signs and symptoms, such asanorexia, nausea, fatigue, weakness, yellow-green halos around visual images, prolonged PR interval.

3. Reducing Fatigue Ensure bed rest to reduce heart rate, stroke volume, BP, and heart contractility; also helps to decrease

residual damage and complications of myocarditis, and promotes healing.o Prolonged bed rest may be required until there is reduction in heart size and improvement of

function. Provide diversional activities for patient. Discuss with patient activities that can be continued after discharge.

PERICARDITIS Pericarditis is an inflammation of the pericardium, the membranous sac enveloping the heart Pericardial effusion is an outpouring of fluid into the pericardial cavity seen in pericarditis Constrictive pericarditis is a condition in which a chronic inflammatory thickening of the pericardium compresses

the heart so it is unable to fill normally during diastole.

Pathophysiology and Etiology Acute idiopathic pericarditis is the most common and typical form; etiology unknown Infection MI; early, 24 to 72 hours; or late, 1 week to 2 years after MI (Dressler's syndrome) Chest trauma, heart surgery, including pacemaker implantation

Clinical Manifestations Pericardial friction rub: scratchy, grating, or creaking sound occurring in the presence of pericardial inflammation Dyspnea: from compression of heart and surrounding thoracic structures

8/22/2019 2013 103 notes 7.docx

18/18

Page 18 of18

IDTER

The Re

i a o and

Ca dio

a cula em


Fever, sweating, chills: due to inflammation of pericardium Dysrhythmias

Diagnostic Evaluation Echocardiogram: most sensitive method for detecting pericardial effusion Chest X-ray: may show heart enlargement ECG: to evaluate for MI WBC and differential elevations indicating infection Pericardiocentesis: for examination of pericardial fluid for etiologic diagnosis

Management The objectives of treatment are targeted toward determining the etiology of the problem; administering

pharmacologic therapy for specified etiology, when known; and being alert to the possible complication of cardiactamponade.

Bacterial pericarditis: penicillin or otherantimicrobial agents

Rheumatic fever: penicillin G and otherantimicrobial agents

Tuberculosis: antituberculosis chemotherapy Systemic lupus erythematosus: corticosteroids Renal pericarditis: dialysis, biochemical control

of end-stage renal disease

Complications Cardiac tamponade Heart failure

Nursing Assessment Evaluate complaint of chest pain. Auscultate heart sounds.

o Listen for friction rub by asking patient to hold breath briefly.o Listen to the heart with patient in different positions.

Evaluate history for precipitating factors.Nursing Diagnoses

Acute Pain related to pericardial inflammation Decreased Cardiac Output related to impaired ventricular expansion

Nursing Interventions

1. Reducing Discomfort Give prescribed drug regimen for pain and symptomatic relief. Relieve anxiety of patient and family by explaining the difference between pain of pericarditis and pain of

recurrent MI. (Patients may fear extension of myocardial tissue damage.) Explain to patient and family that pericarditis does not indicate further heart damage. Encourage patient to remain on bed rest when chest pain, fever, and friction rub occur.

2. Maintaining Cardiac Output Assess heart rate, rhythm, BP, respirations at least hourly Monitor closely for the development of dysrhythmias.

3. Patient Education and Health Maintenance Review all medications with the patient: purpose, adverse effects, dosage, and special precautions.

2013 103 notes 7.docx

Documents

Transcript of 2013 103 notes 7.docx