N4581 EXAM 2 BLUEPRINT

1 N4581 EXAM 2 BLUEPRINT CORONARY ARTERY DISEASE AND ANGINA 1. Describe the pathophysiology, clinical manifestations, risk factors, and treatment of coronary atherosclerosis. Patho: Atherosclerosis is a type of blood vessel disorder resulting in the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen. In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium, which can lead to ischemia of myocardial muscle. Clinical Manifestations: CAD 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 is usually progressive, causing an inadequate blood supply that deprives the cardiac muscle cells of oxygen needed for their survival. The condition is known as ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction. Significant myocardial damage may result in persistently low cardiac output and heart failure. The most common manifestation of myocardial ischemia is the onset of chest pain. Patients with myocardial ischemia may present to an emergency department (ED) or clinic with a variety of symptoms other than chest pain. Some complain of epigastric distress and pain that radiates to the jaw or left arm. Patients who are older or have a history of diabetes or heart failure may report shortness of breath. Many women have been found to have atypical symptoms, including indigestion, nausea, palpitations, and numbness. 2 Risk Factors: ● Highest risk = white, middle-aged men; then african-american women Treatment: ● Decrease myocardial oxygen demand and increase oxygen supply 3 ● Meds ● Oxygen ● Reduce/control risk factors ● Reperfusion therapy 2. Discuss the pathophysiology, clinical manifestations, and treatment of angina pectoris. Patho: If the blockage is temporary, the patient will have reversible (temporary) myocardial ischemia which leads to chest pain; this occurs when O2 demand > than O2 supply. Primary reason for insufficient blood flow is narrowing of the coronary arteries by atherosclerosis. -Chronic stable angina- intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms. Pain usually lasts 3-5 minutes, subsides when precipitating factor is relieved. Pain at rest is unusual. ECG reveals ST-segment depression and/or T wave inversion. -Precipitating factors: Physical exertion, temperature extremes, emotional upset, heavy meals, smoking. ---Silent ischemia: occurs in the absence of any subjective symptoms and is associated with diabetic neuropathy. Confirmed by ECG changes. 4 ----Nocturnal angina: occurs only at night but not necessarily during sleep. ----Angina decubitus: chest pain that occurs only while lying down and is relieved by sitting or standing. ----Prinzmetal’s variant angina: occurs at rest usually in response to spasm of major coronary artery. It is seen in patients with a history of migraine headaches and Raynaud’s phenomenon. Spasm can occur in absence of CAD. can also be brought on by use of cocaine . Decreased blood flow to myocardium, pt experiences chest pain and shows marked transient ST-segment elevation. May occur during REM sleep. May be relieved by moderate exercise or may disappear spontaneously. Cyclic, short bursts of pain at a usual time each day may also occur with this type. CCB and/or nitrates used to control. ----Microvascular angina: is a new concept, may be the cause of heart disease in women. May occur in absence of significant coronary atherosclerosis or coronary spasm. Treatment: nitroglycerin at onset, then every 5 minutes up to 2 additional times if pain not relieved. Can also take nitroglycerin 15-20 minutes prior to doing an activity that produces chest pain. 3. Use the nursing process as a framework for care of patients with angina pectoris. 1. Examine the diagnostic studies pertinent to CAD/angina diagnosis. CAD: 5 C-reactive protein: is a non-specific marker of both acute infection and chronic inflammation. It is increased in many pts with CAD. Chronic exposure to CRP triggers the rupture of plaques. A level above 2.4 mg/L has been associated with a doubled risk of a coronary event compared to levels below 1 mg/L. Angina: ECG reveals ST-segment depression and/or T-wave inversion. The ECG/EKG is one of the primary tools to rule out or confirm UA or an MI. The diagnosis of angina begins with the patient’s history related to the clinical manifestations of ischemia. Laboratory studies are performed; these generally include cardiac biomarker testing to rule out ACS. The patient may undergo an exercise or pharmacologic stress test in which the heart is monitored continuously by an ECG, echocardiogram, or both. The patient may also be referred for a nuclear scan or invasive procedure (e.g., cardiac catheterization, coronary angiography). Both: An elevated CK-MB may indicate cardiac cell death. Rises in 3-9 hours after symptom onset, peaks in 12-18 hours and returns to baseline within 24 to 36 hours after MI. Troponin is found in skeletal and heart muscle. Troponin I and T are specific to heart muscle. When heart cells die, troponin is released into the blood stream. An elevated troponin can be found in the blood stream within 3-8 hours after injury, peaks in 12-16 hours and may remain elevated up to 10 to 14 days. Myoglobin begins to rise within 2 hours and peaks in 3 to 15 hours. 6 Chest X-ray can depict cardiac contours, heart size and configuration, and anatomic changes in individual chambers. Cardiac Stress Tests can also be performed either having the patient actually do physical stress on a tread mill or it can be drug induced. The heart rate is increased while monitoring the EKG for any changes or the pt to have any angina. Computed tomography angiography (CTA) with spiral technology is a noninvasive scan used to quantify calcium deposits in coronary arteries. Currently, EBCT testing is used primarily for risk assessment in asymptomatic patients and to assess for heart disease in patients with atypical symptoms potentially due to cardiac causes. Nuclear Cardiology. One of the most common nuclear imaging tests is the multigated acquisition (MUGA) or cardiac blood pool scan. This test provides information on wall motion during systole and diastole, cardiac valves, and EF. A more invasive diagnostic is a cardiac catheterization. It provides information about CAD, coronary spasm, congenital and valvular heart disease, and ventricular function. Electrophysiologic study (EPS) is the direct study and manipulation of the electrical activity of the heart using electrodes placed inside the cardiac chambers. It provides information on SA node function, AV node conduction, and ventricular conduction According to Hughes: 12-lead ECG, lipid panel 2. Outline nursing interventions & rationales for patients with angina and coronary artery disease. Medications to treat angina 7 Nursing Interventions: Directed patient to stop all activities and sit or rest in bed in a semi-Fowler’s position to reduce the oxygen requirements of the ischemic myocardium. Assess the patient’s angina. Determine whether the angina is the same as the patient typically experiences. Measure vital signs and observing for signs of respiratory distress. Obtain 12-lead ECG and assess for ST-segment and T-wave changes. If the patient has been placed on cardiac monitoring with continuous ST-segment monitoring, the ST segment is assessed for changes. Give nitroglycerin sublingually, and the patient’s response is assessed (relief of chest pain and effect on blood pressure and heart rate). If the chest pain is unchanged or is lessened but still present, nitroglycerin administration is repeated up to three doses. Each time blood pressure, heart rate, and the ST segment (if the patient is on a monitor with ST-segment monitoring capability) are assessed. The nurse administers oxygen therapy if the patient’s respiratory rate is increased or if the oxygen saturation level is 8 decreased. Oxygen is usually given at 2 L/min by nasal cannula, even without evidence of desaturation, although there is no current evidence of a positive effect on patient outcome. If the pain is significant and continues after these interventions, the patient is further evaluated for acute MI and may be transferred to a higher-acuity nursing unit. 3. Describe percutaneous coronary interventional and coronary artery revascularization procedures. PCI is a nonsurgical procedure performed to open coronary arteries through one of the following means: ● Atherectomy: Used to break up and remove plaques within cardiac vessels. ● Stent: Placement of a mesh-wire device that contains no medication to hold an artery open and prevent restenosis. ● Percutaneous transluminal coronary angioplasty: Also referred to simply as angioplasty, this involves inflating a balloon to dilate the arterial lumen and the adhering plaque, thus widening the arterial lumen. This can include stent placement. INDICATIONS ● Can be performed on an elective basis to treat coronary artery disease when there is occlusion of one to two coronary arteries. The area of occlusion is confined, not scattered, and easy to access (proximal). ● Might reduce ischemia during the occurrence of an acute myocardial infarction (MI) by opening coronary arteries and restoring perfusion. It is usually performed within 4 to 6 hr of the onset of manifestations if having a non-ST-elevation (NSTEMI) or myocardial infarction (MI), or within 60 to 90 min for a ST-elevation myocardial infarction (STEMI). ● Might be used as an alternative to coronary artery bypass graft. ● Angioplasty might be used with stent placement to prevent artery reocclusion and to dilate the coronary artery CLIENT PRESENTATION SUBJECTIVE DATA: Chest pain might occur with or without exertion. Pain might radiate to the jaw, left arm, through the back, or to the shoulder. Manifestations might increase in cold weather or with exercise. Other manifestations might include dyspnea, nausea, fatigue, and diaphoresis. OBJECTIVE DATA: ECG changes might include ST elevation, depression, or nonspecific ST changes. Other findings might include bradycardia, tachycardia, hypotension, elevated blood pressure, vomiting, and mental disorientation. Coronary artery bypass grafts ● CABG is an invasive surgical procedure that aims to restore vascularization of the myocardium. 9 ◯ Performed to bypass an obstruction in one or more of the coronary arteries, CABG does not alter the atherosclerotic process but improves the quality of life for clients restricted by painful coronary artery disease. ◯ The procedure is most effective when a client has sufficient ventricular function (ejection fraction greater than 50%). ◯ Older adult clients are more likely to experience transient neurologic changes, toxic effects from cardiac medications, and dysrhythmias. ● Less invasive revascularization procedures have been developed to reduce risk and improve client outcomes (off-pump coronary artery bypass, robotic heart surgery, minimally invasive direct coronary artery bypass). These procedures have characteristics similar to traditional CABG INDICATIONS POTENTIAL DIAGNOSES ● More than 50% blockage of left main coronary artery with anginal episodes (blockage inaccessible to angioplasty and stenting) ● Significant two-vessel disease with unstable angina ● Triple-vessel disease with or without angina ● Persistent ischemia or likely MI following coronary angiography, PCI, or stent placement ● Heart failure or cardiogenic shock with acute MI or ischemia (might not be reasonable for clients who have poor ejection fractions) ● Coronary arteries that are unable to be accessed or treated by angioplasty and stent placement (narrow or calcified) ● Coronary artery disease nonresponsive to medical management ● Heart valve disease CLIENT PRESENTATION SUBJECTIVE DATA: Chest pain can occur with or without exertion. Pain can radiate to jaw, left arm, through the back, or to the shoulder. Effects can increase in cold weather or with exercise. Other findings can include dyspnea, nausea, fatigue, and diaphoresis. OBJECTIVE DATA: ECG changes can include ST elevation, depression, or nonspecific ST changes. Other findings can include bradycardia, tachycardia, hypotension, elevated blood pressure, vomiting, and mental disorientation. 4. Identify the nursing care of a patient who has had a percutaneous coronary interventional procedure for treatment of coronary artery disease. •Post-op vital signs are: • q 15 mins X 4, q 30 mins X 2, q 1 hour X 2 •check circulation, peripheral pulses, color, sensation of extremities. • puncture site for hematoma and bleeding •Assess breathing (conscious sedation) 10 ACUTE CORONARY SYNDROME (MYOCARDIAL INFARCTION) 1. Describe the pathophysiology, clinical manifestations, and treatment of myocardial infarction. Myocardial Infarction is the result of sustained ischemia: (>20 minutes), causing irreversible myocardial cell death (necrosis). When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops. Ischemia= myocardial O2 demand is not met. Ischemia = absolute or relative shortage of the blood supply to an organ. Necrosis of entire thickness of myocardium takes 4 to 6 hours. The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the cardiac muscle). 80 to 90% of all acute MIs are secondary to thrombus formation. Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration.Can have pain that is described as heaviness, constriction, tightness, burning, pressure, or crushing; Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms; It may occur while the patient is active or at rest, or asleep or awake. Commonly occurs in the early morning hours, lasts for 20 minutes or longer and is more severe than usual anginal pain. Some patients may not experience pain but may have “discomfort,” weakness, or shortness of breath. Women may experience atypical discomfort, shortness of breath, or fatigue. Skin: Ashen, clammy, and/or cool to touch.Initial ↑ HR and BP, then ↓ BP (secondary to ↓ in CO). Crackles leading to jugular venous distention. Abnormal heart sounds: S3 or S4 or a new murmur. The patient may have nausea/vomiting, fever.. Initial interventions include the following: Establish an IV, MONA (Morphine, Oxygen, Nitro, Aspirin ) start first with oxygen, and administer sublingual NTG, aspirin, and we give morphine sulfate only if the patient continues to have chest pain after the NTG. We monitor vital signs and pulse oximetry. Emergent PCI is the first line of treatment for patients with confirmed MI. The goal is to open the affected artery within 90 minutes of arrival to a facility with an interventional cardiac catheterization lab which is the treatment of choice for confirmed MI where they can do Balloon angioplasty + Drug-eluting stent(s). Fibrinolytic therapy offers the advantages of availability and rapid administration in facilities that do not have an interventional cardiac catheterization lab and that are too far away for safe transfer of the patient. 2. Use the nursing process as a framework for care of a patient with acute coronary syndrome. a. Analyze the primary goals of nursing care for the patient with an acute myocardial infarction. 11 12 13 14 b. Describe medical therapy and nursing care for the patient with acute myocardial infarction. 15 Acute Coronary Syndrome/Myocardial Infarction Objectives ● Compare modifiable vs. non-modifiable cardiac risk factors and risk factor modification. ● Modifiable: ○ Hyperlipidemia (cholesterol >200, fasting triglycerides >150, ○ HTN, which is defined as a BP > 140/90 mm Hg or >130/80 mm Hg if the patient has diabetes or chronic kidney disease. ○ Cigarette smoking, tobacco use ○ Physical inactivity ○ Obesity ○ Diabetes ○ Metabolic syndrome ● Non-modifiable: age, gender, ethnicity, race, family history, genetic predisposition ● Discuss the use of, contraindications, and adverse reactions to medications prescribed to patients post MI 16 17 18 ● Describe common complications which may occur following Acute Coronary Syndrome/Myocardial Infarction. Once pain is relieved, you may have to deal with denial in a patient who interprets the absence of pain as an absence of cardiac disease. You must be competent in ECG interpretation so that dysrhythmias causing further deterioration of cardiovascular status are identified and treated. Included are an assessment of heart and lung sounds and inspection for evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). •Dysrhythmias (most common) •Post Cath Bleeding •Patient given thrombin inhibitors •ASA •Oral antiplatelet drugs •Cardiogenic Shock (more details later) •Change in vital signs (↑ HR, ↓ B/P) •Crackles in lung -> left heart failure •Abnormal heart sounds •S3 or S4 •New murmur -> papillary muscle rupture (rare and fatal) •Pericarditis = inflammation of the sac surrounding the heart (pericardium) –Occurs 2-3 days after MI –Excessive fluid can collect within the pericardium – this MAY reduce the stretch during diastole -> ↓ filling -> ↓ cardiac output -> ↓B/P –Characterized by chest pain that is aggravated; •on inspiration, by movement or coughing •pain is relieved by sitting in forward position. •may have a friction rub (grating sound. “like walking on fresh snow”) •treat with NSAIDS/ASA •Dressler Syndrome = a type of pericarditis –Inflammation associated with Dressler's syndrome is believed to be an immune 19 system response following damage to heart tissue or the pericardium, such as a heart attack, surgery or traumatic injury. –similar S&S to above ● Describe medical therapy and nursing care for the patient with acute myocardial infarction. Nursing MGMT: O2 and meds, VS, bed rest with HOB elevation, monitor I&O/tissue perfusion, Monitor complications, report changes, evaluate interventions. Possible indicated invasive procedures: PTCA, Coronary artery stent, CABG, cardiac surgery Initial interventions include the following: Establish an IV, MONA (Morphine, Oxygen, Nitro, Aspirin ) start first with oxygen, and administer sublingual NTG, aspirin, and we give morphine sulfate only if the patient continues to have chest pain after the NTG. Fibrinolytic therapy offers the advantages of availability and rapid administration in facilities that do not have an interventional cardiac catheterization lab and that are too far away for safe transfer of the patient. Inclusion criteria for fibrinolytic therapy include (1) chest pain > 20 minutes that is typical of acute MI that is ≤6 hours in duration, (2) 12-lead ECG findings (ST segment elevated in at least 2 leads that face the same area of the heart) consistent with acute MI, and (3) no absolute contraindications. Depending on the drug selected, therapy is administered in one IV bolus or over a period of time (30 to 90 minutes). Evaluate heart rhythm, vital signs, and pulse oximetry and assess the heart and lungs frequently to evaluate the patient’s response to therapy. A major concern with fibrinolytic therapy is reocclusion of the artery. The site of the thrombus is unstable, and another clot may form or spasm of the artery may occur. Minor bleeding (e.g., surface bleeding from IV sites, gingival bleeding) is expected and is controlled by applying a pressure dressing or ice packs. Also monitor the patient for signs of changes in LOC – indication of bleeding into the brain. If it works you will see a return of ST the segment to baseline, Relief of chest pain, Reperfusion dysrhythmias (less reliable). Morphine sulfate is the drug of choice for chest pain that is unrelieved by NTG. β-Adrenergic blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility. ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI with an EF ≤ 40%. Dysrhythmias are the most common complication so many patients are on antidysrhythmic medications. All patients with elevated triglycerides and LDL cholesterol should receive cholesterol-lowering drugs. Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate and 20 promote the comfort of bowel evacuation. This prevents straining and resultant vagal stimulation from the Valsalva maneuver. Identify the risk factors associated with a myocardial infarction. Review the difference between MI and Angina. If artery blockage is temporary, the patient will have reversible (temporary) myocardial ischemia which leads to Angina (chest pain); this occurs when O2 demand > O2 supply. 21 Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis. Myocardial infarction is sustained ischemia: (>20 minutes), causing irreversible myocardial cell death (necrosis). Understand the purpose of the various lab/diagnostic tests used when an MI is suspected. •Blood pressure •Blood glucose •Lipid panel. The lipid panel includes a measurement of serum triglycerides, LDL, and HDL. HDL = healthy/good cholesterol. Should, on average, be > 50. LDL = lousy/bad cholesterol. Should be < 100. Total cholesterol should be <200. Triglycerides <150 •A height and weight. Height and weight values, used to calculate a Body Mass Index or BMI, generate a standardized number. A BMI of 30 or more indicates obesity. •Assess her peripheral pulses -> screen for peripheral vascular disease. Echo -> probe w/ultrasound placed on chest (non-invasive) and sound waves used to assesses the movement of the heart structures and can calculate the ejection fraction. The ejection fraction provides valuable information of left ventricular function. Transesophageal Echocardiogram (TEE) -> probe w/ultrasound transducer is swallowed; may involve contrast medium. Pt must be NPO at least 6 hours prior, remove dentures. IV sedation and local anesthetic, maybe bite block. Will need to be driven home. Review the nursing management pre and post coronary revascularization procedures and surgeries. Nursing care requires understanding of hemodynamics and diligent observations. Some facilities don’t allow new grads to care for this type of patient. ICU for first 24 to 36 hours 22 post-op; Endotracheal tube connected to mechanical ventilation; Extubation within 12 hours; Epicardial pacing wires for emergency pacing of the heart; Pulmonary artery catheter; Urinary catheter to monitor urine output; NG tube for gastric decompression. 23 Review supportive devices used to manage complications of an MI such as Intra-aortic balloon pump (IABP) and left ventricular assist devices (LVADs) along with the 24 complications associated with their use. Ventricular Assist Device -> A ventricular assist device (VAD) is a mechanical pump that's used to support heart function and blood flow in people who have weakened hearts. The device takes blood from the ventricle of the heart and helps pump it to the body and vital organs, just as a healthy heart would VADs can be used as -”bridge to recovery” for patients who require temporary assistance for reversible ventricular failure -”bridge to transplant” for patients with end stage heart failure until a donor organ becomes available for transplant (most common) -”destination therapy” for patients with end stage heart failure who are not candidates for or decline heart transplantation and have the VAD implanted for permanent use. Complications: bleeding disorders, hemorrhage, thromboemboli, hemolysis, infection, kidney injury, right-sided heart failure, multisystem failure, and mechanical. Intraaortic balloon pump: IABP. increases coronary blood flow to the heart muscle and decreases the heart’s workload through a process called counterpulsation. Placed in the aorta- useful in hemodynamically unstable patients because they decrease SVR, PAWP, PAP, leading to improved CO. Review indications for cardiac surgery and complications that may arise post operatively and the associated hemodynamic changes. Indications: -Fail medical management -Have left main coronary artery or 3-vessel disease -Are not candidates for PCI (eg lesions are long or difficult to access) -Have failed PCI and continue to have chest pain -Have DM -When long term benefits of CABG are superior to those of PCI 25 26 Hemodynamic Monitoring 27 1. Identify normal hemodynamic pressure parameters and two primary reasons for using each a. CVP: Normal: 2-8 mmHg Measures preload in the right side of the heart High CVP: right-sided heart failure, volume overload Low CVP: dehydration In addition to obtaining pressure readings, the CVP catheter is used for infusing IV fluids, administering IV medications, and drawing blood specimens. 28 b. Arterial line PAD Normal: 4-12 mmHg Measures volume on the left side of the heart. c. PA Catheter PAWP Normal: 6-12 mmHg Measures volume/preload on left side of heart; Each chamber has an associated wave form. High = left-sided heart failure (too much volume). 29 The proximal lumen can be used to measure right atrial pressure (CVP), infuse IV fluids, and obtain venous blood samples. The distal lumen can be used to measure PAPs (PA systolic, PA diastolic, mean PA pressure, and PA wedge pressure). This lumen is not used for IV fluid administration. 30 2. Examine the nursing assessment, complications, and interventions which are appropriate for the patient with each of these. See above. Hemodynamics Objectives ● Identify normal hemodynamic pressure parameters. 31 ● Differentiate how to adjust each parameter using medications or fluids. -To Increase Preload: Volume expanders such as Crystalloids: Normal Saline, Lactated 32 Ringers; Colloids: Hetastarch, Albumin; or Blood Products: PRBCs, Whole blood. How do I know if they worked? My preload numbers come up -To Decrease Preload: diuretics such as furosemide, bumetanide, torsemide; or venous dilators: morphine, nitroglycerin, nitroprusside. How do I know if they worked? My preload numbers come down -To Increase Afterload: Vasopressors: dopamine (higher doses), epinephrine, Norepinephrine (Levophed), Phenylaphrine Hydrochlorie (Neo-Synephrine), Vasopressin. How do I know they worked? The SVR comes up along with the BP. -To Decrease Afterload: Vasodilators: nitroprusside, nitroglycerin (higher doses), PDE inhibitors (Milrinone), calcium channel blockers (Nicardipine, Nifedipine), ACE inhibitors, hydralazine, Nesiritide (Natrecor). How do I know they worked? The SVR comes down along with the BP and the skin becomes pinker and warmer -To Increase contractility: positive inotropic agents; epinephrine, norepinephrine (levophed), isoproterenol (isuprel), dopamine, dobutamine (dobutrex), digitalis like drugs, calcium and PDE inhibitors (milrinone). How do I know they worked? CO increases, UO increases, cap refill improves, skin becomes warmer and pinker -To decrease contractility: negative inotropic agents: beta adrenergic blockers, calcium channel blockers. ● List two primary reasons for using CVP monitoring See above. ● List the indications for insertion of a PA catheter and the nursing assessment and interventions which are appropriate for the patient with a PA catheter ● Describe the complications which may occur due to a PA catheter: insertion, maintenance, and removal. See above. ● List the indications and preparation for insertion of an arterial line. Intra-arterial BP monitoring is used to obtain direct and continuous BP measurements in critically ill patients who have severe hypertension or hypotension. Arterial catheters are also useful when arterial blood gas measurements and blood samples need to be obtained frequently. 33 Site preparation and care are the same as for CVP catheters. The catheter flush solution is the same as for pulmonary artery catheters. A transducer is attached, and pressures are measured in millimeters of mercury (mm Hg). The nurse monitors the patient for complications, which include local obstruction with distal ischemia, external hemorrhage, massive ecchymosis, dissection, air embolism, blood loss, pain, arteriospasm, and infection. ● Discuss nursing assessment and interventions appropriate for the patient with an arterial line. The radial artery is the usual site selected. However, placement of a catheter into the radial artery can further impede perfusion to an area that has poor circulation. As a result, the tissue distal to the cannulated artery can become ischemic or necrotic. Patients with diabetes, peripheral vascular disease, or hypotension, receiving IV vasopressors, or having had previous surgery are at highest risk for this complication. Traditionally, collateral circulation to the involved extremity was assessed by using the Allen test. To perform the Allen test, the hand is elevated and the patient is asked to make a fist for 30 seconds. The nurse compresses the radial and ulnar arteries simultaneously, causing the hand to blanch. After the patient opens the fist, the nurse releases the pressure on the ulnar artery. If blood flow is restored (hand turns pink) within 6 seconds, the circulation to the hand may be adequate enough to tolerate placement of a radial artery catheter. Evidence suggests that pulse oximetry and plethysmography are additional reliable methods for assessing circulation to the hand Review the function of the pulmonary artery and what complications may occur during insertion or while in use. Complications from the use of hemodynamic monitoring systems are uncommon and can include pneumothorax, infection, and air embolism. The nurse observes for signs of pneumothorax during the insertion of catheters using a central venous approach (CVP and pulmonary artery catheters). The longer any of these catheters are left in place (after 72 to 96 hours), the greater the risk of infection. Air emboli can be introduced into the vascular system if the stopcocks attached to the pressure transducers are mishandled during blood drawing, administration of medications, or other procedures that require opening the system to air. Therefore, nurses handling this equipment must demonstrate competence prior to caring independently for a patient requiring hemodynamic monitoring. Monitor for dysrhythmias while inserting. 34 Pulmonary artery pressure monitoring is used in critical care for assessing left ventricular function, diagnosing the etiology of shock, and evaluating the patient’s response to medical interventions (e.g., fluid administration, vasoactive medications). Review the effects of shock on hemodynamic parameters. CVP decreases in hypovolemic, increases in cardiogenic Neurogenic shock: drop in CO and HR, life threatening decrease in BP Hemodynamic shock: inability to compensate can lead to sustained decreased CO and BP. Further explanation below Review PA occlusion or wedge pressure (PAOP/PAWP) waveform vs PA waveform and how PAOP/PAWP is measured. Afterload in the right side of the heart is measured by: Pulmonary Artery Pressure (PAP) Pulse pressure analysis uses an arterial pressure waveform to continuously estimate the patient’s stroke volume. During insertion of the pulmonary artery catheter, the bedside monitor is observed for pressure and waveform changes, as well as dysrhythmias, as the catheter progresses through the right heart to the pulmonary artery. pulmonary artery wedge pressure is achieved by inflating the balloon tip, which causes it to float more distally into a smaller portion of the pulmonary artery until it is wedged into position. This is an occlusive maneuver that impedes blood flow through that segment of the pulmonary artery. Therefore, the wedge pressure is measured immediately and the balloon deflated promptly to restore blood flow What are the complications that may occur during PAOP/PAWP measuring? However, obtaining a pulmonary artery wedge pressure may cause the leads to move out of pacing position. The endocardial and epicardial wires are connected to a temporary generator, which is about the size of a small paperback book. Review the categories of shock types and then the individual shock states within the category. Cardiogenic shock Cardiac pump failure occurs due to a direct cardiac cause, such as MI (especially anterior wall infarction), heart failure, cardiomyopathy, dysrhythmias, and valvular rupture or stenosis. Older adult clients are at increased risk for MI and cardiomyopathy. Hypovolemic Shock Excessive fluid loss from diuresis, vomiting, or diarrhea; or blood loss secondary to surgery, trauma, gynecologic/obstetric causes, burns, and diabetic ketoacidosis. Older 35 adult clients are more prone to dehydration due to decreased fluid and protein intake and the use of medications, such as diuretics. Minimal amounts of fluid loss (vomiting, diarrhea) can cause the older adult client to become dehydrated. Obstructive shock Cardiac pump failure occurs due to an indirect cardiac factor (blockage of great vessels, pulmonary artery stenosis, pulmonary embolism, cardiac tamponade, tension pneumothorax, aortic dissection). Distributive shock Divided into three types: ○ Neurogenic: Loss of sympathetic tone causing massive vasodilation. Head trauma, spinal cord injury, and epidural anesthesia are among the causes. ○ Septic: Endotoxins and other mediators causing massive vasodilation. Most common cause is gram-negative bacteria. ■ Urosepsis is more frequent in older adult clients due to increased use of catheters in long-term care facilities and late detection of urinary tract infection (decreased sensation of burning, urgency). ○ Anaphylactic: Allergen exposure results in an antigen-antibody reaction causing massive vasodilation. Common causes include antibiotics, foods (such as peanuts), latex, and bee stings. Review the pathophysiology of each type of shock. Review the stages of shock. Initial: No visible changes in client parameters; only changes on the cellular level Compensatory (non-progressive): Measures to increase cardiac output to restore tissue perfusion and oxygenation Progressive: Compensatory mechanisms beginning to fail Refractory: Irreversible shock and total body failure Review the medical and nursing management of shocks. 36 37 38 Review the use of fluids vs vasopressors in the various shock states. Vasopressors and inotropes are medications used to create vasoconstriction or increase cardiac contractility, respectively, in patients with shock. The hallmark of shock is decreased perfusion to vital organs, resulting in multiorgan dysfunction and eventually death. Vasopressors increase vasoconstriction, which leads to increased systemic vascular resistance (SVR). Increasing the SVR leads to increased mean arterial pressure (MAP) and increased perfusion to organs. Inotropes increase cardiac contractility which improves cardiac output (CO), aiding in maintaining MAP and perfusion to the body. 39 What are the hemodynamic changes associated with each type of shock? 40 Nursing interventions to prevent CLABSI 41 42 Diagnostic tests used to diagnose sepsis – lactic acid and procalcitonin The lactate level is elevated because of the maldistribution of blood. Inflammatory markers such as WBC counts, plasma C-reactive protein (CRP), and procalcitonin levels are also elevated Review the body system involvement in MODS. How many body systems must be affected? Two or more. 43 How to determine if the body system is affected? While it is not possible to predict MODS, clinical severity assessment tools may be used to anticipate patient risk of organ dysfunction and mortality. These clinical assessment tools include APACHE (Acute Physiology and Chronic Health Evaluation); SAPS (Simplified Acute Physiology Score); PIRO (Predisposing factors, the Infection, the host Response, and Organ dysfunction); and SOFA score. Review the pathophysiology associated with MODS. MODS may be a complication of any form of shock, but it is most commonly seen in patients with sepsis and is a result of inadequate tissue perfusion. The precise mechanism by which MODS occurs remains unknown. However, MODS frequently occurs toward the end of the continuum of septic shock when tissue perfusion cannot be effectively restored. It is not possible to predict which patients who experience shock will develop MODS, partly because much of the organ damage occurs at the cellular level and, therefore, cannot be directly observed or measured. The clinical presentation of MODS is insidious; tissues become hypoperfused at both a microcellular and macrocellular level, eventually causing organ dysfunction that requires mechanical and pharmacologic intervention to support organ function. Organ failure 44 usually begins in the lungs, and cardiovascular instability, as well as failure of the hepatic, GI, renal, immunologic, and central nervous systems, follows. Review the medical management for a patient with MODS. If preventive measures fail, treatment measures to reverse MODS are aimed at (1) controlling the initiating event, (2) promoting adequate organ perfusion, (3) providing nutritional support, and (4) maximizing patient comfort. (This is literally all it says in the book). Review the S&S of DIC. Bruises (ecchymoses) and bleeding (petechiae) may appear in the skin. Coagulation times (e.g., prothrombin time, activated partial thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require replacement therapy to achieve hemostasis 45 Review pathophysiology and medical management of DIC. Compare the use of heparin vs platelets in the treatment of patients with DIC. Platelets are transfused to correct severely low platelet levels, control bleeding (with factor replacement), or prior to an invasive procedure 46 A controversial treatment strategy is to interrupt the thrombosis process through the use of heparin infusion. Heparin may inhibit the formation of microthrombi and thus permit perfusion of the organs (skin, kidneys, or brain) to resume. Heparin use was traditionally reserved for patients in whom thrombotic manifestations predominated or in whom extensive blood component replacement failed to halt the hemorrhage or increased fibrinogen and other clotting levels. In the absence of bleeding, prophylactic doses of unfractionated heparin or low–molecular-weight heparin (LMWH) may be used to prevent venous thromboembolism (VTE), whereas therapeutic doses of unfractionated heparin may be used when severe thrombosis predominates Review the various blood products and indications for use and goals of therapy. ● Platelets: control or prevent bleeding w/thrombocytopenia ● Packed RBC’s: Increase O2 carrying capacity in anemic patients + acute blood loss ● Whole blood: massive blood loss ● Fresh frozen plasma: Increase clotting factors in pts w/demonstrated coagulation deficiency: ○ DIC / hemorrhage / massive transfusion / liver dz / vitK deficiency / excess warfarin ● Leucocytes: WBC transfusion Review the process utilized when preparing to and administering a blood transfusion. 47 Review the cultural and religious considerations when giving blood products. A patient’s religious and cultural beliefs may significantly impact their decision whether to consent to a procedure such as a blood transfusion. Differences in moral perspectives can complicate the provision of quality nursing care. The patient who has mental capacity, is fully informed of the benefits and risks of a procedure, and is at least 18 years of age has the right to sign or refuse to sign an informed consent. In this 48 particular case scenario, although his mother and the surgeon know his decision to refuse blood products will likely end in his death, only the patient has the autonomy to make this decision, regardless of his young age. The nurse should support the autonomous decision that the patient makes, even when his decision to refuse blood transfusions may cause the nurse to experience moral distress. Review the complications of blood transfusions and various types of transfusion reactions. 49 50 STRUCTURAL CARDIAC DISORDERS 1. Define valvular disorders of the heart and describe the pathophysiology, clinical manifestations, as well as the medical and nursing management of patients with mitral and aortic disorders. Stenosis: (constriction or narrowing) is seen in the pressure differences (ie the higher the difference, the greater the stenosis) Regurgitation: (also called incompetence or insufficiency) incomplete closure of the 51 valve results in the backward flow of blood. Mitral Stenosis: obstruction to blood flowing from the left atrium into the left ventricle. Most frequently as a result of rheumatic heart disease; causes scarring of valve leaflets and chordae tendineae; contractures develop with adhesions between commissures of the leaflets. Stenotic mitral valve assumes ‘fish mouth’ shape caused by thickening and shortening of valve strictures. This results in obstruction: ^ left atrial pressure and volume and hypertrophy of pulmonary vessels leading to HR increases, CO decreases and pulmonary pressure increase. -Manifestations: exertional dyspnea due to reduced lung compliance; palpitations from afib; fatigue; accentuated first heart sound; low pitched, rumbling diastolic murmur; the patient may present with hoarseness (from atrial enlargement pressing on laryngeal nerve); hemoptysis (from pulmonary HTN); chest pain (from decreased CO and coronary perfusion) or may have seizures or present with a stroke (from emboli) Acute mitral insufficiency can result from endocarditis, chest trauma or MI. CO decreases dramatically, cascading into pulmonary edema and shock. Treatment for acute is emergent mitral valve replacement. Mitral Insufficiency: blood flowing back from the left ventricle into the left atrium during systole. Often edges of mitral valve do not close completely during systole because leaflets and chordae tendineae have thickened and fibrosed, resulting in their contraction. Most common causes are degenerative changes of mitral valve (ie mitral valve prolapse) and ischemia of the LV. Chronic mitral insufficiency may result from rheumatic heart disease, degenerative changes associated with aging, or left ventricular dilation. Volume overload can be reflected backward to the pulmonary circulation, but pulmonary and right sided symptoms usually do not develop until late in dx process. -Manifestations: fatigue, palpitations, and sometimes SOB. Aortic stenosis: obstruction of blood flow from the left ventricle into aorta during systole. May develop as result of rheumatic fever, calcification of a congenital bicuspid valve, or calcific degeneration. Left ventricular hypertrophy and dilation results and increased LV pressures are reflected backward through the LA and pulmonary vasculature. Increases myocardial o2 consumption because of the increased myocardial mass. Diminished CO may lead to angina and syncope. -Manifestations: exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Reduced CO leads to decreased tissue perfusion, pulmonary HTN, and HF. symptoms develop when valve orifice becomes about ⅓ of normal size. Auscultation typically reveals a normal or soft S1, diminished or absent S2, a systolic murmur and a prominent S4. Aortic Insufficiency: Chronic aortic insufficiency due to rheumatic fever, reactive arthritis and aneurysm of ascending aorta. LV hypertrophy ensues. Eventually increased LV pressure is reflected back into LA and pulmonary circulation. Acute aortic insufficiency due to blunt chest trauma, ruptured aortic aneurysm or infective 52 endocarditis is life-threatening emergency. Physiologic consequences include retrograde blood flow from ascending aorta back into LV which results in volume overload. Initially LV compensates by dilation and hypertrophy but contractility eventually declines leading to pulmonary HTN and LV failure. -Manifestations: chronic- fatigue, low DBP, widened pulse pressure and angina, exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Acute- sx of sudden CV collapse; LV exposed to aortic pressure during diastole resulting in sudden weakness; severe dyspnea; angina and hypotension. In severe aortic regurgitation can feel ‘water-hammer’ pulse (a strong quick beat that collapses immediately). May hear soft or absent S1; presence of S3 or S4; and a soft high pitched diastolic murmur. Nursing: •Collect a detailed health history -> due to the many causes of valvular heart disease. •Patient education; vegetations (substances such as calcium and cholesterol) that weaken the valve leaflets can “flake” off and can lead to; •emboli formation causing a stroke. •Infection causing endocarditis -> microbes “floating in the blood” •Assess for abnormal cardiac rhythms – A. Fib. Valve disorders lead to an increased work load to the heart muscle -> assess for the development of heart failure Medical: •Continuous cardiac monitoring, 12-lead ECG and chest x-ray on arrival to the ED. •Cardiac catheterization (discussed in the ACS & MI presentation) à to assess coronary artery patency and obtain measurements of intracardiac pressures •Echocardiogram •An echocardiogram will assess valve structure/function, measure the size of each cardiac chamber and measure the ejection fraction 2. Describe types of cardiac valve repair and replacement procedures used to treat valvular problems and care needed by patients who undergo these procedures. Repair, rather than replacement, of a cardiac valve is referred to as valvuloplasty. We see the non-surgical interventions used more on our elderly population who may not do well on bypass. The type of valvuloplasty depends on the cause and type of valve dysfunction. Repair may be made to commissures between the leaflets in a procedure known as commissurotomy, to the annulus of the valve by annuloplasty, to leaflets, or to chordae by chordoplasty. Valvular reconstructions has several advantages: Eliminates need for long-term anticoagulation, Decreases risk of thromboembolism and endocarditis, Decreases need for reoperation, Increases survival rates. Common procedures: Commissurotomy (moderate mitral stenosis), Annuloplasty or prosthetic ring. For high-risk patients and those who are not suitable for open-heart surgery, another option is now available - transcatheter aortic valve replacement (TAVR) - a less 53 invasive procedure that does not require open-heart surgery; it is indicated for relief of aortic stenosis in patients with symptomatic heart disease due to severe native calcific aortic stenosis. An alternative treatment for some patients with valvular heart disease is the percutaneous transluminal balloon valvuloplasty (PTBV) procedure. During PTBV, the fused commissures are split open. Balloon valvuloplasty is used for mitral, tricuspid, and pulmonic stenosis, and less often for aortic stenosis. The PTBV procedure is generally indicated for older adults and for those who are poor surgery candidates Patients who have undergone percutaneous balloon valvuloplasty with or without percutaneous valve replacement will need to be assessed for signs and symptoms of heart failure and emboli: listening for changes in heart sounds at least every 4 hours, and providing the patient with the same care as for postprocedure cardiac catheterization or percutaneous transluminal coronary angioplasty. After undergoing percutaneous balloon valvuloplasty, the patient usually remains in the hospital for 24 to 48 hours. Patients who have undergone surgical valvuloplasty or valve replacements are admitted to the ICU. Vital signs are assessed every 5 to 15 minutes until stable and then every 2 to 4 hours. IV medications may be needed to increase or decrease blood pressure and treat dysrhythmias or altered heart rates. Patient assessments are conducted hourly initially and then every 2- 4 focusing on neurologic, respiratory, and cardiovascular systems. Patient education is very important so they understand about anticoagulant therapy, explaining the need for frequent follow-up appointments and blood laboratory studies. 54 Patients who take warfarin (Coumadin) have individualized target international normalized ratios, usually between 2 and 3.5 for mitral valve replacement and 1.8 and 2.2 for aortic valve replacement. Patients who have been treated with an annuloplasty ring or a tissue valve replacement usually require anticoagulation for only 3 months unless there are other risk factors such as atrial fibrillation or a history of thromboembolism. Aspirin is prescribed with warfarin for patients with bioprostheses or at high risk for embolic events (e.g., history of embolic event or having two or more preexisting conditions: diabetes, hypertension, coronary artery disease, congestive heart failure, older than 75 years). Patients with a mechanical valve prosthesis (including annuloplasty rings and other prosthetic materials used in valvuloplasty) require education to prevent infective endocarditis. Patients may be at risk for infective endocarditis that results from bacteria entering the bloodstream and adhering to abnormal valve structures or prosthetic devices.. Antibiotic prophylaxis is necessary before dental procedures involving manipulation of gingival tissue, the periapical area of the teeth, or perforation of the oral mucosa (not including routine anesthetic injections, placement of orthodontic brackets, or loss of deciduous teeth). Antibiotic therapy should also be used before invasive procedures especially those involving the respiratory tract (e.g., biopsy of respiratory mucosa, tonsillectomy, and adenectomy). 55 3. Identify the pathophysiology, clinical manifestations, as well as the medical and nursing management of patients with cardiomyopathies. Cardiomyopathy is disease of the heart muscle that is associated with cardiac dysfunction. It is classified according to the structural and functional abnormalities of the 56 heart muscle: dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), restrictive or constrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), and unclassified cardiomyopathy. The pathophysiology of all cardiomyopathies is a series of events that culminate in impaired cardiac output. Decreased stroke volume stimulates the sympathetic nervous system and the renin–angiotensin–aldosterone response, resulting in increased systemic vascular resistance and increased sodium and fluid retention, which place an increased workload on the heart. These alterations can lead to heart failure Patients with cardiomyopathy may remain stable and without symptoms for many years. As the disease progresses, so do the symptoms. Frequently, dilated or restrictive cardiomyopathy is first diagnosed when the patient presents with signs and symptoms of heart failure (e.g., DOE, fatigue). Patients with cardiomyopathy may also report PND, cough (especially with exertion), and orthopnea, which may lead to a misdiagnosis of bronchitis or pneumonia. Other symptoms include fluid retention, peripheral edema, and nausea, which are caused by poor perfusion of the gastrointestinal system. The patient also may experience chest pain, palpitations, dizziness, nausea, and syncope with exertion. However, with HCM, cardiac arrest (i.e., sudden cardiac death) may be the initial manifestation in young people, including athletes Medical management is directed toward identifying and managing possible underlying or precipitating causes; correcting the heart failure with medications, a low-sodium diet, and an exercise/rest regimen; and controlling dysrhythmias with antiarrhythmic medications and possibly with an implanted electronic device, such as an ICD. Systemic anticoagulation to prevent thromboembolic events is usually recommended. If the patient has signs and symptoms of congestion, fluid intake may be limited to 2 L each day. Patients with HCM should avoid dehydration and may need beta-blockers (atenolol [Tenormin], metoprolol [Lopressor], sotalol [Betapace], propranolol [Inderal]) to maintain cardiac output and minimize the risk of left ventricular outflow tract (LVOT) obstruction during systole. Nursing Interventions: ● IMPROVING CARDIAC OUTPUT AND PERIPHERAL BLOOD FLOW: rest is indicated; sitting up with their legs down is helpful in pooling venous blood in the periphery and reducing preload. Determining a need for supplemental oxygen. Ensuring that medications are taken as prescribed. Ensure that the patient receives or chooses food selections that are appropriate for a low-sodium diet ● INCREASING ACTIVITY TOLERANCE AND IMPROVING GAS EXCHANGE: Plans the patient’s activities so that they occur in cycles, alternating rest with activity periods. 57 ● REDUCING ANXIETY: Spiritual, psychological, and emotional support. Interventions are directed toward eradicating or alleviating perceived stressors. ● DECREASING THE SENSE OF POWERLESSNESS: Patients often go through a grieving process when cardiomyopathy is diagnosed. The patient is assisted in identifying the things in life that he or she has lost and their emotional responses to the loss . The nurse assists the patient in identifying the amount of control that he or she still has over life, such as making food choices, managing medications, and working with the patient’s primary provider to achieve the best possible outcomes. ● PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE 4. Analyze the management of the patient with a heart transplant. NURSING ACTIONS -Prepare the client for the procedure (NPO status and informed consent). -Monitor postoperatively: vital signs, SaO2, incision drainage, and pain management. -Monitor for complications. Organ transplant recipients are at risk for infection, thrombosis, and rejection. CLIENT EDUCATION -Take diuretics in the early morning and early afternoon. -Restrict fluid and sodium as instructed. Regulate potassium intake as instructed to prevent high or low potassium levels. A dietitian can help with menu planning. -Check weight daily at the same time, and notify the provider for a weight gain of 2 lb in 24 hr or 5 lb in 1 week. -Schedule regular follow-up visits with the provider. -Obtain the pneumococcal and yearly influenza vaccines. Patients who have had heart transplantations are constantly balancing the risk of rejection with the risk of infection and diseases such as cancer. They must adhere to a complex regimen of diet, medications, activity, follow-up laboratory studies, biopsies of the transplanted heart (to diagnose rejection), and clinic visits. There are three classes of medications that are prescribed for a transplant patient to help minimize rejection: corticosteroids, calcineurin inhibitors, and antiproliferative agents. Because the heart is denerved, the patient will not experience chest pain and medications working on the sympathetic and parasympathetic nerves will not be effective on these patients. Though the transplanted heart usually has a faster rate, bradycardia could occur – atropine will not be effective so this patient would need a pacemaker. 58 5. Use the nursing process as a framework of care for the patient with a cardiomyopathy and the patient with pericarditis. The inflammatory process of pericarditis may lead to an accumulation of fluid in the pericardial sac (pericardial effusion) and increased pressure on the heart, leading to cardiac tamponade. ● Causes of Pericarditis ○ Idiopathic or nonspecific causes ○ Infection: usually viral (e.g., human immune deficiency virus, coxsackievirus, influenza); rarely bacterial (e.g., staphylococci, streptococci, meningococci, gonococci, gram-negative rods, Borrelia [Lyme disease], tuberculosis); mycotic (fungal); and parasitic ○ Disorders of connective tissue: systemic lupus erythematosus, rheumatic fever, rheumatoid arthritis, polyarteritis, and scleroderma ○ Sarcoidosis ○ Hypersensitivity states: immune reactions, medication reactions, and serum sickness ○ Disorders of adjacent structures: myocardial infarction, dissecting aneurysm, pleural and pulmonary disease (pneumonia) ○ Neoplastic disease: caused by metastasis from lung or breast cancer, leukemia, and primary (mesothelioma) neoplasms ○ Radiation therapy of chest and upper torso (peak occurrence 5–9 months after treatment) ○ Trauma: chest injury, cardiac surgery, cardiac catheterization, implantation of pacemaker, or implantable cardioverter defibrillator ○ Kidney injury and uremia ● Manifestations ○ Chest pain, may be located beneath the clavicle, in the neck, or in the left trapezius (scapula) region. Remains fairly constant, but it may worsen with deep inspiration or movement ○ Creaky or scratchy friction rub heard most clearly at the left lower sternal border. ○ Mild fever, increased WBC count, anemia, elevated ESR or C-reactive protein level. ○ Nonproductive cough or hiccup. ○ Dyspnea, as well as respiratory splinting due to pain upon inspiration ○ signs and symptoms of heart failure may occur ○ The heart rate may increase to maintain cardiac output. ● Assessment and Diagnostic Findings 59 ○ The diagnosis most often is made on the basis of history, signs, and symptoms. ○ An echocardiogram may detect inflammation, pericardial effusion or tamponade, and heart failure. It may help confirm the diagnosis and may be used to guide pericardiocentesis . ○ CT imaging may be the best diagnostic tool for determining size, shape, and location of pericardial effusions and may be used to guide pericardiocentesis. ○ Cardiac MRI may assist with detection of inflammation and adhesions. ○ Because the pericardial sac surrounds the heart, a 12-lead ECG may show concave ST elevations in many, if not all, leads (with no reciprocal changes) and may show depressed PR segments or atrial dysrhythmias ● Medical Management ○ Determine the cause, administer therapy for treatment and symptom relief, and detect signs and symptoms of cardiac tamponade. When cardiac output is impaired, the patient is placed on bed rest until fever, chest pain, and friction rub have subsided ○ Analgesic medications and NSAIDs such as aspirin or ibuprofen (Motrin) may be prescribed for pain relief during the acute phase. ○ Pericardiocentesis rarely is necessary. It may be performed to assist in identification of the cause or relieve symptoms, especially if there are signs and symptoms of heart failure or tamponade. ● Nursing Management ○ Patients with acute pericarditis require pain management with analgesics, assistance with positioning, and psychological support ○ Pain may be relieved with a forward-leaning or sitting position. ○ To minimize complications, the nurse helps the patient with activity restrictions until pain and fever subside. As the patient’s condition improves, the nurse encourages gradual increases of activity. ○ Assessment ■ The primary symptom of pericarditis is pain, which is assessed by evaluating the patient in various positions. ○ Planning and Goals ■ The patient’s major goals may include relief of pain and absence of complications. ○ Nursing Interventions ■ RELIEVING PAIN ■ MONITORING AND MANAGING POTENTIAL COMPLICATIONS ● Pericardial Effusion. Abnormal accumulation of fluid between the pericardial linings (i.e., in the pericardial sac) 60 ● Cardiac Tamponade. Signs and symptoms of cardiac tamponade may begin with the patient reporting shortness of breath, chest tightness, or dizziness ■ PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE Cardiac Disorders Objectives ● Discuss three common indications for cardiovascular surgery. Coronary Artery Bypass, Valvular Surgery, Congenital Heart Defects. ○ CABG: Recommended for those who: ■ Fail medical management ■ Have left main coronary artery or 3-vessel dz ■ Are not candidates for PCI (lesions long or difficult to access) ■ Have failed PCI w/ongoing chest pain ■ Have DM ○ Valvular surgery: procedure depends on valve involved + pathology & severity of dz + patient’s clinical condition → all valve surgeries are palliative (not curative) ■ Stenosis (constriction/narrowing) ● Aortic stenosis: ○ Causes: rheumatic fever or calcifications on valve ○ Patho: obstruction of flow from LV to aorta →LV hypertrophy + ↑ myocardial oxygen consumption → ↓CO → ↓tissue perfusion, pulmonary HTN, HF ○ Manifestations: classic triad: angina/syncope/exertional dyspnea ● Mitral stenosis: ○ Causes: rheumatic heart dz, congenital mitral stenosis, RA, Lupus ○ Patho: thickening/shortening of valve structures (“fish mouth” appearance) → obstruction of blood flow → pressure difference b/t LA & LV (during diastole/filling) → ↑pressure + volume LA → ↑pulmonary vascular pressure + hypertrophy of pulmonary vessels ○ Manifestations: exertional dyspnea (d/t ↓ lung compliance) ■ Loud S1 (closing of stenosed valve) + diastolic murmur ■ Fatigue + palpitations from A-fib may also occur ■ May have hoarseness, hemoptysis, chest pain, seizures, stroke ■ Regurgitation (incomplete closure → backward flow of blood) ● Mitral regurgitation: ○ Causes: MI, rheumatic heart dz, mitral valve prolapse, ischemi