NSG-430 Exam 2

heart failure

-Complex clinical syndrome resulting in insufficient blood supply/oxygen to tissues and organs -Involves diastolic or systolic dysfunction -Ejection fraction (EF) is amount of blood pumped by LV with each heart beat -Associated with CVDs: -↑ In incidence and prevalence -Better survival after cardiac events -Aging population -Costly -Most common cause for hospital admission in adults over age 65 -Review risk factors Clinical Manifestations: -Edema: •Common sign of HF •It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion). •If the patient is in bed, sacral and scrotal edema may develop. •Pressing the edematous skin with the finger may leave a transient depression (pitting edema). •The development of dependent edema or a sudden weight gain of more than 3 lb (1.4 kg) in 2 days is often a sign of ADHF, an exacerbation of chronic HF. •It is important to note that not all lower extremity edema is a result of HF. •Hypoproteinemia, immobility, venous insufficiency, and certain drugs can cause peripheral edema. -Nocturia: •The tendency to urinate excessively during the night. •Chronic HF is frequently associated with poor renal perfusion and function. •Patients develop increased peripheral and systemic edema. •At night when lying flat, extravascular fluid is reabsorbed from the interstitial spaces back into the circulatory system. •This results in increased perfusion to the kidneys. The increased renal blood flow results in diuresis. •The patient may complain of having to urinate frequently throughout the night. -Pleural Effusion: •Is a common complication in HF. •There are two pleural layers or membranes: the visceral pleura lines the lungs, whereas the parietal pleura lines the chest cavity. •Normally a small amount of fluid is between the two layers for lubrication and to aid breathing. •A pleural effusion occurs when excess fluid builds up in the pleural cavity of the lungs secondary to increasing pressure in the pleural capillaries. •Fluid then moves from these capillaries into the pleural space. •Pleural effusions may result in symptoms of dyspnea, cough, and chest pain -Dysrhythmias (atrial and ventricular): •Chronic HF causes enlargement of the chambers of the heart. This enlargement can cause changes in the normal electrical pathways. •When numerous sites in the atria fire spontaneously and rapidly (atrial fibrillation), the organized atrial depolarization (contraction) no longer occurs. •Atrial fibrillation also promotes thrombus formation within the atria. Thrombi may break loose and form emboli. •This places patients with atrial fibrillation at risk for stroke. •They require treatment with anticoagulants, cardioversion, ablation, and antidysrhythmic drugs. •Patients with HF are also at risk for ventricular dysrhythmias (e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). •Patients with decreased LV function are at the greatest risk for SCD. •Guidelines recommend implantation of a prophylactic implantable cardioverter-defibrillator (ICD). -Left Ventricular Thrombus: •With ADHF or chronic HF, the enlarged LV and decreased CO combine to increase the risk of thrombus formation in the LV. •Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and worsen the patient's perfusion. •The development of emboli from the thrombus also places the patient at risk for stroke. -Hepatomegaly: •HF can lead to severe hepatomegaly, especially with RV failure. •The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver function. •Eventually liver cells die, fibrosis occurs, and cirrhosis can develop -Renal Failure: •The decreased CO that accompanies chronic HF results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure Diuretics: -Diuretics are used to reduce edema, pulmonary venous pressure, and preload. If excess extracellular fluid is removed, blood volume returning to the heart can be reduced and cardiac function improved. -Diuretics act on the kidney by promoting excretion of sodium and water. -Many varieties of diuretics are available. Loop diuretics (e.g., bumetanide [Bumex]) are potent diuretics. These drugs act on the ascending loop of Henle to promote sodium, chloride, and water excretion. Problems in using loop diuretics include reduction in serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs. -Thiazide diuretics inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. They can be added to loop diuretics to obtain results if patients become resistant to loop diuretics. Thiazide diuretics also can cause severe reductions in potassium levels. -Diuretics are effective in relieving the congestive symptoms of HF. However, their use does activate the SNS and RAAS, which can exacerbate the HF syndrome. -In chronic HF, the lowest effective dose of diuretic should be used. -Diuretics are the mainstay of treatment in patients with volume overload. -They act to decrease sodium reabsorption at various sites within the nephrons, thereby enhancing sodium and water loss. -Decreasing intravascular volume with the use of diuretics reduces venous return (preload) and subsequently the volume returning to the LV. This allows the LV to pump more efficiently. -CO is increased, pulmonary vascular pressures are decreased, and gas exchange is improved. Loop diuretics (e.g., furosemide [Lasix]) can be given by IV push and act rapidly in the kidneys. -Monitor potassium levels (hypokalemia) Vasodilators: -IV nitroglycerin is a vasodilator that reduces circulating blood volume. It also improves coronary artery blood flow by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. -When titrating IV nitroglycerin, monitor BP frequently (every 5 to 10 minutes) to avoid hypotension. -Sodium nitroprusside (Nipride) is a potent IV vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. -Complications of IV sodium nitroprusside include hypotension and thiocyanate toxicity, which can develop after 48 hours of use. -Sodium nitroprusside is given in an ICU, since symptomatic hypotension is the main adverse effect. -Nesiritide, given IV, is a recombinant form of BNP. It causes both arterial and venous dilation. The main hemodynamic effects of nesiritide include (1) a reduction in PAWP and (2) a decrease in systemic BP. -Although classified as a vasodilator, nesiritide is also a neurohormonal blocking agent. It can be used for short-term treatment of ADHF. -Nesiritide does not require titration after the initial IV bolus. It can be given in the emergency department (ED) and non-ICU setting. Because the main adverse effect of nesiritide is symptomatic hypotension, monitor BP closely. Morphine: -Morphine sulfate reduces preload and afterload. It is frequently used in the treatment of HF and acute coronary syndrome -It dilates both pulmonary and systemic blood vessels. When morphine is used, the patient often experiences relief from dyspnea and, consequently, the anxiety often associated with dyspnea. -Use morphine cautiously in patients with ADHF. Morphine is related to more adverse events, including a greater need for mechanical ventilation, more ICU admissions, prolonged hospitalization, and higher mortality rates in these patients. Positive Inotropes: -Inotropic therapy increases myocardial contractility. Drugs include β-agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], norepinephrine [Levophed]), the phosphodiesterase inhibitor milrinone (Primacor), and digitalis. -The β-agonists are only used as a short-term treatment of ADHF. -Milrinone is a phosphodiesterase inhibitor that has been called an inodilator. It increases myocardial contractility (inotropic effect) and promotes peripheral vasodilation. -Inhibition of phosphodiesterase increases cyclic adenosine monophosphate (cAMP). This enhances calcium entry into the cell and improves myocardial contractility. -Milrinone increases CO and reduces BP (decrease afterload). Like dopamine and dobutamine, this drug is available only for IV use. Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity. -Digitalis is a positive inotrope that improves LV function. Digitalis increases contractility but also increases myocardial oxygen consumption. Because digitalis requires a loading dose and time to work, it is not recommended for the initial treatment of ADHF. -Currently, inotropic therapy is only recommended for use in the short-term management of patients with ADHF who have not responded to conventional drug therapy (e.g., diuretics, vasodilators, morphine). More About Drug Therapy: -β-Adrenergic Blockers: •β-Blockers directly block the negative effects of the SNS (e.g., increased heart rate) on the failing heart. -Vasodilators: •Nitrates cause vasodilation by acting directly on the smooth muscle of the vessel wall. •Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries. -BiDil: •Combination therapy with hydralazine and isosorbide dinitrate (Bidil) may be helpful in African American patients with HF who are getting optimal therapy with ACE inhibitors and β-blockers. •The same benefit is not found in white patients. •The combination of the two drugs is also associated with a significant improvement in LV EF and exercise tolerance. •Although the evidence of benefit is stronger in African American patients, the combination therapy may be used in patients of other races who are already on optimal therapy. -Positive Inotropes: •Digitalis preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action). Etiology of Heart Failure: -HF may be caused by any interference with the normal mechanisms regulating cardiac output (CO). -CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR). -Any changes in these factors can lead to decreased ventricular function and HF. -The major causes of HF may be divided into two subgroups: primary and precipitating -Primary causes include: •Hypertension, including hypertensive crisis •Coronary artery disease, including myocardial infarction •Rheumatic heart disease •Congenital heart defects (e.g., ventricular septal defect) •Pulmonary hypertension •Cardiomyopathy (e.g., viral, postpartum, substance abuse) •Hyperthyroidism •Valvular disorders (e.g., mitral stenosis) •Myocarditis -Precipitating causes often increase the workload of the ventricles, resulting in an acute condition that results in decreased cardiac function: •Anemia (decreased oxygen supply increases workload of heart to meet the demand) •Infection (increased oxygen demand) •Thyrotoxicosis (increased heart rate and workload) •Hypothyroidism (increased risk for atherosclerosis) •Dysrhythmias (decreased CO and increased workload) •Bacterial endocarditis (infection increases workload, can also cause valvular disorders) •Obstructive sleep apnea •Pulmonary embolism (increased workload to pump blood into lungs) •Paget's disease (increased workload secondary to increased vasculature bed) •Nutritional deficiencies (decreased cardiac function increases workload) •Hypervolemia (increased preload increases workload) Compensatory Mechanisms: -Renin-Angiotensin-Aldosterone-System (RAAS) -Neurohormonal response: RAAS •Endothelin is produced •Cytokines are released -Neurohormonal response: SNS catecholamines -Ventricular remodeling: •Dilation •Hypertrophy -This is an example of how the body tries to maintain homeostasis but may induce other problems; example, hypertrophy; the heart gets larger, the normal stretch of the cardiac muscle becomes weaker, decreases the cardiac output and decreases end organ perfusion, so you can see how important it is to manage heart failure. Counterregulatory Mechanisms: -The body's ability to try to maintain balance is demonstrated by several counterregulatory processes. -Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are hormones produced by the heart muscle -Normal level for BNP is < 100pg/mL -ANP is released from the atria and BNP is released from the ventricles in response to increased blood volume in the heart. -The natriuretic peptides have renal, cardiovascular, and hormonal effects. -Renal effects include (1) increased glomerular filtration rate and diuresis, and (2) excretion of sodium (natriuresis). -Cardiovascular effects include vasodilation and decreased BP. -Hormonal effects include (1) inhibition of aldosterone and renin secretion and (2) interference of ADH release. -The combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS in patients with HF. -Nitric oxide (NO) and prostaglandin are counterregulatory substances released from the vascular endothelium in response to the compensatory mechanisms activated in HF. -Like the natriuretic peptides, NO and prostaglandin work to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload. -Compensated HF occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion. -Decompensated HF occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

mitral valve prolapse

-Mitral valve prolapse (MVP) is an abnormality of the mitral valve leaflets and the papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the left atrium during systole. -It is the most common form of valvular heart disease in the United States. -The use of the term prolapse can be misleading because it is used even when the valve is working normally. -MVP is usually benign with the valve closing effectively, but serious complications can occur, including MR, IE, SCD, HF, and cerebral ischemia. -Although the etiology of MVP is unknown, there is an increased familial incidence in some patients. -Can mimic an MI -M-mode and 2-D echocardiography are used to confirm MVP. -MVP covers a broad range of severity. -Most patients are asymptomatic and remain so for their entire lives. -About 10% of those with MVP become symptomatic. -A characteristic of MVP is a murmur from regurgitation that is louder during systole. -MVP does not alter S1 or S2 heart sounds. -Severe MR is an uncommon but serious complication of MVP. -Dysrhythmias, most commonly ventricular premature contractions, paroxysmal supraventricular tachycardia, and ventricular tachycardia, may cause palpitations, light-headedness, and dizziness. -IE may occur in patients with mitral regurgitation associated with MVP. -Patients may or may not have chest pain. The cause of the chest pain is not known. It may be the result of abnormal tension on the papillary muscles. If chest pain occurs, episodes tend to occur in clusters, especially during periods of emotional stress. -Dyspnea, palpitations, and syncope may occasionally accompany the chest pain and do not respond to antianginal treatment (e.g., nitrates). -Valvular surgery for MR -β-blockers may be given to control palpitations and chest pain. -Patients with MVP generally have a benign, manageable course unless problems related to mitral regurgitation develop. No accepted medical therapy appears to delay the need for valve surgery in this group. Patient Teaching: -Encourage the patient to stay hydrated, exercise regularly, and avoid caffeine. -Teach patient the importance of antibiotic prophylaxis for endocarditis before undergoing certain procedures if the patient has MVP with regurgitation. -Instruct patient to take drugs as prescribed (e.g., β-blockers to control palpitations, chest pain). -Advise patient to adopt healthy eating habits. Avoid caffeine because it is a stimulant and may exacerbate symptoms. -Counsel patient who uses diet pills or other over-the-counter drugs to check for common ingredients that are stimulants (e.g., caffeine, ephedrine) as these will exacerbate symptoms. -Encourage the patient to begin (or maintain) an exercise program to achieve optimal health. -Instruct patient to contact HCP or emergency medical services (EMS) if symptoms develop or worsen (e.g., palpitations, fatigue, shortness of breath, anxiety).

acute coronary syndrome

-When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops. -ACS includes the spectrum of UA, non-ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI). -When patients first present with chest pain, ST-elevations on the 12-lead ECG are most likely indicative of a STEMI. -The ECG should always be compared to a previous ECG whenever possible. -For patients with chest pain who do not show ST-elevation or ST-T wave changes on the ECG, it is difficult to distinguish between UA and NSTEMI until serum cardiac biomarkers are measured. -On the cellular level, the heart muscle becomes hypoxic within the first 10 seconds of a total coronary occlusion. Heart cells are deprived of oxygen and glucose needed for aerobic metabolism and contractility. -Anaerobic metabolism begins and lactic acid accumulates. -In ischemic conditions, heart cells are viable for approximately 20 minutes. -Irreversible heart damage starts after 20 minutes if there is no collateral circulation Etiology and Pathophysiology: -ACS is caused by the decline of a once stable atherosclerotic plaque. -The previously stable plaque ruptures, releasing substances into the vessel. -This stimulates platelet aggregation and thrombus formation. -This area may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI). -What causes a coronary plaque to suddenly become unstable is not well understood, but systemic inflammation (described earlier) is thought to play a role. -Patients with suspected ACS require immediate hospitalization. ECG Changes: -The 12-lead ECG is a major diagnostic tool used to evaluate patients with ACS. -The ECG changes are in response to ischemia, injury, or infarction (necrosis) of myocardial cells. -The leads facing the area of involvement demonstrate the definitive ECG changes. -The leads facing opposite the area involved in ACS often demonstrate reciprocal (opposite) ECG changes. -In addition, the pattern of ECG changes among the 12 leads provides information on the coronary artery involved in ACS ECG Changes: -Typical ECG changes that are seen in myocardial ischemia include ST-segment depression and/or T wave inversion. -ST-segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line. -Depression in the ST segment and/or T wave inversion occurs in response to an inadequate supply of blood and oxygen, which causes an electrical disturbance in the myocardial cells. -Once treated (adequate blood flow is restored), the ECG changes will resolve, and the ECG will return to the patient's baseline. -Myocardial injury represents a worsening stage of ischemia that is potentially reversible but may evolve to MI. -The typical ECG change seen during injury is ST-segment elevation. -ST-segment elevation is significant if it is greater than or equal to 1 mm above the isoelectric line. -If treatment is prompt and effective, it is possible to restore oxygen to the myocardium and avoid or limit infarction. -The absence of serum cardiac markers confirms this. Interprofessional Care: -It is extremely important to quickly diagnose and treat a patient with ACS to preserve heart muscle. -Obtain a 12-lead ECG and start continuous ECG monitoring. -Position the patient in an upright position unless contraindicated and initiate oxygen by nasal cannula to keep oxygen saturation above 93%. -Establish an IV route to provide an access for emergency drug therapy. -Give sublingual NTG and 162-325 mg of aspirin (chewable) if not given before arrival at the ED. -Morphine sulfate is given for pain unrelieved by NTG. -A high-dose statin (atorvastatin [Lipitor]) is started if not already taking prior to the hospitalization. -The patient will usually receive ongoing care in a critical care unit or telemetry unit, where continuous ECG monitoring is available. -Dysrhythmias are treated according to agency protocols. -Some patients are started on glycoprotein IIb/IIIa inhibitors (e.g., eptibibatide) either before catheterization or at the time of PCI. -Monitor vital signs, including pulse oximetry, frequently during the first few hours after admission and closely thereafter. -Maintain bed rest and limitation of activity for 12 to 24 hours, with a gradual increase in activity unless contraindicated. -For patients with UA and NSTEMI, aspirin and heparin (UH or LMWH) are recommended. -Dual antiplatelet therapy (e.g., aspirin and clopidogrel) and heparin are recommended for NSTEMI patients. -Cardiac catheterization with possible PCI is considered for both UA and NSTEMI patients once the patient is stabilized and angina is controlled or if angina returns or increases in severity -For patients with STEMI, reperfusion therapy is initiated. -Reperfusion therapy can include emergent PCI (preferred) or thrombolytic therapy for STEMI. -The goal in the treatment of STEMI is to save as much heart muscle as possible. -Dual antiplatelet therapy and heparin are also used. -Emergent PCI is the first line of treatment for patients with confirmed STEMI (i.e., ST-elevation on the ECG and/or positive cardiac biomarkers). -The goal is to open the blocked artery within 90 minutes of arrival to a facility that has an interventional cardiac catheterization laboratory. -In this case, the patient will undergo a cardiac catheterization to locate and assess the severity of the blockage(s), determine the presence of collateral circulation, and evaluate LV function. -During the procedure, a bare metal stent (BMS) or drug-eluting stent (DES) is inserted into the blocked coronary artery. -Patients with severe LV dysfunction may require the addition of IABP therapy and/or inotropes (e.g., dobutamine). -A small percentage of patients may require emergent CABG surgery. -The advantages of PCI (compared to thrombolytic therapy) include the following: (1) it provides an alternative to surgical intervention; (2) it is performed with local anesthesia; (3) the patient is ambulatory shortly after the procedure; (4) the length of hospital stay is approximately 3 to 4 days after MI compared with the 4 to 6 days with CABG surgery, thus reducing hospital costs; and (5) the patient can return to work several weeks sooner after PCI compared to 6- to 8-week convalescence after CABG. -Advances in PCI techniques have significantly reduced the need for emergent CABG. Currently, there are more PCIs than CABGs performed in the United States. -Thrombolytic (fibrinolytic) therapy is only indicated for patients with a STEMI. -It offers the advantages of availability and rapid administration in agencies that do not have an interventional cardiac catheterization laboratory or one is too far away to transfer the patient safely. -Treatment of STEMI with thrombolytic therapy aims to limit the infarction size by dissolving the thrombus in the coronary artery and reperfusing the heart muscle. -The goal is to give the thrombolytic within 30 minutes of the patient's arrival to the ED. -All thrombolytics are given IV. -Because all thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a postoperative site). -Therefore patient selection is important because minor or major bleeding can be a complication of therapy. -Inclusion criteria for thrombolytic therapy are (1) chest pain less than 12 hours with 12-lead ECG findings consistent with acute STEMI and (2) no absolute contraindications. -Patients with chest pain lasting 12-24 hours with ECG changes supporting STEMI may be considered for thrombolytic therapy. -Each hospital has a protocol for giving thrombolytic therapy. However, there are several common factors. -Draw blood to obtain baseline laboratory values and start two or three lines for IV therapy. -All other invasive procedures are done before the thrombolytic agent is given to reduce the possibility of bleeding in the patient. -Depending on the drug selected, therapy is given 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. -Regularly assess for changes in neurologic status as this may indicate cerebral bleeding. -When reperfusion occurs (i.e., the coronary artery that was blocked is opened and blood flow is restored to the heart muscle), several clinical signs may occur. •The most reliable sign is the return of the ST segment to baseline on the ECG. •Other signs include a resolution of chest pain, and an early, rapid rise of the cardiac biomarkers within 3 hours of therapy and peaking within 12 hours. •These levels increase as the necrotic heart cells release proteins into the circulation after perfusion is restored to the area. •The presence of reperfusion dysrhythmias (e.g., accelerated idioventricular rhythm) is a less reliable sign of reperfusion. •These dysrhythmias are generally self-limiting and do not require aggressive treatment. -A major concern with thrombolytic 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. Therefore, IV heparin therapy is started -Coronary revascularization with CABG surgery is recommended for patients who (1) fail medical management, (2) have left main coronary artery or three-vessel disease, (3) are not candidates for PCI (e.g., blockages are long or difficult to access), or (4) have failed PCI and continue to have chest pain. -CABG may also be the option for patients with diabetes, LV dysfunction, or chronic kidney disease. -CABG surgery and PCI are considered palliative treatment for CAD and not a cure. -CABG surgery consists of the placement of arterial or venous grafts to transport blood between the aorta, or other major arteries, and the heart muscle distal to the blocked coronary artery (or arteries). -CABG surgery requires a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). -During CPB, blood is diverted from the patient's heart to a machine. Here it is oxygenated and returned (via a pump) to the patient. -This allows the surgeon to operate on a quiet, nonbeating, bloodless heart while perfusion to vital organs is maintained. -The procedure may involve one or more grafts using the internal mammary artery (IMA), saphenous vein, radial artery, gastroepiploic artery, and/or inferior epigastric artery. Grafts: -The internal mammary artery (IMA) is the most common artery used for bypass graft. -It is left attached to its origin (the subclavian artery) but then dissected from the chest wall. Next, it is anastomosed (connected with sutures) to the coronary artery distal to the blockage. -Saphenous veins are also used for bypass grafts. The surgeon endoscopically removes the saphenous vein from one or both legs. A section is sutured into the ascending aorta near the native coronary artery opening and then sutured to the coronary artery distal to the blockage. The use of antiplatelet and statin therapy after surgery improves vein graft patency. -Radial artery is another potential graft -Thick muscular artery that is prone to spasm -Calcium channel blockers and long-acting nitrates can control the spasms -Patency rates are not as good as IMA but better than saphenous veins -Minimally invasive direct coronary artery bypass (MIDCAB) offers patients with disease of the left anterior descending or right coronary artery an approach to surgical treatment that does not involve a sternotomy and CPB. •The technique requires several small incisions between the ribs or a mini thoracotomy. •A thoracoscope or robotic assistance is used to dissect the IMA from the chest. •A mechanical stabilizer immobilizes the operative site. The IMA is then sutured to the left anterior descending or right coronary artery. •Some patients undergo hybrid procedures where they have a MIDCAB for the left anterior descending artery and undergo a PCI of a second or third artery at a later time. -OPCAB: •The off-pump coronary artery bypass (OPCAB) procedure uses a median sternotomy to access all coronary vessels. •OPCAB is performed on a beating heart (no CPB) using mechanical stabilizers. •OPCAB is associated with less blood loss, less renal dysfunction, less postoperative atrial fibrillation, and fewer neurologic complications. •It is estimated that less than 20% of CABG procedures are OPCAB procedures. •OPCAB is primarily used for patients with multiple comorbidities who should avoid CPB. -TECAB: •This technique uses a robot in performing CABG surgery. This procedure is done without the use of CPB or with the use of CPB using femoral access. •TECAB is used for limited bypass grafting. The benefits include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time. -Transmyocardial Laser Revascularization: •Transmyocardial laser revascularization is an indirect revascularization procedure. •It is used for patients with advanced CAD who are not candidates for traditional CABG surgery and who have persistent angina despite maximum medical therapy. •The procedure involves the use of a high-energy laser to create channels in the heart muscle to allow blood flow to ischemic areas. •The procedure can be done using a left thoracotomy approach or in combination with CABG surgery. •It is as an adjunctive therapy when bypass grafts cannot be placed. Drug Therapy: -IV NTG (Tridil) is used in the initial treatment of the patient with ACS: •The goal of therapy is to reduce anginal pain and improve coronary blood flow. •IV NTG decreases preload and afterload while increasing the myocardial oxygen supply. •The onset of action is immediate. •Titrate NTG to control and stop chest pain. •Because hypotension is a common side effect, BP is closely monitored during this time. •Patients who do become hypotensive are often volume depleted and can benefit from an IV fluid bolus. -Morphine is the drug of choice for chest pain that is unrelieved by NTG: •As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility, and decreasing BP and HR. •In addition, morphine can help reduce anxiety and fear. •In rare situations, morphine can depress respirations. •Monitor patients for signs of bradypnea or hypotension, conditions to avoid in myocardial ischemia and infarction. -β-Blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility: •The use of these drugs in patients who are not at risk for complications of MI (e.g., cardiogenic shock, bradycardia or hypotension) reduces the risk of reinfarction and the occurrence of HF. •β-Blockers are continued indefinitely. -Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers inhibitors should be started within the first 24 hours if the BP is stable and there are no contraindications: •They are continued indefinitely in patients recovering from STEMI or NSTEMI, with heart failure, or an EF of 40% or less. •The use of ACE inhibitors can help prevent ventricular remodeling and prevent or slow the progression of HF. •For patients who cannot tolerate ACE inhibitors (e.g., angioedema, cough), ARBs should be considered. -Dysrhythmias are the most common complications after an MI: •In general, they are self-limiting and are not treated aggressively unless they are life threatening (e.g., sustained ventricular tachycardia). -A lipid panel is obtained on all patients with ACS: •All patients with ACS or diagnosed with CAD should receive lipid-lowering drugs indefinitely, unless contraindicated. -After an MI, the patient may be predisposed to constipation because of bed rest and opioid administration: •Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate bowel movements. •This prevents straining and the resultant vagal stimulation from the Valsalva maneuver. •Vagal stimulation produces bradycardia and can provoke dysrhythmias. Nutritional Therapy: -Initially, patients may be NPO (nothing by mouth), except for sips of water, until stable (e.g., pain free, nausea resolved). -You advance the diet as tolerated to a low-salt, low-saturated fat, and low-cholesterol diet. Acute Care: -Priority interventions are aimed at decreasing the oxygen needs of a compromised heart muscle and reducing the risk of complications. -Provide NTG, morphine sulfate, and supplemental oxygen as needed to eliminate or reduce chest pain. -Ongoing evaluation and documentation of the effectiveness of the interventions is important. -Maintain continuous ECG monitoring while in the ED and ICU and after transfer to a step-down or general unit. -Dysrhythmias need to be identified quickly and treated. -During the initial period after MI, ventricular fibrillation is the most common lethal dysrhythmia. -In many patients, premature ventricular contractions or ventricular tachycardia precedes this dysrhythmia. -Monitor the patient for the presence of reinfarction or ischemia by monitoring the ST segment for shifts above or below the baseline of the ECG. -Silent ischemia can occur without subjective symptoms (e.g., chest pain). It is noted by ST segment changes only. Notify the HCP if you see ST segment changes without any clinical symptoms. -Perform a physical assessment to detect deviations from the patient's baseline findings. -Assess heart and breath sounds and any evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). -In addition to routine vital signs and pulse oximetry, monitor intake and output at least once a shift. -It is important to promote rest and comfort with any degree of heart damage. -Bed rest may be ordered for the first few days after an MI involving a large portion of the LV. A patient with an uncomplicated MI (e.g., angina resolved, no signs of complications) may rest in a chair within 8 to 12 hours after the event. -The use of a commode or bedpan is based on patient preference. -When sleeping or resting, the body requires less work from the heart than it does when active. -It is important to plan nursing and other interventions to ensure adequate rest periods free from interruption. -Comfort measures that can promote rest include a quiet environment, use of relaxation therapy (e.g., guided imagery), and assurance that staff are nearby and responsive to the patient's needs. -Phase 1 of cardiac rehab occurs in the hospital. It is important that the patient understands the reasons why activity is limited but not completely restricted. -Gradually increase the patient's cardiac workload through more demanding physical tasks so that the patient can achieve a discharge activity level adequate for home care. -Phase 2 of rehab begins when the patient is discharged home and continues for 2 to 12 weeks. -Phase 3 is long-term maintenance for optimal cardiac health. -To some degree anxiety is present in all patients with ACS. -Your role is to identify the source of anxiety and assist the patient in reducing it. -If the patient is afraid of being alone, allow a caregiver to sit by quietly or check in with the patient frequently. -For anxiety caused by lack of information, provide teaching based on the patient's stated need and level of understanding. -Answer the patient's questions with clear, simple explanations. -It is important to start teaching at the patient's level rather than to present a prepackaged program. -For example, patients generally are not ready to learn about the pathology of CAD. -The earliest questions usually relate to how the disease affects perceived control and independence. -Examples include the following: When will I leave the intensive care unit? When can I be out of bed? When will I be discharged? When can I return to work? How many changes will I have to make in my life? Will this happen again? -Often the patient may not be able to ask the most serious concern of ACS patients: Am I going to die? -Even if a patient denies this concern, it is helpful for you to start conversation by remarking that fear of dying is a common concern among most patients who have experienced ACS. -This gives the patient "permission" to talk about an uncomfortable and fearful topic. -The emotional and behavioral reactions of a patient vary but often follow a predictable response pattern. -Your role is to understand what the patient is currently experiencing and to support the use of constructive coping styles. -Assess the support structure of the patient and caregiver. -Determine how you can help maximize the support system. -Often the patient is separated from the most significant support system at the time of hospitalization. -Your role can include talking with the caregiver(s), informing them of the patient's progress, allowing the patient and caregiver to interact as necessary, and supporting the caregivers who will be able to provide the necessary support to the patient. -Open visitation is helpful in decreasing anxiety and increasing support for the patient with ACS. Procedural Care: -Patients with ACS may undergo coronary revascularization with PCI or CABG surgery. -The major nursing responsibilities for the care of the patient following PCI involve: •Monitoring for signs of recurrent angina •Frequent assessment of vital signs, including HR and rhythm •Evaluation of the catheter insertion site for signs of bleeding •Neurovascular assessment of the involved extremity •Maintenance of bed rest per institution policy -For patients having CABG surgery, care is provided in the ICU for the first 24 to 36 hours. -Ongoing and intensive monitoring of the patient's hemodynamic status is critical. -The patient will have numerous invasive lines for monitoring cardiac status and other vital organs. These include: •A pulmonary artery catheter for hemodynamic monitoring •An intraarterial line for continuous BP monitoring •Pleural and mediastinal chest tubes for chest drainage •Continuous ECG monitoring •An endotracheal tube connected to mechanical ventilation •Epicardial pacing wires for emergency pacing of the heart •A urinary catheter to monitor urine output •NG tube for gastric decompression -Most patients will be extubated within 6 hours and transferred to a step-down unit within 24 hours for continued monitoring of cardiac status. -Many of the postoperative complications that develop after CABG surgery relate to the use of CPB. -Major consequences of CPB are systemic inflammation, which includes complications of -Bleeding and anemia from damage to red blood cells and platelets -Fluid and electrolyte imbalances -Hypothermia as blood is cooled as it passes through the CPB machine -Infections -Focus your nursing care on: •Assessing the patient for bleeding (e.g., chest tube drainage, incision sites) •Hemodynamic monitoring •Checking fluid status •Replacing blood and electrolytes as needed •Restoring temperature (e.g., warming blankets) •Postoperative dysrhythmias, specifically atrial dysrhythmias, are common in the first 3 days after CABG surgery. •Many of the postoperative complications that develop after CABG surgery relate to the use of CPB. •Beta-blockers should be restarted as soon as possible after surgery (unless contraindicated) to reduce the incidence of AF. CABG Nursing Care: -Nursing care for the patient with a CABG involves caring for the surgical sites (e.g., chest, arm, leg). -Care of the leg incision is minimal since endoscopy is used to harvest the vein. -Chest incisions are usually closed with Dermabond and do not require dressings. -Management of the chest wound, which involves a sternotomy, is similar to that of other chest surgeries. -Care of the radial artery harvest site includes monitoring sensory and motor function of the hand. -The patient with radial artery harvest should be on a calcium channel blocker for approximately 3 months to reduce the incidence of arterial spasm at the arm or anastomosis site. -Other interventions include strategies to manage pain and prevent venous thromboembolism (e.g., early ambulation, sequential compression device) and respiratory complications (e.g., use of incentive spirometer, splinting during coughing and deep-breathing exercises). -Postoperatively, patients may experience some cognitive dysfunction. This includes impairment of memory, concentration, language comprehension, and social integration. -Patients may inexplicably cry or become teary. -Postoperative cognitive dysfunction (POCD) can manifest days to weeks after surgery and may remain a permanent disorder Evaluation of Expected Outcomes: -The overall expected outcomes are that the patient with ACS: •Maintains stable signs of effective cardiac output •Reports relief of pain •Reports decreased anxiety and increased sense of self-control •Achieves a realistic program of activity that balances physical activity with energy-conserving activities •Describes the disease process, measures to reduce risk factors, and rehabilitation activities necessary to manage the therapeutic regimen

acute kidney injury

Acute kidney injury (AKI): -Term used to encompass the entire range of the syndrome, including a very slight deterioration in kidney function to severe impairment. -Characterized by a rapid loss of kidney function -Accompanied by a rise in serum creatinine level and/or a reduction in urine output -Severity of dysfunction can range from a small increase in serum creatinine or reduction in urine output to the development of azotemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood). -Can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium, with or without a reduction in urine output. -Impacts the kidney in three different ways: pre-renal, intra-renal, and post-renal Pre-Renal Causes: -Factors that reduce systemic circulation causing reduction in renal blood flow -Severe dehydration, heart failure, ↓CO -This causes ↓ to the glomerular filtration rate (GFR), leading to oliguria -There is no damage to the kidney tissue (parenchyma) -Caused by a decrease in circulating blood volume (e.g., severe dehydration, heart failure, decreased cardiac output) -Readily reversible with appropriate treatment. -Autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone attempt to preserve blood flow to essential organs -Prerenal azotemia results in a reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention, and decreased urine output. -Prerenal conditions contribute to intrarenal disease if renal ischemia is prolonged. -If decreased perfusion persists for an extended time, the kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage). Autoregulatory Mechanisms: -GOAL: to preserve blood flow -With a decrease in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone attempt to preserve blood flow to essential organs. -Prerenal azotemia results in a: •Reduction in the excretion of sodium (less than 20 mEq/L) •Increased salt and water retention •Decreased urine output. Intra-Renal Causes: -Causes include conditions that cause direct damage to kidney tissue like infection, autoimmune disease, and other causes -This results in impaired nephron function -Prolonged ischemia: renal ischemia is the deficiency of blood in one or both kidneys usually due to functional constriction or actual obstruction of a blood vessel -Nephrotoxins, penicillins, cephalosporins, sulfonamides, thiazide diuretics, furosemide, NSAIDs, rifampicin, and IV contrast are other examples -Nephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules. -Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction. -Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI. -There are a number of drugs that cause direct toxicity to the renal tubules (acute tubular necrosis), such as aminoglycosides, amphotericin, and cyclosporins Post-Renal Causes: -Causes include mechanical obstruction of outflow: •Benign prostatic hyperplasia •Prostate cancer •Calculi •Trauma •Extrarenal tumors •Bilateral ureteral obstruction -As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function. -Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive decline in kidney function. -If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. -Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis. -Postrenal causes of AKI account for less than 10% of AKI cases. RIFLE: -Clinically, AKI may progress through phases: oliguric, diuretic, and recovery. -When a patient does not recover from AKI, then CKD may develop. -The RIFLE classification is used to describe the stages of AKI (Table 46-3).: •Risk (R) is the first stage of AKI, is followed by Injury (I), which is the second stage. Then AKI increases in severity to the final or third stage Failure (F). •The two outcome variables are Loss (L) and End-stage renal disease (E). Assessment: -Measure vital signs -Measure fluid intake and output -Examine urine -Assess general appearance -Observe dialysis access site -Mental status/level of consciousness -Oral mucosa -Lung sounds -Heart rhythm -Laboratory values -Diagnostic test results -Know patient preparations/ management for diagnostic tests Oliguric Phase: -Urinary changes: the most common initial manifestation of AKI is oliguria, a reduction in urine output to less than 400 mL/day. -Oliguria usually occurs within 1 to 7 days of the injury to the kidneys. -If the cause is ischemia, oliguria often occurs within 24 hours. -The oliguric phase lasts on average about 10 to 14 days but can last months in some cases. -The longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function. -About 50% of patients will not be oliguric, making the initial diagnosis more difficult. -Changes in urine output generally do not correspond to changes in glomerular filtration rate (GFR). -However, changes in urine output are often helpful in differentiating the etiology of AKI. For example, anuria (no urine output) is usually seen with urinary tract obstruction, oliguria is commonly seen with prerenal causes, and nonoliguric AKI is seen with acute interstitial nephritis and ATN. -A urinalysis may show casts, RBCs, and white blood cells (WBCs). -The casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules. -Urinary specific gravity (measure of the concentration of solutes in the urine) is normally 1.003-1.030. -Urine osmolality is used to measure the number of dissolved particles in the urine. Urine osmolality range is 300-1300 mOsm/kg. As a measure of urine concentration, it is more accurate than specific gravity. -Fluid volume: •Hypovolemia may exacerbate AKI •Decreased urine output •Fluid retention •Neck veins distended •Bounding pulse •Edema •Hypertension •Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions -Metabolic acidosis: •Impaired kidney cannot excrete hydrogen ions •Serum bicarbonate production is decreased •Severe acidosis develops •Kussmaul respirations -Sodium balance: •Damaged tubules cannot conserve sodium. The urinary excretion of sodium may increase, resulting in normal or below-normal levels of serum sodium. •Excessive intake of sodium should be avoided because it can lead to volume expansion, hypertension, and HF. •Uncontrolled hyponatremia or water excess can lead to cerebral edema. -Potassium excess: •The kidneys normally excrete 80% to 90% of the body's potassium. •In AKI the serum potassium level increases because the kidney's normal ability to excrete potassium is impaired. •Hyperkalemia risk is increased if AKI is caused by massive tissue trauma because the damaged cells release additional potassium into the extracellular fluid. •Bleeding and blood transfusions may cause cellular destruction, releasing more potassium into the extracellular fluid. •Metabolic acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the extracellular fluid. •Although patients with hyperkalemia are often asymptomatic, some may complain of weakness with severe hyperkalemia. •Because cardiac muscle is intolerant of acute increases in potassium, emergency treatment of hyperkalemia is needed. •Acute or rapid development of hyperkalemia may result in clinical signs that are apparent on electrocardiogram (ECG). •These changes include peaked T waves, widening of the QRS complex, and ST segment depression. -Hematologic disorders: leukocytosis -Waste product accumulation: elevated BUN and serum creatinine levels -Neurologic disorders: fatigue and difficulty concentrating; seizures, stupor, coma Diuretic Phase: -During the diuretic phase of AKI, daily urine output usually is around 1 to 3 L but may reach 5 L or more. -The high urine volume is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. -In this phase, the kidneys have recovered their ability to excrete wastes, but not to concentrate the urine. -Large losses of fluid and electrolytes require the patient be monitored for hyponatremia, hypokalemia, and dehydration. -The diuretic phase may last 1 to 3 weeks. Near the end of this phase, the patient's acid-base, electrolyte, and waste product (BUN, creatinine) values stabalize. -Recovery phase: •The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to decrease. •Major improvements occur in the first 1 to 2 weeks of this phase, but kidney function may take up to 12 months to stabilize. •The outcome of AKI is influenced by the patient's overall health, severity of kidney failure, and the number type of complications. •Some individuals do not recover and progress to end-stage renal disease. •The older adult is less likely to have a complete recovery of kidney function. •Patients who recover may achieve clinically normal kidney function, but remain in an early stage of CKD. Diagnostic Studies: -Thorough history -Serum creatinine -Urinalysis -Kidney ultrasonography -Renal scan -CT scan -Renal biopsy -Obtaining an MRI or magnetic resonance angiography (MRA) study with the contrast media gadolinium is not advised in patients with kidney failure. -Administration of gadolinium can be potentially fatal. •In patients with kidney failure, contrast-induced nephropathy (CIN) can occur when contrast medium for diagnostic studies causes nephrotoxic injury. •In patients with diabetes receiving metformin, the drug should be held for 48 hours prior to and after the use of contrast media to decrease the risk of lactic acidosis. •The best way to avoid CIN is to avoid exposure to contrast media by using other diagnostic tests such as ultrasound. •Nephrogenic systemic fibrosis is also a concern Planning: -The first step is to determine if there is adequate intravascular volume and cardiac output to ensure adequate perfusion of the kidneys. -Diuretic therapy may be administered and usually includes loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) or an osmotic diuretic (e.g., mannitol). -If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful. -Closely monitor fluid intake during the oliguric phase of AKI. -The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g., respiration, diaphoresis). -Hyperkalemia: •Insulin and sodium bicarbonate •Calcium carbonate •Sodium polystyrene sulfonate (Kayexalate) -Types of renal replacement therapy (RRT) include peritoneal dialysis (PD, not frequently used), intermittent hemodialysis (HD), and continuous renal replacement therapy (CRRT, cannulation of artery and vein) -The most common indications for RRT in AKI are: •Volume overload, resulting in compromised cardiac and/or pulmonary status •Elevated serum potassium level •Metabolic acidosis (serum bicarbonate level less than 15 mEq/L [15 mmol/L]) •BUN level greater than 120 mg/dL (43 mmol/L) •Significant change in mental status •Pericarditis, pericardial effusion, or cardiac tamponade Nutritional Therapy: -The goal of nutritional management in AKI is to provide adequate calories to prevent catabolism despite the restrictions necessary to prevent electrolyte disorders, fluid disorders, and azotemia. -Nutritional intake must maintain adequate caloric intake (providing 30 to 35 kcal/kg and 0.8 to 1.0 g of protein per kilogram of desired body weight) to prevent the further breakdown of body protein for energy purposes. -Adequate energy should be primarily from carbohydrate and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. -Supplementation of essential amino acids can be given for amino acid replacement. -Sodium is restricted as needed to prevent edema, hypertension, and heart failure. -Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat. -Fat emulsion IV infusions given as a nutritional supplement provide a good source of nonprotein calories -If a patient cannot maintain adequate oral intake, enteral nutrition is the preferred route for nutritional support -When the gastrointestinal (GI) tract is not functional, parenteral nutrition is necessary to provide adequate nutrition. -The patient treated with parenteral nutrition may need daily HD or CRRT to remove the excess fluid. -Concentrated formulas of parenteral nutrition are available to minimize fluid volume. Implementation: -Observe and record accurate intake and output. -Measure daily weights with the same scale at the same time each day to allow for the evaluation and detection of excessive gains or losses of body fluid (1 kg is equivalent to 1000 mL of fluid). -Assess for the common signs and symptoms of hypervolemia (in the oliguric phase) or hypovolemia (in the diuretic phase), potassium and sodium disturbances, and other electrolyte imbalances that may occur in AKI -Because infection is the leading cause of death in AKI, meticulous aseptic technique is critical. -If a patient with renal failure has an infection, it is important to recognize that the temperature may not always be elevated. Patients with kidney failure have a blunted febrile response to an infection (e.g., pneumonia). -If antibiotics are used to treat an infection, the type, frequency, and dosage must be carefully considered because the kidneys are the primary route of excretion for many antibiotics. -Nephrotoxic drugs should be used judiciously. -Perform skin care, and take measures to prevent pressure ulcers as mobility may be impaired. -Mouth care is important for preventing stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates the mucous membranes. -Regulate protein and potassium intake -Follow-up care -Teaching -Appropriate referrals Gerontologic Considerations: -Although the causes of AKI in older adults are similar to younger adults, they are at an increased risk for AKI. -Dehydration is a predisposing factor and tends to occur much more frequently in older adults. -Dehydration can occur from polypharmacy (diuretics, laxatives, and drugs that suppress appetite or consciousness), acute febrile illnesses, and immobility from being bedridden. -Other common causes of AKI in the older adult include hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders (e.g., prostatic hyperplasia), surgery, infection, and contrast media. -Mortality rates are similar for older and younger patients. -Patients over 65 years of age are less likely to recover from AKI. -Despite this, a patient's chronologic age is not a barrier to offering renal replacement therapy.

valvular heart disease

Heart has: -Two atrioventricular valves: •Mitral •Tricuspid -Two semilunar valves: •Aortic •Pulmonic Types of valvular heart disease depend on: -Valve(s) affected -Type of dysfunction •Stenosis •Regurgitation Stenosis: -Constriction/ narrowing -Forward blood flow is impeded -Pressure differences on two sides of open valve reflect degree of stenosis -The higher the difference in pressure, the greater the stenosis Regurgitation: -Incompetence/ insufficiency -Incomplete closure of valve leaflets -Results in backward flow of blood Nursing Assessment: Subjective Data: -Past medical history: rheumatic fever, infective endocarditis; congenital defects, heart attack, chest trauma, cardiomyopathy; syphilis, Marfan's syndrome, streptococcal infections -IVDA, fatigue -Palpitations, weakness, activity intolerance, dizziness, fainting -DOE, cough, hemoptysis, orthopnea, PND -Angina or atypical chest pain Objective Data: -Fever -Diaphoresis, flushing, cyanosis, clubbing, peripheral edema -Crackles, wheezes, hoarseness -S3 and S4 -Dysrhythmias: including atrial fibrillation, premature ventricular contractions, tachycardia -↑ or ↓ in pulse pressure; hypotension -Water-hammer or thready peripheral pulses -Hepatomegaly, ascites -Unexplained weight gain Functional Health Patterns: -Health perception-health management: IV drug abuse, fatigue -Activity-exercise: palpitations; generalized weakness, activity intolerance; dizziness, fainting; dyspnea on exertion, cough, hemoptysis, orthopnea -Sleep-rest: paroxysmal nocturnal dyspnea -Cognitive-perceptual: angina or atypical chest pain Diagnostic Studies: -Diagnosis of valvular heart disease includes information from the patient's history and physical examination and a variety of tests. -A CT scan of the chest with contrast is the gold standard for evaluating aortic disorders. -An echocardiogram reveals valve structure, function, and heart chamber size. -Transesophageal echocardiography and Doppler color-flow imaging help diagnose and monitor valvular heart disease progression. -Chest x-ray reveals the heart size, altered pulmonary circulation, and valve calcification. -An ECG identifies heart rate, rhythm, and any ischemia or ventricular hypertrophy. -Heart catheterization detects pressure changes in the heart chambers, records pressure differences across the valves, and measures the size of valve openings. Interprofessional Care: -An important aspect of conservative management of valvular heart disease is prophylactic antibiotic therapy to prevent recurrent RF and IE. -Treatment depends on the valve involved and disease severity. -It focuses on preventing exacerbations of HF, acute pulmonary edema, thromboembolism, and recurrent endocarditis. -HF is treated with vasodilators (e.g., nitrates, ACE inhibitors), positive inotropes (e.g., digoxin), β-blockers, diuretics, and a low-sodium diet. -Anticoagulant therapy prevents and treats systemic or pulmonary emboli. -It is used prophylactically in patients with atrial fibrillation. -Atrial dysrhythmias are common and treated with calcium channel blockers, β-blockers, anti-dysrhythmic drugs, or electrical cardioversion. -An alternative treatment for some patients with valvular heart disease is percutaneous transluminal balloon valvuloplasty (PTBV). -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 procedure is done in the heart catheterization laboratory. It involves threading a balloon-tipped catheter from the femoral artery or vein to the stenotic valve. -The balloon is inflated in an attempt to separate the valve leaflets. -A single- or double-balloon technique may be used for the PTBV procedure. -Currently, the use of a single Inoue balloon with hourglass shape allows sequential inflation. -This technique is the most popular because it is easy and has good results with few complications (e.g., left ventricular perforation). -The PTBV procedure is generally indicated for older adults and for those who are poor surgery candidates. -The long-term results of PTBV are similar to surgical commissurotomy. -The decision for surgical intervention depends on the patient's clinical state using the New York Heart Association classification system for functional disability. -The type of surgery can be valve repair or valve replacement. -The procedure that is used depends on the (1) valves involved, (2) pathology and severity of the disease, and (3) patient's clinical condition. -Valve repair is usually the surgical procedure of choice. It has a lower operative mortality rate than valve replacement and is often used in mitral or tricuspid valvular heart disease. -Although valve repair avoids the risks of replacement, it may not restore total valve function. -Mitral commissurotomy (valvulotomy) is the procedure of choice for patients with pure mitral stenosis. -The less precise closed method of commissurotomy has generally been replaced by the open method. -In the closed procedure, the surgeon inserts a dilator through the apex of the left ventricle into the opening of the mitral valve. -The direct vision procedure, or open procedure, requires the use of cardiopulmonary bypass. -The surgeon removes thrombi from the atrium and makes a commissure incision. Next, the fused chordae are separated by splitting the papillary muscle and debriding the calcified valve. -Open surgical valvuloplasty involves repair of the valve by suturing the torn leaflets, chordae tendineae, or papillary muscles. -It is primarily used to treat mitral or tricuspid regurgitation. -Minimally invasive valvuloplasty surgery involves a ministernotomy or parasternal approach. -It may include robotic and thoracoscopic surgical systems. -Results compare with those of the open procedure. -In addition, shorter lengths of stay, fewer blood transfusions, less pain, and lower risk of sternal infection and postoperative atrial fibrillation have been reported. -For patients with mitral or tricuspid regurgitation, further valve repair or reconstruction using annuloplasty is an option. -Annuloplasty involves reconstruction of the annulus, with or without the aid of prosthetic rings. -Valve replacement is also an option -Prosthetic valves are categorized as mechanical or biologic (tissue) valves. -Mechanical valves are manufactured from artificial materials and consist of combinations of metal alloys, pyrolytic carbon, and Dacron. -Biologic valves are constructed from bovine, porcine, and human (cadaver) heart tissue and usually contain some man-made materials. -A "decellularizing" process removes the cadaver cells from the valve. This lowers the risk of immune response and tissue rejection. -Biologic valves are asymmetric in shape and produce a more natural pattern of blood flow compared to mechanical valves. -Asymmetric mechanical valve prototypes are being tested. -Mechanical prosthetic valves are more durable and last longer than biologic valves. However, they have an increased risk of thromboembolism, and require long-term anticoagulation therapy. -The main risk of mechanical valves is bleeding from the use of anticoagulants. -Biologic valves do not require anticoagulation therapy because of their low thrombogenicity. However, they are less durable and tend to cause early calcification, tissue degeneration, and stiffening of the leaflets. -The choice of valves depends on many factors. For example, if a patient cannot take an anticoagulant (e.g., women of childbearing age), a biologic valve is considered. -A mechanical valve may be best for a younger patient because it is more durable. -For patients over age 65, durability is less important than the risks of bleeding from anticoagulants, so most receive a biologic valve. -A wide variety of prosthetic valves are available for use. -Desirable valves are nonthrombogenic and durable, and create minimal stenosis. -Prolonged waiting time for aortic valve replacement is associated with greater mortality, and should be done on a semi-urgent basis. Nursing Implementation: -Diagnosing and treating streptococcal infections and providing prophylactic antibiotics for patients with a history of RF are critical to prevent acquired rheumatic valve disease. The patient at risk for endocarditis and any patient with certain heart conditions must also receive prophylactic antibiotics. -The patient must adhere to ordered therapies. -The person with a history of RF, endocarditis, and congenital heart disease should know the symptoms of valvular heart disease so early medical treatment may begin. -A patient with progressive valvular heart disease may need outpatient care or hospitalization for management of HF, endocarditis, embolic disease, or dysrhythmias. -HF is the most common reason for ongoing medical care. -Your role is to implement therapeutic interventions and evaluate their effects. -Design activities considering the patient's limitations. An appropriate exercise plan can increase cardiac tolerance, but activities that cause fatigue and dyspnea should be limited. -Strenuous physical exercise should be avoided because damaged valves may not handle the increased CO demand. -Develop your patient's care plan to emphasize conserving energy, setting priorities, and taking planned rest periods. -Consider a referral to a vocational counselor if the patient has a physically or emotionally demanding job. -Tobacco use should be discouraged. -Perform ongoing cardiac assessments to monitor the effectiveness of drugs. -The patient on anticoagulation therapy (e.g., warfarin [Coumadin]) after surgery for valve replacement must have the international normalized ratio (INR) checked regularly to determine proper dosage and adequacy of therapy. -INR values of 2.5 to 3.5 are therapeutic for patients with mechanical valves Patient Teaching: -Teach the actions and side effects of drugs to achieve compliance. -The patient must understand the importance of prophylactic antibiotic therapy to prevent IE. If the valve disease was caused by RF, ongoing prophylaxis to prevent recurrence is necessary. -Teach the patient about anticoagulation therapy -Teach the patient when to seek medical care. -Any manifestations of infection, HF, signs of bleeding, and any planned invasive or dental procedures require the patient to notify the health care provider. -When valvular heart disease can no longer be managed medically, surgery is necessary. -The patient must know that valve surgery is not a cure, and that regular follow-up with a HCP is needed. -Finally, encourage patients to obtain and wear a Medic Alert device. Evaluation: Maintain -Adequate tissue and organ perfusion -Achieve fluid and electrolyte balance -Achieve optimal level of activity -Verbalizes understanding of disease process and appropriate measures to prevent complications

acute decompensated heart failure (ADHF)

-Mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results. -Sudden onset of signs and symptoms of HF -Requires urgent medical care -Life threatening condition, both of the ventricles are failing, end organ perfusion is greatly impacted -Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures (universal finding) Clinical Manifestations: -In acute decompensated HF (ADHF), the pulmonary venous pressure increases caused by failure of the LV. This results in engorgement of the pulmonary vascular system. -As a result, the lungs become less compliant, and there is increased resistance in the small airways. To help compensate, the lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. -This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (Pao2). -If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove. Interstitial edema occurs at this point. •Tachypnea develops and the patient becomes symptomatic (e.g., short of breath). -If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema). -As the disruption becomes worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid. -This is accompanied by a worsening of the arterial blood gas values (i.e., lower Pao2 and possible increased partial pressure of carbon dioxide in arterial blood [Paco2] and progressive respiratory acidemia). -Based on hemodynamic and clinical status, patients can be categorized into one of four groups: 1. Dry-warm 2. Dry-cold 3. Wet-warm (most common) 4. Wet-cold -A patient is "wet" due to volume overload (e.g., congestion, dyspnea), but "warm" due to adequate perfusion (warm skin, positive pulses). Pulmonary Edema: -This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid. -The most common cause of pulmonary edema is left-sided HF secondary to CAD. -As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the alveolar-capillary interface. -Increased pulmonary capillary hydrostatic pressure causes fluid to move from the vascular space into the pulmonary interstitial space. -Lymphatic flow increases in an attempt to pull fluid back into the vascular or lymphatic space. -Failure of lymphatic flow and worsening of left heart failure result in further movement of fluid into the interstitial space and into the alveoli. -Most commonly associated with left-sided HF -Clinical manifestations of pulmonary edema are distinct: •The patient has dyspnea and orthopnea (unable to lie flat due to shortness of breath). •Jugular venous distention is often present and is the most sensitive and specific sign for elevated LV filling pressures. •The patient is usually anxious, pale, and possibly cyanotic. •The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. •Respiratory rate is often greater than 30 breaths/minute, and use of accessory muscles to breathe may be seen. •There may be wheezing and coughing with the production of frothy, blood-tinged sputum. •Breath sounds may reveal crackles and wheezes throughout the lungs. •The absence of crackles does not rule out ADHF as many patients with a history of chronic HF develop increased lymphatic drainage of the alveolar edema. •The patient's HR is rapid, and an abnormal S3 or S4 heart sound may be auscultated. •BP may be elevated or decreased depending on the severity of the HF. Diagnostics: -Diagnosing HF is often difficult. -Patient signs and symptoms are not highly specific and may mimic those associated with many other medical conditions (e.g., anemia, lung disease). -A primary goal in diagnosis is to find the underlying cause of HF. -An echocardiogram is a common diagnostic tool used in patients with HF. It provides information on the EF. This helps to differentiate between HFpEF and HFrEF. An echocardiogram also provides information on the structure and function of the heart valves. Heart chamber enlargement or stiffness can also be assessed. -Other useful tests include electrocardiogram (ECG), chest x-ray, 6-minute walk test, multi-gated acquisition (MUGA) scan, cardiopulmonary exercise stress test, and heart catheterization. -Studies for obstructive sleep apnea may be done in select patients. An endomyocardial biopsy (EMB) may be done as part of a heart catheterization in select acutely ill patients who develop unexplained, new onset HF that is unresponsive to usual care -Laboratory studies also aid in the diagnosis of HF. In general, BNP levels correlate positively with the degree of LV failure. -Many agencies routinely measure the N-terminal prohormone of BNP (NT-proBNP). This is a more precise test to aid in the diagnosis of HF. Levels are temporarily higher in patients receiving nesiritide (Natrecor) and may be high in patients with chronic, stable HF. -Increases in BNP or NT-proBNP levels can be caused by conditions other than HF. -These include pulmonary embolism, renal failure, and acute coronary syndrome. Interprofessional Care: -Patients with ADHF need continuous monitoring and assessment. This is done in an intensive care unit (ICU) if the patient is unstable. In the ICU, monitor heart rhythm and oxygen saturation continuously. -Assess vital signs and urine output at least every hour. -The patient may have hemodynamic monitoring, including arterial BP and pulmonary artery pressures. -If a pulmonary artery catheter is placed, evaluate CO and pulmonary artery wedge pressure (PAWP). Therapy is titrated to maximize CO and reduce PAWP. A normal PAWP is generally between 8 and 12 mm Hg. Patients with ADHF may have a PAWP as high as 30 mm Hg. -Provide supplemental oxygen to help increase the percentage of oxygen in inspired air. -In severe pulmonary edema, the patient may need noninvasive positive pressure ventilation (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation. BiPAP is also effective in decreasing preload. -Some patients with ADHF require hospitalization but are more stable. They are often admitted to a telemetry or stepdown unit for treatment. Assess these patients every 4 hours (e.g., vital signs, pulse oximetry) for adequate oxygenation. -Record intake and output and daily weights to evaluate fluid status. -If the patient has dyspnea, place in a high Fowler's position with the feet horizontal in the bed or dangling at the bedside. This position helps decrease venous return because of the pooling of blood in the extremities. This position also increases the thoracic capacity, allowing for improved breathing. -Ultrafiltration (UF), or aquapheresis, is an option for the patient with volume overload. It is a process to remove excess salt and water from the patient's blood. -UF can rapidly remove intravascular fluid volume while maintaining hemodynamic stability. The ideal patients for UF are those with major pulmonary or systemic volume overload who have shown resistance to diuretics and are hemodynamically stable. -UF also may be an appropriate adjunctive therapy for patients with HF and coexisting renal failure. -In the ICU, circulatory assist devices are used to manage patients with worsening HF. The intraaortic balloon pump (IABP) is a device that increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. -The IABP is useful in hemodynamically unstable patients because it decreases pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO. -Ventricular assist devices (VADs) can be used to maintain the pumping action of a heart that cannot effectively pump. A VAD is a mechanical pump that is surgically implanted. -Once the patient is more stable, determination of the cause of ADHF is important. -Diagnosis of systolic or diastolic HF will then direct further treatment protocols. Drug Therapy: -Same for other forms of heart failure

dialysis

-Movement of fluid/molecules across a semipermeable membrane from one compartment to another -Clinically, dialysis is a technique in which substances move from the blood through a semipermeable membrane and into a dialysis solution (dialysate). -Used to correct fluid and electrolyte imbalances and to remove waste products in kidney failure -Can be used to treat drug overdoses -Two methods of dialysis available: •Peritoneal dialysis (PD) •Hemodialysis (HD) -Begun when patient's uremia can no longer be adequately treated conservatively -Initiated when GFR < 15 mL/min/1.73 m2 -In PD the peritoneal membrane acts as the semipermeable membrane. -In HD an artificial membrane (usually made of cellulose-based or synthetic materials) is used as the semipermeable membrane and is in contact with the patient's blood. -This criterion can vary widely in different clinical situations, and the nephrologist determines when to start dialysis based on the patient's clinical status. -Certain uremic complications, including encephalopathy, neuropathies, uncontrolled hyperkalemia, pericarditis, and accelerated hypertension, indicate a need for immediate dialysis. -ESRD treated with dialysis because: •There is a lack of donated organs •Some patients are physically or mentally unsuitable for transplantation •Some patients do not want transplants -An increasing number of individuals, including older adults and those with complex medical problems, are receiving maintenance dialysis. -A patient's chronologic age is not a factor in determining candidacy for dialysis. General Principles of Dialysis: -Diffusion: movement of solutes from an area of greater concentration to an area of lesser concentration -Solutes and water move across the semipermeable membrane from the blood to the dialysate or from the dialysate to the blood in accordance with concentration gradients. -In kidney failure, urea, creatinine, uric acid, and electrolytes (potassium, phosphate) move from the blood to the dialysate with the net effect of lowering their concentration in the blood. -RBCs, WBCs, and plasma proteins are too large to diffuse through the pores of the membrane. -Small-molecular-weight substances can pass from the dialysate into a patient's blood, so the purity of the water used for dialysis is monitored and controlled. -Osmosis: movement of fluid from an area of lesser concentration of solutes to area of greater concentration -Ultrafiltration: water and fluid removal, results when there is an osmotic gradient or pressure gradient across membrane, excess fluid moves into dialysate -Glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood. -In PD, excess fluid is removed by increasing the osmolality of the dialysate (osmotic gradient) with the addition of glucose. -In HD, the gradient is created by increasing pressure in the blood compartment (positive pressure) or decreasing pressure in the dialysate compartment (negative pressure). -Extracellular fluid moves into the dialysate because of the pressure gradient. -The excess fluid is removed by creating a pressure differential between the blood and the dialysate solution with a combination of positive pressure in the blood compartment or negative pressure in the dialysate compartment. Vascular Access Catheter: -Temporary double-lumen vascular access catheter for acute hemodialysis. -Soft, flexible dual-lumen tube is attached to a Y-hub. -The distance between the arterial intake and the venous return lumina typically provides recirculation rates of 5% or less.

myocardial infarction (MI)

-A myocardial infarction occurs because of abrupt stoppage of blood flow through a coronary artery from a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis). -Most MIs occur in the setting of preexisting CAD. -When a thrombus develops, blood flow to the heart muscle beyond the blockage stops, resulting in necrosis. -A STEMI caused by an occlusive thrombus creates ST-elevation in the ECG leads facing the area of infarction. -A STEMI is an emergency situation. In order to limit the infarct size, the artery must be opened within 90 minutes of presentation. -This can be done either by PCI or thrombolytic (fibrinolytic) therapy. PCI is the preferred treatment if a hospital is capable of performing PCI. -NSTEMI, caused by a non-occlusive thrombus, does not cause ST elevation on the 12-lead ECG. -Patients may or may not develop ST-T wave changes in the leads affected by the infarction. -NSTEMI patients do not go to the catheterization laboratory emergently but usually undergo the procedure within 12 to 72 hours if there are no contraindications. -Thrombolytic therapy is not indicated for NSTEMI patients. -With either a NSTEMI or STEMI, an echocardiogram may show hypokinesis (worsening myocardial contractility) or akinesis (absent myocardial contractility) in the necrotic area(s). -The degree of LV dysfunction depends on the area of the heart involved and size of the infarction. Myocardial Infarction from Occlusion: -The acute MI process evolves over time. -The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the heart muscle). -If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness of the heart muscle to become necrosed. -If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as 12 hours. -The majority of MIs affect the LV and are usually described based on the location of damage (e.g., anterior, inferior, lateral, septal, or posterior wall infarction). -The location of the MI and ECG changes correlate with the involved coronary artery. -For example, in most people, the right coronary artery provides blood to the inferior and posterior LV walls. -Blockage of the right coronary artery results in an inferior wall and/or posterior wall MI. -Anterior wall infarctions result from blockages in the left anterior descending artery. -Blockages in the left circumflex artery usually cause lateral LV wall MIs. -Damage can occur in more than one location, especially if more than one coronary artery is involved (e.g., anterolateral MI). -Right ventricular MIs are much less common and treated differently than LV MIs. -Not everyone develops collateral circulation, but if present, the degree of collateral circulation influences the severity of the MI. -An individual with a long history of CAD may develop good collateral circulation to provide the area surrounding the infarction site with a blood supply. This is one reason why a younger person may have a more serious first MI than an older person with the same degree of blockage. Nursing Assessment: -Severe chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. -Persistent and unlike any other pain, it is usually described as heavy, pressure, tight, burning, constricted, or crushing feeling. -Common locations are substernal or epigastric areas. -When epigastric pain is present, the patient may relate it to indigestion and take antacids without relief. -The pain may radiate to the neck, lower jaw, and arms or to the back. -It may occur while the patient is active or at rest, asleep, or awake. -It often occurs in the early morning hours. -It usually lasts for 20 minutes or longer and is more severe than usual anginal pain. -Not everyone who has an MI has classic symptoms. -Some patients may not experience pain but may have "discomfort," weakness, nausea, indigestion, or shortness of breath. -Although women and men have more similarities than differences in their acute MI symptoms, some women may experience atypical discomfort, shortness of breath, or fatigue. -Patients with diabetes may experience silent (asymptomatic) MIs because of cardiac neuropathy or may manifest atypical symptoms (e.g., dyspnea). -An older patient may experience a change in mental status (e.g., confusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia. -During the initial phase of MI, the ischemic heart cells release catecholamines (norepinephrine and epinephrine) that are normally found in these cells. -This results in release of glycogen, diaphoresis, increased HR and BP, and vasoconstriction of peripheral blood vessels. -On physical examination, the patient's skin may be ashen, clammy, and cool to touch. -The patient may experience nausea and vomiting. -These symptoms can result from reflex stimulation of the vomiting center by the severe pain. -They can also result from vasovagal reflexes initiated from the area of the infarcted heart muscle. -The temperature may increase to 100.4° F (38° C) within the first 24-48 hours. The temperature elevation may last for as long as 4-5 days. This increase in temperature is due to a systemic inflammatory process caused by the death of heart cells. -In response to the release of catecholamines, BP and HR may initially increase. -The BP may later drop because of decreased cardiac output (CO). -If severe enough, this may result in decreased renal perfusion and urine output. -Crackles, if present, may persist for several hours to several days, suggesting LV dysfunction. -Jugular venous distention, hepatic engorgement, and peripheral edema may indicate right ventricular dysfunction. -Examination may reveal abnormal heart sounds that may seem distant. -Other abnormal sounds suggesting LV dysfunction are S3 and S4. -In addition, a loud holosystolic murmur may develop. -This may indicate a ventricular septal defect, papillary muscle rupture, or valve dysfunction. -Perform a focused physical assessment for the following clinical manifestations: •Anxiety, fearfulness, restlessness, distress; cool, clammy, pale skin; tachycardia or bradycardia, pulsus alternans (alternating weak and strong heartbeats), pulse deficit, dysrhythmias (especially ventricular), S3, S4, ↑ or ↓ BP, murmur Healing Process: -The body's response to cell death is the inflammatory process. -Within 24 hours, leukocytes infiltrate the area of cell death. -The proteolytic enzymes of the neutrophils and macrophages begin to remove necrotic tissue by the fourth day. -During this time, the necrotic muscle wall is thin. -The necrotic zone of a STEMI is identified by ECG changes (e.g., lowering of the ST-segments, T-wave inversion, pathologic Q wave) within a day or two. -At this point, the neutrophils and monocytes have cleared the necrotic debris from the injured area, and the collagen matrix that will eventually form scar tissue is laid down. -By 6 weeks after MI, scar tissue has replaced necrotic tissue and the injured area is considered healed. -Often, the scarred area is less compliant than the surrounding area. -This condition may be manifested by abnormal wall motion on an echocardiogram or nuclear imaging, LV dysfunction, altered conduction patterns, or heart failure (HF). -These changes in the infarcted heart muscle also cause changes in the unaffected areas. -In an attempt to compensate for the damaged muscle, the normal myocardium will hypertrophy and dilate. -This process is called ventricular remodeling. -Remodeling of normal myocardium can lead to the development of late heart failure (HF), especially in the person with atherosclerosis of other coronary arteries and/or an anterior MI. -ACE inhibitors are given to limit ventricular remodeling. Complications: -Any condition that affects the heart cells' sensitivity to nerve impulses (e.g., ischemia, electrolyte imbalances, SNS stimulation) can cause dysrhythmias that adversely affect the damaged heart muscle. -Dysrhythmias are the most common complication after an MI. They occur in 80% to 90% of patients. -Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common cause of death in patients in the prehospital period. -If a patient survives a cardiac arrest, initiate a therapeutic hypothermia protocol as soon as possible. -Bradycardias (e.g., complete heart block) develop when key areas of the conduction system are destroyed. -VT or VF most often occur within the first 4 hours after the onset of pain, and they are the most common cause of death in the prehospitalization period. -Premature ventricular contractions (PVCs) may precede VT and VF. -Life-threatening ventricular dysrhythmias must be treated immediately. -With reperfusion, it is not uncommon to see PVCs, asymptomatic nonsustained VT, and idioventricular rhythms. -These rhythms are not associated with an increased risk of sudden cardiac death (SCD) and are not treated unless the patient is symptomatic. -Heart failure (HF) is a complication that occurs when the right or left heart's pumping action is reduced. -Depending on the severity and extent of the injury, left-sided HF occurs initially with subtle signs such as mild dyspnea, restlessness, agitation, or slight tachycardia. -Other signs indicating the onset of left-sided HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds on auscultation of the heart, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea. -Signs of right-sided HF include jugular venous distention, hepatic congestion, or lower extremity edema. -Cardiogenic shock occurs when oxygen and nutrients supplied to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction. -Patient is going to die unless you stop it -This occurs less often with the early and rapid treatment of STEMI with PCI or thrombolytic therapy. -When cardiogenic shock does occur, it is associated with a high death rate. -Cardiogenic shock requires aggressive management. This includes control of dysrhythmias, intraaortic balloon pump (IABP) therapy, and support of contractility with vasoactive drugs. -Goals of therapy are to maximize oxygen delivery, reduce oxygen demand, and prevent complications (e.g., acute kidney injury). Papillary Muscle Dysfunction: -May occur if the infarcted area includes or is near the papillary muscle that attaches to the mitral valve. -Papillary muscle rupture is a rare and life-threatening complication. -It causes immediate and massive mitral valve regurgitation with no time for the heart to compensate. -Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium. -This condition aggravates an already damaged LV by reducing CO even further. There is rapid clinical decline of the patient. -Treatment includes afterload reduction with nitroprusside (Nipride) and/or IABP therapy, and immediate cardiac surgery with mitral valve repair or replacement. Left Ventricular Aneurysm: -Results when the infarcted heart wall is thin and bulges out during contraction. This can develop within a few days, weeks, or months. -It is more common with anterior MIs. -The patient with a ventricular aneurysm may experience HF, dysrhythmias, and angina. -Besides ventricular rupture, which is usually fatal, ventricular aneurysms can hide thrombi that can lead to an embolic stroke. -Anticoagulation therapy is recommended for these patients if not contraindicated. -A new loud systolic murmur heard in patients with acute MI may signal ventricular septal wall rupture. -Depending on the size of the defect and degree of right and LV dysfunction, HF and cardiogenic shock may occur. -The patient must receive emergency repair, either surgically or percutaneously. -The defect can quickly expand and lead to hemodynamic compromise. -LV free wall rupture is an emergent clinical situation. Rapid hemodynamic compromise and death ensues if not treated immediately. -Although this is a rare complication, death rates are high. -Free wall rupture is seen more frequently in patients suffering their first MI, patients with anterior MIs, older adults, and women. Acute Pericarditis: -Pericarditis is an inflammation of the visceral and/or parietal pericardium -May occur 2 to 3 days after an acute MI. -Pericarditis is characterized by mild to severe chest pain that increases with inspiration, coughing, and movement of the upper body. -Sitting in a forward position often relieves the pain. -Assess the patient with suspected pericarditis for the presence of a friction rub over the pericardium. -The sound is best heard with the diaphragm of the stethoscope at the mid to lower left sternal border. It may be persistent or intermittent. Fever may also be present. -Diagnosis of pericarditis can be made with serial 12-lead ECGs. Typical ECG changes include diffuse ST-segment elevations. This reflects the inflammation of the pericardium. -Treatment includes pain relief with high doses of aspirin (e.g., 650 mg every 4-6 hours). Serum Cardiac Biomarkers After MI: -Serum cardiac biomarkers are proteins released into the blood from necrotic heart muscle after an MI. -These biomarkers are important in the diagnosis of MI. -Cardiac-specific troponin has two subtypes: cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI). -These biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase (CK-MB). -Serum levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days. -Serial cardiac biomarkers are drawn over 24 hours (e.g., every 8 hours x3). -The presence of biomarkers helps to differentiate between a diagnosis of UA (negative biomarkers) and NSTEMI (positive biomarkers). -CK levels begin to rise at about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours. -The CK enzymes are fractionated into bands. The CK-MB band is specific to heart muscle cells and help to quantify myocardial damage. -Myoglobin is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours. -Although it is one of the first serum cardiac biomarkers to appear after an MI, it lacks cardiac specificity. Its role in diagnosing MI is limited

urinary tract calculi

-1 to 2 million in United States have nephrolithiasis -More common in men -Average age at onset: 20-55 years -Increased incidence: •White persons •Family history of stone formation •Previous history •Summer months -Except for struvite (magnesium ammonium phosphate) stones associated with UTI, stone disorders are more common in men than in women. -Stone formation is more frequent in white persons than in African Americans. -The incidence is also higher among persons with a family history of stone formation. -Stones can recur in up to 50% of patients. -Stone formation occurs more often in the summer months, thus supporting the role of dehydration in this process. Etiology and Pathophysiology: -No single theory for all cases -Factors involved: •Metabolic •Genetic •Climatic •Lifestyle •Occupational influences -Crystals, when in a supersaturated concentration, can precipitate and unite to form a stone. -Keeping urine dilute and free flowing reduces the risk of recurrent stone formation in many individuals. -The term calculus refers to the stone, and lithiasis refers to stone formation. Types: -Calcium phosphate -Calcium oxalate -Uric acid -Cystine -Struvite (magnesium ammonium phosphate): the worst -Although calcium stones are the most common, stone composition may be mixed. History: -Previous episodes -Prescribed and OTC medications -Dietary supplements -Family history Clinical Manifestations: -Can be found in various locations in the urinary tract -Renal colic: •Sudden severe pain due to obstruction •Flank area, back, or lower abdomen -Common sites of obstruction: •Ureteropelvic junction (UPJ): dull pain in costovertebral flank, renal colic •Ureterovesicular junction (UVJ) -"Kidney stone dance": patients with renal colic have a hard time being still; they go from walking to sitting to lying down, and then they repeat the process -Mild shock with cool, moist skin -Pain moves to lower quadrant of abdomen as stone nears UVJ -Testicular versus labial pain -Both sexes experience groin pain -UTI symptoms: dysuria, fever, chills Diagnostics: -Noncontrast helical (spiral) CT: commonly used in patients with renal colic; quick and noninvasive, requires no IV contrast -Ultrasound used in some situations -Complete urinalysis to assess for: •Hematuria •Crystalluria •Urinary pH: useful in the diagnosis of struvite stones and renal tubular acidosis (tendency for alkaline or high pH) and uric acid stones (tendency for acidic or low pH). -Retrieval and analysis of stones -Patients who form stones recurrently should have a 24- hour urinary measurement of serum calcium, phosphorus, sodium, potassium, magnesium, oxalate, citrate, sulfate, bicarbonate, uric acid, BUN, creatinine, and total volume Interprofessional Care: -Acute attack: •Treat renal colic pain: opioids •Infection •Obstruction: -Tamsulosin (Flomax) and Terazosin (Hytrin): α-adrenergic blockers that relax the smooth muscle in the ureter, can be used to facilitate stone passage by relaxing the smooth muscle in the ureters. -These drugs may also relax the muscle of the prostate in men with benign prostatic hyperplasia (BPH). -Assessment of cause Evaluation of Cause of Stone Formation: -Family history of stone formation -Geographic location -Nutritional assessment: intake of vitamins A and D -Activity pattern: active or sedentary -History of prolonged illness with immobilization or dehydration, -Any history of disease or surgery involving the GI or GU tract Teaching: -Adequate hydration -Dietary sodium restrictions -Dietary changes -Drugs to minimize stone formation Treatment of Struvite Stones: -Antibiotics to control infection: may be difficult to control infection if the stone remains in place -Acetohydroxamic acid: may be used to treat kidney infections that result in the continual formation of struvite stones. Acetohydroxamic acid inhibits the chemical action caused by the persistent bacteria and thus retards struvite stone formation. -Surgical removal of stone if the infection cannot be controlled Indications for endourology, lithotripsy, or open surgical stone removal include: -Stones too large for passage -Stones associated with bacteriuria -Causing impairment in renal function -Causing persistent pain, nausea, or paralytic ileus Surgeries: -If the stone is located in the bladder, a cystoscopy is done to remove small stones (endourologic procedure). •Flexible ureteroscopes, inserted via a cystoscope, can be used to remove stones from the renal pelvis and upper urinary tract. -For large stones, a cystolitholapaxy is done. In this procedure, large stones can be broken up with an instrument called a lithotrite (stone crusher). •The bladder is then irrigated and the crushed stones washed out. -In a cystoscopic lithotripsy, an ultrasonic lithotrite is used to pulverize (break up) stones. -Laser lithotripsy is used to fragment ureteral and large bladder stones. •A ureteroscope is used to get close to the stone. •A small fiber is inserted up the endoscope so that the tip (which emits the laser energy) can come in contact with the stone. •A holmium laser in direct contact with the stone is commonly used to break up the stone. -In extracorporeal shock-wave lithotripsy (ESWL), the patient receives anesthetic (spinal or general) to ensure that the patient's position is maintained during the procedure. •Fluoroscopy or ultrasound is used to focus the lithotripter on the affected kidney, and a high-voltage spark generator produces high-energy acoustic shock waves that shatter the stone without damaging the surrounding tissues. •The stone is broken into fine sand (steinstrasse) and excreted in the urine. -In percutaneous ultrasonic lithotripsy, an ultrasonic probe is placed in the renal pelvis via a percutaneous nephroscope inserted through a small incision in the flank, and the probe is then positioned against the stone. •The patient is given general or spinal anesthetic, and the probe produces ultrasonic waves, which break the stone into sandlike particles. -In electrohydraulic lithotripsy, the probe is positioned directly on a stone, but it breaks the stone into small fragments that are removed by forceps or by suction. •A continuous saline irrigation flushes out the stone particles, and all of the outflow drainage is strained so that the particles can be analyzed. •The calculi can also be removed by basket extraction. -In percutaneous nephrolithotomy, a nephroscope is inserted into the renal pelvis through a track (with the use of a sheath) in the skin in the patient's back. •The kidney stones can be fragmented with ultrasonic, electrohydraulic, or laser lithotripsy. •The stone fragments are removed, and the pelvis is irrigated. -Pyelolithotomy -Ureterolithotomy -Cystotomy Nutritional Therapy: -To manage an obstructing stone, the patient should drink adequate fluids to avoid dehydration. -Forcing excessive fluids is not advised because this has not proved effective in facilitating spontaneous "passage" (excretion) of stones via the urine, and it may also increase the pain or precipitate the development of renal colic. -Increasing the fluid intake is particularly important for patients at risk for dehydration, including those who (1) are active in sports, (2) live in a dry climate, (3) perform physical exercise, (4) have a family history of stone formation, and/or (5) work outside or in an occupation that requires a great deal of physical activity. -Water is the preferred fluid. -Consumption of colas, coffee, and tea should be limited because high intake of these beverages tends to increase rather than diminish the risk of recurring urinary calculi. -A low-sodium diet is recommended because high sodium intake increases calcium excretion in the urine. Planning: -Relief of pain -No urinary tract obstruction -Knowledge of ways to prevent recurrence of stones Nursing Implementation: -Adequate fluid intake is important to produce a urine output of approximately 2 L/day. -Moderately active, ambulatory persons should drink about 3 L/day. -Fluid intake will need to be higher in the active person who works outdoors or who regularly engages in athletic activities. -Dietary restriction of purines may be helpful for the patient at risk for developing uric acid stones. -Teach the patient the dosage, scheduling, and potential side effects of drugs used to reduce the risk of stone formation -Some patients may be taught to self-monitor urinary pH, or urinary output. -Pain management and patient comfort are primary nursing responsibilities in managing an obstructing stone and renal colic -To ensure that any spontaneously passed stones are retrieved, strain all urine voided by the patient, using gauze or a urine strainer. -Encourage ambulation to promote movement of the stone from the upper to the lower urinary tract. -To ensure safety, tell the patient who is experiencing acute renal colic to ask for assistance when ambulating, particularly if opioid analgesics are being given.

asystole

-Asystole represents the total absence of ventricular electrical activity. -Occasionally, P waves are seen. -No ventricular contraction occurs because depolarization does not occur. -Patients are unresponsive, pulseless, and apneic. -Asystole is a lethal dysrhythmia that requires immediate treatment. -Always assess the rhythm in more than one lead. -The prognosis of a patient with asystole is extremely poor. -Asystole is usually a result of advanced heart disease, a severe cardiac conduction system disturbance, or end-stage HF. -Generally the patient with asystole has end-stage heart disease or has a prolonged arrest and cannot be resuscitated. -Treatment consists of CPR with initiation of ACLS measures. -These include definitive drug therapy with epinephrine and/or vasopressin, and intubation.

sudden cardiac death

-Death from a cardiac cause -Majority of SCDs result from ventricular dysrhythmias: •Ventricular tachycardia •Ventricular fibrillation -Prodysrhythmia: •Life-threatening dysrhythmias caused by antidysrhythmia drugs •Severe LV dysfunction increases risk •Digoxin and class IA, IC, and III antidysrhythmia drugs -Most susceptible first few days of drug therapy: •Monitored in-patient for several days

Torsades de Pointes

-French for "twisting of the points" -Polymorphic VT associated with a prolonged QT interval of the underlying rhythm. -May be med-related -Treatment same as VT but also include magnesium as treatment: reduces irritability

normal sinus rhythm

-Normal sinus rhythm refers to a rhythm that starts in the SA node at a rate of 60 to 100 times per minute and follows the normal conduction pathway. -Rhythm is regular. -The P wave precedes each QRS complex and has a normal shape and duration. -The PR interval is normal, and the QRS complex has a normal shape and duration.

nursing management for chronic stable angina and ACS

-Obtain the following health information from the patient: •Past health history: previous history of CAD, chest pain/angina, MI, valve disease (e.g., aortic stenosis), heart failure, or cardiomyopathy; hypertension, diabetes, anemia, lung disease; hyperlipidemia -Drugs: use of antiplatelets/ anticoagulants, nitrates, angiotensin-converting enzyme inhibitors, β-adrenergic blockers, calcium channel blockers; antihypertensive drugs; lipid-lowering drugs; over-the-counter drugs (e.g., vitamin and herbal supplements) -History of present illness: description of events related to current illness, including any self-treatments and response. -Also obtain the following important health information related to pertinent functional health patterns: •Health perception-health management: family history of heart disease; sedentary lifestyle; tobacco use; exposure to environmental smoke •Nutritional-metabolic: indigestion, heartburn, nausea, belching, vomiting •Elimination: urinary urgency or frequency, straining at stool •Activity-exercise: palpitations, dyspnea, dizziness, weakness •Cognitive-perceptual: substernal chest pain or pressure (squeezing, constricting, aching, sharp, tingling), possible radiation to jaw, neck, shoulders, back, or arms •Coping-stress tolerance: stressful lifestyle, depression; anger, anxiety; feeling of impending doom Nursing Diagnoses: -Decreased cardiac output related to altered contractility and altered heart rate and rhythm -Acute pain related to an imbalance between myocardial oxygen supply and demand -Anxiety related to perceived or actual threat of death, pain, and/or possible lifestyle changes -Activity intolerance related to general weakness secondary to decreased cardiac output and poor lung and tissue perfusion -Ineffective health management related to lack of knowledge of disease process, risk factor reduction, rehabilitation, home activities, and medications Planning (overall goals): -Relief of pain -Preservation of heart muscle -Immediate and appropriate treatment -Effective coping with illness-associated anxiety -Participation in a rehabilitation plan -Reduction of risk factors

paroxysmal supraventricular tachycardia (PSVT)

-Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His. -Identification of the ectopic focus is often difficult even with a 12-lead ECG as it requires recording the dysrhythmia as it starts. -The HR is 150 to 220 beats/minute, and the rhythm is regular or slightly irregular. -The P wave is often hidden in the preceding T wave. If seen, it may have an abnormal shape. -The PR interval may be shortened or normal, and the QRS complex is usually normal. -PSVT occurs because of a reentrant phenomenon (reexcitation of the atria when there is a one-way block). -Usually a PAC triggers a run of repeated premature beats. -Paroxysmal refers to an abrupt onset and ending. -Termination is sometimes followed by a brief period of asystole (absence of all cardiac electrical activity). -In the normal heart, PSVT is associated with overexertion, emotional stress, deep inspiration, and stimulants such as caffeine and tobacco. -PSVT is also associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale. Clinical Manifestations: -Clinical significance of PSVT depends on the associated symptoms -HR is 150-220 beats/minute (add for clarification) -Prolonged episode of HR > 180 leads to decreased cardiac output and stroke volume -Hypotension -Dyspnea -Angina Treatment: -Treatment for PSVT includes vagal stimulation and drug therapy. -Common vagal maneuvers include Valsalva, carotid massage, and coughing. -IV adenosine (Adenocard) is the first drug of choice to convert PSVT to a normal sinus rhythm. This drug has a short half-life (10 seconds) and is well tolerated by most patients. -IV β-blockers (e.g., sotalol [Betapace]), calcium channel blockers (e.g., diltiazem [Cardizem]), and amiodarone (Cordarone) can also be used. -If vagal stimulation and drug therapy are ineffective and the patient becomes hemodynamically unstable, direct current (DC) cardioversion is used. -Give chemicals first: 6 mg of adenosine helps to rest the heart rate -After chemicals, then give shock -If taken for a long period of time, amiodarone hurts the cardiac muscle

nervous system control of heart

-The autonomic nervous system plays an important role in the rate of impulse formation, speed of conduction, and strength of cardiac contraction. -The components of the autonomic nervous system that affect the heart are the vagus nerve fibers of the parasympathetic nervous system and nerve fibers of the sympathetic nervous system. -Stimulation of the vagus nerve causes a decreased rate of firing of the SA node and slowed impulse conduction of the AV node. -Stimulation of the sympathetic nerves increases SA node firing, AV node impulse conduction, and cardiac contractility.

pacemakers

-The artificial cardiac pacemaker is an electronic device used to pace the heart when the normal conduction pathway is damaged. -The basic pacing circuit consists of a power source (battery-powered pulse generator) with programmable circuitry, one or more pacing (conducting) leads, and the myocardium. -The electrical signal (stimulus) travels from the pulse generator, through the leads, to the wall of the myocardium. The heart muscle is "captured" and stimulated to contract -Current pacemakers are small, sophisticated, and physiologically precise. -They pace the atrium and/or one or both of the ventricles. -Fixed pacemakers always have a consistent rate -Most pacemakers are demand pacemakers. This means that they sense the heart's electrical activity and fire only when the HR drops below a preset rate. -Demand pacemakers have two distinct features: (1) a sensing device that inhibits the pacemaker when the HR is adequate and (2) a pacing device that triggers the pacemaker when no QRS complexes occur within a preset time period. -In addition to antibradycardia pacing, devices now include antitachycardia and overdrive pacing. -Antitachycardia pacing involves the delivery of a stimulus to the ventricle to end tachydysrhythmias (e.g., VT). -Overdrive pacing involves pacing the atrium at rates of 200 to 500 impulses/minute in an attempt to terminate atrial tachycardias (e.g., atrial flutter with a rapid ventricular response). -A permanent pacemaker is implanted totally within the body. -The power source is placed subcutaneously, usually over the pectoral muscle on the patient's nondominant side. -The pacing leads are placed transvenously to the right atrium and/or one or both ventricles and attached to the power source. -This graphic displays a dual-chamber rate-responsive pacemaker from Medtronic, Inc. -Pacing leads in both the atrium and the ventricle enable a dual-chamber pacemaker to sense and pace in both heart chambers. -Permanent pacemakers are inserted to treat patients with chronic heart problems in which the heart beats too slowly to adequately support the body's circulation (i.e., AV heart blocks, sick sinus syndrome, atrial fibrillation with slow ventricular response, severe heart failure, cardiomyopathy, bundle branch block). -New technology and research are focused on miniaturized, leadless permanent pacemakers. -Most candidates for the new device are patients who need single-chamber pacing for atrial fibrillation with AV block. -The device is placed in the right ventricle. -The lack of a transvenous lead and subcutaneous pulse generator is a major shift in cardiac pacing. Temporary Pacemakers: -A temporary pacemaker is one that has the power source outside the body. -Temporary pacemakers are attached to a programmable external power source. -There are three types of temporary pacemakers: transvenous, epicardial, and transcutaneous: •Transvenous: through central line •Epicardial: through chest wall post surgery •Transcutaneous: through skin in emergency Epicardial Pacing: -Epicardial pacing involves attaching an atrial and ventricular pacing lead to the epicardium during heart surgery. -The leads are passed through the chest wall and attached to the external power source. -Epicardial pacing leads are placed prophylactically in case any bradydysrhythmias or tachydysrhythmias occur in the early postoperative period. Transcutaneous Pacing: -A transcutaneous pacemaker (TCP) is used to provide adequate HR and rhythm to the patient in an emergency situation. -Placement of the TCP is a noninvasive, temporary procedure used until a transvenous pacemaker is inserted or until more definitive therapy is available. -The TCP consists of a power source and a rate, and voltage-control device that attaches to two large, multifunction electrode pads. -Position one pad on the anterior part of the chest, usually on the V4 lead position, and the other pad on the back between the spine and the left scapula at the level of the heart. -When programming the TCP, always use the lowest current that results in a ventricular contraction (capture) to minimize patient discomfort. -Before starting TCP therapy, it is important to tell the patient what to expect. -Explain that the muscle contractions created by the pacemaker when the current passes through the chest wall are uncomfortable. -Reassure the patient that the TCP is temporary and that it will be replaced with a transvenous pacemaker as soon as possible. -Whenever possible, provide analgesia and/or sedation while the TCP is in use. -The TCP consists of a power source and a rate- and voltage-control device that attaches to two large, multifunction electrode pads. -Position one pad on the anterior part of the chest, usually on the V4 lead position, and the other pad on the back between the spine and the left scapula at the level of the heart. -The pads can be used for both pacing and defibrillation. -Patients with temporary or permanent pacemakers will be ECG monitored to evaluate the status of the pacemaker. -Pacemaker malfunction primarily involves a failure to sense or a failure to capture. -Failure to sense occurs when the pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately. •This can result in the pacemaker firing during the excitable period of the cardiac cycle resulting in VT. •Failure to sense is caused by fibrosis around the tip of the pacing lead, battery failure, sensing set too high, or dislodgement of the electrode. -Failure to capture occurs when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction. •This lack of pacing when needed can result in serious bradycardia or asystole. •Failure to capture is caused by pacer lead damage, battery failure, dislodgement of the electrode, electrical charge set too low, or fibrosis at the electrode tip. -Failure to capture pacer spike: charge was delivered, but you didn't get anything -Complications of invasive temporary (i.e., transvenous) or permanent pacemaker insertion include infection and hematoma formation at the insertion site, pneumothorax, failure to sense or capture, perforation of the atrial or ventricular septum by the pacing lead, lead misplacement, and appearance of "end-of-life" battery power on testing the pacemaker. -Several measures can prevent or assess for complications. These include prophylactic IV antibiotic therapy before and after insertion, post-insertion chest x-ray to check lead placement and to rule out the presence of a pneumothorax, careful observation of insertion site, and continuous ECG monitoring of the patient's rhythm. Postprocedure Care: -After the pacemaker has been inserted, the patient can be out of bed once stable. -Have the patient limit arm and shoulder activity on the operative side to prevent dislodging the newly implanted pacing leads. -Observe the insertion site for signs of bleeding and check that the incision is intact. -Note any temperature elevation or pain at the insertion site and treat as ordered. -Most patients are discharged the next day if stable. -Patient teaching is important

implantable cardioverter-defibrillator (ICD)

-The implantable cardioverter-defibrillator (ICD) is an important technology for patients who (1) have survived SCD, (2) have spontaneous sustained VT, (3) have syncope with inducible ventricular tachycardia/ fibrillation during EPS, and (4) are at high risk for future life-threatening dysrhythmias (e.g., have cardiomyopathy). -The use of ICDs has significantly decreased heart mortality rates in these patients. -The ICD consists of a lead system placed via a subclavian vein to the endocardium. -A battery-powered pulse generator is implanted subcutaneously, usually over the pectoral muscle on the patient's nondominant side. -The pulse generator is similar in size to a pacemaker. Most systems are single-lead systems. -The ICD sensing system monitors the HR and rhythm, and identifies VT or VF. -After the sensing system detects a lethal dysrhythmia, the device delivers a 25-joule or less shock to the patient's heart. -If the first shock is unsuccessful, the device recycles and can continue to deliver shocks. -In addition to defibrillation capabilities, ICDs are equipped with antitachycardia and antibradycardia pacing capabilities. -These devices use algorithms that detect dysrhythmias and determine the appropriate response. -They can initiate overdrive pacing of supraventricular and ventricular tachycardias, sparing the patient painful defibrillator shocks. -They also provide backup pacing for bradydysrhythmias that may occur after defibrillation discharges. -Preprocedure and postprocedure nursing care of the patient undergoing ICD placement is similar to the care of a patient undergoing permanent pacemaker implantation (discussed shortly). -Recent research has focused on a totally subcutaneous ICD (S-ICD). -The S-ICD pulse generator is placed under the skin on the left side of the chest and the electrode is placed under the skin above the sternum. -The system delivers a shock when VT or VF is detected. -Since the S-ICD does not have any electrodes implanted in the heart, it has no pacing capability. -Patients experience a variety of emotions. These include fear of body image change, fear of recurrent dysrhythmias, expectation of pain with ICD discharge (described as a feeling of a blow to the chest), and anxiety about going home. -Encourage patients and caregivers to participate in local or online ICD support groups Patient and Caregiver Teaching: 1. Follow up with a HCP for routine checks of the function of the ICD. This is often done by interrogating the device using a telephone. 2. Report any signs of infection at incision site (e.g., redness, swelling, drainage) or fever to your HCP immediately. Keep incision dry for 4 days after insertion or as instructed. 3. Avoid lifting arm on ICD side above shoulder until approved. 4. Discuss resuming sexual activity with your HCP. It is usually safe to resume sexual activity once your incision is healed. 5. Avoid driving until cleared by your HCP. This decision is usually based on the ongoing presence of dysrhythmias, the frequency of ICD firings, your overall health, and state laws regarding drivers with ICDs. 6. Avoid direct blows to ICD site. 7. Avoid large magnets and strong electromagnetic fields because these may interfere with the device. You should not have a magnetic resonance imaging (MRI) scan unless the ICD is approved as MRI safe or there is a protocol in place for patient safety during the procedure. 8. Travel is not restricted. Inform security (e.g., airport, train station, public buildings) of presence of ICD because it may set off the metal detector. If hand-held screening wand is used, it should not be placed directly over the ICD. Manufacturer information may vary regarding the effect of metal detectors on the function of the ICD. 9. Avoid standing near antitheft devices in doorways of stores and public buildings. You should walk through them at a normal pace. 10. If your ICD fires, call your HCP immediately. •If your ICD fires and you feel sick, contact the emergency medical services (EMS) system. •If your ICD fires more than once, contact EMS. 11. You should obtain and wear a Medic Alert ID device at all times. 12. Always carry the ICD identification card and a current list of your drugs. 13. Consider joining an ICD support group. 14. Caregivers should learn cardiopulmonary resuscitation (CPR).

pericarditis

-An inflammatory process of the pericardial sac -The pericardial sac contains 10 to 15 mL of serous fluid -The pericardium serves as an anchoring function and provides lubrication to decrease friction between heart contractions -Pericarditis can be transmitted through a virus, fungus, or bacteria -When pericarditis goes into the heart, it is known as endocarditis Infectious Causes: -Viral (ex: COVID can cause pericarditis) -Bacterial -Fungal Noninfectious Causes: -Renal failure -Acute myocardial infarction -Neoplasms (cancer) -Trauma -Radiation -Dissecting aortic aneurysm -Myxedema Hypersensitive or Autoimmune Causes: -Dressler syndrome -Rheumatic fever -Drug reactions: procainamide, hydralazine •Procainamide is used for dysrhythmias, but it prolongs the QT and decreases the contractility of the heart Clinical Manifestations/ Complications: -Progressive frequent severe, sharp chest pain; worse when lying flat or with deep inspiration -Pain that radiates to the neck, arms, or left shoulder -The hallmark finding is the PERICARDIAL FRICTION RUB -Cardiac tamponade, pericardial effusion increases in volume resulting in compression of the heart -Phrenic nerve compression can cause hiccups and compression of the laryngeal nerve -Pericardial effusion build up of fluid in the pericardium -Pericardial tamponade: too much fluid-compression-reduced cardiac filling and less output -Tamponade: occurs when extra fluid builds up in the pericardium; measured with hemodynamic monitoring, catheter is put in the right atrium -Assesses if the chambers of the heart have too much fluid or not enough -Patients with pericarditis often don't want to lay flat Diagnostic Studies: -ECG changes, ST changes -Echocardiogram -CT and/or MRI -CRP, CBC, ESR -Pericardiocentesis: relieves tamponade-samples of fluid for testing Interprofessional Care: -Identify causes; think about why we would use these medications -Antibiotics to treat bacterial pericarditis -NSAIDS -Corticosteroids -Pericardiocentesis -Pericardial window for persisting fluid or tamponade Nursing Management: -Management of pain and anxiety -Client on bedrest with head of bed 45 degrees -Administer medications as ordered.

aortic valve regurgitation

-Aortic regurgitation (AR) may be the result of primary disease of the aortic valve leaflets, the aortic root, or both. -Trauma, IE, or aortic dissection can cause acute AR and constitutes a life-threatening emergency. -Chronic AR is generally the result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions, such as ankylosing spondylitis or reactive arthritis. -AR causes retrograde (backward) blood flow from the ascending aorta into the left ventricle during diastole. This results in volume overload. -The left ventricle initially compensates for chronic AR by dilation and hypertrophy. -Myocardial contractility eventually declines and blood volume in the left atrium and pulmonary bed increases. -This leads to pulmonary hypertension and right ventricular failure. Clinical Manifestations of Acute AR: -Sudden signs of cardiovascular collapse -Severe dyspnea -Chest pain -Hypotension, indicating left ventricular failure -Cardiogenic shock, a life-threatening emergency Clinical Manifestations of Chronic AR: -May be asymptomatic for years -Exertional dyspnea, orthopnea, paroxysmal dyspnea -Angina -"Water-hammer" pulse if severe -Soft or absent S1 -S3 or S4 -Murmur

atrial flutter

-Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium or, less commonly, the left atrium. -Atrial rate is 200 to 350 beats/minute. -The ventricular rate will vary based on the conduction ratio. In 2:1 conduction, the ventricular rate is typically found to be approximately 150 beats/minute. -Atrial rhythm is regular, and ventricular rhythm is usually regular. -The PR interval is variable and not measurable. -The QRS complex is usually normal. -Because the AV node can delay signals from the atria, there is usually some AV block in a fixed ratio of flutter waves to QRS complexes. -Atrial flutter rarely occurs in a healthy heart. It is associated with CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism, and the use of drugs such as digoxin, quinidine, and epinephrine. -The high ventricular rates (greater than 100 beats/minute) and loss of the atrial "kick" (atrial contraction reflected by a sinus P wave) that are associated with atrial flutter decrease CO. -This can cause serious consequences such as HF, especially in the patient with underlying heart disease. -Patients with atrial flutter have an increased risk of stroke because of the risk of thrombus formation in the atria from the stasis of blood. -Warfarin (Coumadin) is given to prevent stroke in patients who have atrial flutter. Treatment: -The primary goal in treatment of atrial flutter is to slow the ventricular response by increasing AV block. -Drugs used to control ventricular rate include calcium channel blockers (such as diltiazem) and β-blockers. -Antidysrhythmia drugs are used to convert atrial flutter to sinus rhythm (e.g., ibutilide [Corvert]) or to maintain sinus rhythm (e.g., amiodarone, flecainide [Tambocor], dronedarone [Multaq]). -Electrical cardioversion may be performed to convert the atrial flutter to sinus rhythm in an emergency (i.e., the patient is hemodynamically unstable) and electively. -Radiofrequency catheter ablation is the treatment of choice for atrial flutter. -The procedure is done in the EP laboratory and involves placing a catheter in the right atrium. -Using a low-voltage, high-frequency form of electrical energy, the ectopic foci are ablated (or destroyed), the dysrhythmia is ended, and normal sinus rhythm is restored.

aortic valve stenosis

-Congenital aortic stenosis is generally found in childhood, adolescence, or young adulthood. -In older adults, aortic stenosis (AS) is a result of RF or degeneration. -AS due to rheumatic heart disease accompanies mitral valve disease. -Isolated AS is usually nonrheumatic in origin. -The incidence of rheumatic aortic valve disease has been decreasing, but degenerative stenosis is increasing as the population ages. -AS causes obstruction of blood flow from the left ventricle to the aorta during systole. -The effect is left ventricular hypertrophy and increased myocardial oxygen consumption because of the increased myocardial mass. -As the disease progresses and compensatory mechanisms fail, reduced CO leads to decreased tissue perfusion, pulmonary hypertension, and HF. -Left untreated, severe AS has approximately a 50% mortality rate at one year. Clinical Manifestations: -Manifestations of AS develop when the valve orifice becomes about one third its normal size. -Classic Triad: •Angina •Syncope •Exertional dyspnea -Reflects left ventricular failure -Auscultatory Findings: •Normal to soft S1 •Diminished or absent S2 •Systolic murmur •Prominent S4 -The prognosis is poor for patients who exhibit manifestations and whose valve obstruction is not fixed. -Nitroglycerin is used cautiously to treat angina as it can significantly reduce preload and BP and can worsen chest pain.

circulatory assist devices (CADs)

-Decrease cardiac work and improve organ perfusion -Drug therapy is no longer adequate -Provide interim support when: •Recovering from acute injury •Stabilizing before surgical repair •Awaiting heart transplantation -Types: •Intraaortic Balloon Pump (IABP) •Ventricular Assist Devices (VAD) •Implantable Artificial Heart Intraaortic Balloon Pump (IABP): -Provides temporary circulatory assistance by reducing afterload inserted in femoral artery -Benefits: •Decreased ventricular workload •Increased myocardial perfusion •Augment circulation -Temporary use only -During systole the balloon is deflated, which helps with ejection of blood into the periphery. -In early diastole, the balloon begins to inflate. -In late diastole, the balloon is totally inflated, which augments aortic pressure and increases the coronary perfusion pressure. -This increases coronary and cerebral blood flow. -Complications: 1)Thrombus and embolus formation 2)Thrombocytopenia 3)Ischemia to periphery, kidneys, bowel 4)Infection 5)Mechanical malfunction: •Improper timing of balloon inflation •Balloon leak •Malfunction of balloon or console Ventricular Assist Devices (VADs): -Short- and long-term support for failing heart -Bridge while awaiting transplant -Allows more mobility and longer term than IABP -Shunts blood from left atrium or ventricle to device, then to the aorta -Internal or external -Types: left, right, or biventricular -A VAD is a pump that we use for patients who have reached end-stage heart failure. -We surgically implant the LVAD, a battery-operated, mechanical pump, which then helps the left ventricle (main pumping chamber of the heart) pump blood to the rest of the body -LVADs can be used as bridge-to-transplant therapy: this is a life-saving therapy for patients awaiting a heart transplant. -Patients use the LVAD until a heart becomes available. In some cases, the LVAD is able to restore the failing heart, eliminating the need for a transplant. -Destination therapy: some patients are not candidates for heart transplants. -In this case, patients can receive long-term treatment using an LVAD, which can prolong and improve patients' lives -Patients undergo a screening process to see if this treatment is an appropriate option for the individual. -There are also artificial implantable hearts available for a specific patient population. Implantable Artificial Heart: -Fully implantable device -Can sustain the body's circulatory system: •Bridge to transplantation •Replacement for heart in patient not eligible for transplant -Risks: •Infection •Thrombus •Stroke CADs Nursing Management: -Goals: •Recovery through ventricular improvement •Receive artificial heart •Heart transplantation -Many patients die or choose to no longer seek treatment, causing death -Emotional support for patient and caregiver essential -Frequent assessments and observe for complications -Patient may be mobile and will require an activity plan -In-depth teaching if discharged to home

defibrillation

-Defibrillation is the treatment of choice to end VF and pulseless VT. -It is most effective when the myocardial cells are not anoxic or acidotic. -Rapid defibrillation (within 2 minutes) is critical to a successful patient outcome. -Defibrillation involves the passage of an electric shock through the heart to depolarize the myocardial cells. -The goal is that the following repolarization of heart cells will allow the SA node to resume the role of pacemaker. -Defibrillators deliver energy using a monophasic or biphasic waveform. -Monophasic defibrillators deliver energy in one direction, and biphasic defibrillators deliver energy in two directions. -Biphasic defibrillators deliver shocks at lower energies and with fewer postshock ECG dysrhythmias than monophasic defibrillators. -LifePak contains a monitor, defibrillator, and transcutaneous pacemaker. -An automatic external defibrillator (AED) is a defibrillator that has rhythm detection capability and the ability to advise the operator to deliver a shock using hands-free defibrillator pads. -Proficiency in the use of the AED is a part of the basic life support course for HCPs. -You should be familiar with the operation of the type of defibrillator used in your clinical setting. -The following general steps are taken for defibrillation: 1. CPR should be in progress until the defibrillator is available. 2. Turn the defibrillator on, and select the proper energy level. 3. Check to see that the synchronizer switch is turned off. 4. Apply conductive materials (e.g., defibrillator gel pads) to the chest, one to the right of the sternum just below the clavicle, and the other to the left of the apex. 5. Charge the defibrillator using the button on the defibrillator or the paddles. 6. Position the paddles firmly on the chest wall over the conductive material. 7. Call and look to see that everyone is "all clear" to ensure that staff are not touching the patient or the bed at the time of discharge. 8. Deliver the charge by depressing buttons on both paddles simultaneously. -Hands-free, multifunction defibrillator pads are available and are placed on the chest as described above. -Connect the cables from the pads to the defibrillator. -Charge and discharge the defibrillator using buttons on the defibrillator. -It is still essential that you ensure that all staff are clear before the defibrillator is discharged.

tricuspid valve stenosis

-Diseases of the tricuspid and pulmonic valves are uncommon, with stenosis occurring more frequently than regurgitation. -Tricuspid stenosis occurs almost exclusively in patients with RF or who abuse IV drugs. -Tricuspid stenosis results in right atrial enlargement and elevated systemic venous pressures. -Clinical manifestations: peripheral edema, ascites, hepatomegaly; diastolic low-pitched murmur with increased intensity during inspiration

dysrhythmias

-Dysrhythmias result from disorders of impulse formation, conduction of impulses, or both. -The heart has specialized cells in the SA node, atria, AV node, and bundle of His and Purkinje fibers (His-Purkinje system), which can fire (discharge) spontaneously. -Normally, the SA node is the pacemaker of the heart. It spontaneously fires 60 to 100 times per minute. -A secondary pacemaker from another site may fire in two ways. -If the SA node fires more slowly than a secondary pacemaker, the electrical signals from the secondary pacemaker may "escape." -The secondary pacemaker will then fire automatically at its intrinsic rate. -These secondary pacemakers may start from the AV node at a rate of 40 to 60 times per minute or the His-Purkinje system at a rate of 20 to 40 times per minute. -Another way that secondary pacemakers can start is when they fire more rapidly than the normal pacemaker of the SA node. -Triggered beats (early or late) may come from an ectopic focus or accessory pathway (area outside the normal conduction pathway) in the atria, AV node, or ventricles. -This results in a dysrhythmia, which replaces the normal sinus rhythm.

first-degree AV block

-First-degree AV block is a type of AV block in which every impulse is conducted to the ventricles but the time of AV conduction is prolonged. -After the impulse moves through the AV node, the ventricles usually respond normally. -HR is normal and rhythm is regular. -The P wave is normal, the PR interval is prolonged (greater than 0.20 second), and the QRS complex usually has a normal shape and duration. -First-degree AV block is associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (e.g., hypokalemia), vagal stimulation, and drugs such as digoxin, β-blockers, calcium channel blockers, and flecainide. -First-degree AV block is usually not serious but can be a sign of higher degrees of AV block. -Patients with first-degree AV block are asymptomatic. -There is no treatment for first-degree AV block. -Changes to potentially causative situations may be considered. -Monitor patients for any new changes in heart rhythm (e.g., more serious AV block).

cardiomyopathy

-Group of diseases that directly affect the structure or function of the myocardium. CMP classification: -Primary: etiology of the heart disease is unknown -Secondary: known myocardial disease is known and causes CMP -Dilated: acute or chronic onset due to infection or other processes: •Vent. Dilation, impaired systole, atrial enlargement, stasis of blood in LV -Hypertrophic: asymmetric LEFT Ventricular Hypertrophy (no dilation): •Impaired diastolic LV filling (unable to relax): obstructed LV outflow •Most common cause of sudden cardiac death (SCD) in young/athletes -Restrictive: impaired diastolic filling and stretch (uncommon): •Impaired diastolic filling and stretch with normal systole •Unknown etiology Causes: -Dilated: more severely ill: •Cardiotoxic agents: alcohol, cocaine, doxorubicin •Coronary artery disease •Hypertension •Genetic (autosomal dominant) •Metabolic disorders •Muscular dystrophy •Myocarditis •Pregnancy •Valve disease -Hypertrophic: males, SCD: •Aortic stenosis •Genetic (autosomal dominant) •Hypertension -Restrictive: exercise intolerance: •Amyloidosis •Endomyocardial fibrosis •Neoplastic tumor •Post-radiation therapy •Sarcoidosis •Ventricular thrombus Clinical Manifestations: -Progresses to Heart Failure: •Decreased exercise capacity, fatigue •Dyspnea at rest and PND and orthopnea •Dry cough •Palpitations •Abdominal bloating, hepatomegaly, JVD, nausea vomiting anorexia •S3, S4, murmurs •Dysrhythmias •Pulmonary crackles •Edema •Weak peripheral pulses •Pallor •Blood flow stasis causes can lead to embolization Diagnostic Assessment: •History and physical examination •Electrocardiogram •b-Type natriuretic peptide (BNP) •Chest x-ray •Echocardiogram •Nuclear imaging studies •Heart catheterization •Endomyocardial biopsy Drug Therapy: •Nitrates (except in hypertrophic CMP) •β-Blockers •Antidysrhythmics •ACE inhibitors •Diuretics •Digitalis (except in hypertrophic CMP unless used to treat atrial fibrillation) •Anticoagulants (if indicated) Surgical Intervention and Devices: •Ventricular assist device •Cardiac resynchronization therapy •Implantable cardioverter-defibrillator •Surgical repair •Heart transplantation •Cardiac rehabilitation •Palliative and hospice care -Care is like that of heart failure

premature atrial contraction

-HR varies with the underlying rate and frequency of the PAC. The rhythm is irregular. -The P wave has a different shape from that of the P wave originating from the SA node or it may be hidden in the preceding T wave. -The PR interval may be shorter or longer than the PR interval coming from the SA node, but it is within normal limits. -The QRS complex is usually normal. -If the QRS interval is greater than or equal to 0.12 second, abnormal conduction through the ventricles is present. -A premature atrial contraction (PAC) is a contraction starting from an ectopic focus in the atrium (i.e., a location other than the SA node) and coming sooner than the next expected sinus beat. -The ectopic signal starts in the left or right atrium and travels across the atria by an abnormal pathway. This creates a distorted P wave. -At the AV node, it may be stopped (nonconducted PAC), delayed (lengthened PR interval), or conducted normally. -If the signal moves through the AV node, in most cases it is conducted normally through the ventricles. Causes: -In a normal heart, a PAC can result from: •Emotional stress •Physical fatigue •Caffeine •Tobacco •Alcohol •Hypoxia, •Electrolyte imbalances •Disease states such as hyperthyroidism, chronic obstructive pulmonary disease (COPD), and heart disease, including CAD and valvular disease. -In persons with healthy hearts, isolated PACs are not significant. Clinical Manifestations: -Patients may report palpitations or a sense that their hearts "skipped a beat." -In persons with heart disease, frequent PACs may indicate enhanced automaticity of the atria, or a reentry mechanism. -Such PACs may warn of or start more serious dysrhythmias (e.g., supraventricular tachycardia). Treatment: -Depends on the patient's symptoms. -Withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be needed. -β-blockers may be used to decrease PACs.

unstable angina and MI diagnostic studies

-In addition to the patient's history of pain, risk factors, and health history, the primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac biomarkers. -The 12-lead ECG is one of the primary tools to diagnose UA or an MI (STEMI or NSTEMI). -Whenever possible, it should be compared to a previous ECG. -Changes in the QRS complex, ST-segment, and T-wave caused by ischemia and infarction can develop slowly or quickly with UA and MI. -The ECG must be read carefully, since changes can be absent or subtle at first. For this reason, serial 12-lead ECGs are done. -For diagnostic and treatment purposes, it is important to distinguish between STEMI and NSTEMI/UA. -STEMI patients usually have a complete coronary occlusion. -ST elevation is first seen on the 12-lead ECG. Within a few hours to days, T-wave inversion and pathologic Q waves develop. -Patients with NSTEMI or UA usually have transient thrombosis or incomplete coronary occlusion. These patients often develop ST depression or T wave inversion on the initial ECG. They usually do not develop pathologic Q waves. -Because MI is a dynamic process that evolves over time, serial ECGs are done to show the evolution of ischemia, injury, infarction, and resolution of the infarction Coronary Angiography: -The patient with a STEMI must undergo coronary angiography within 90 minutes of presentation or receive thrombolytic therapy within 30 minutes in agencies without PCI capability. -This will open the totally occluded artery and limit the infarction size. -The patient with UA or NSTEMI may or may not undergo coronary angiography to evaluate the extent of the disease. -Guidelines suggest that it is reasonable to do coronary angiography on stable but high-risk patients with UA or NSTEMI within 12-72 hours after presentation. -If appropriate, a PCI is performed at this time. Some patients may be treated only with conservative medical management. Pharmacologic Stress Testing: -When the ECG and serum cardiac biomarkers do not confirm MI, other measures for diagnosing CAD are considered. -To assess for ischemia or infarction, pharmacologic stress testing may be done when a patient has an abnormal but nondiagnostic ECG and negativebiomarkers

sinus bradycardia

-In sinus bradycardia, the conduction pathway is the same as that in sinus rhythm but the SA node fires at a rate less than 60 beats/minute. -The rhythm is regular. -The P wave precedes each QRS complex and has a normal shape and duration. -The PR interval is normal, and the QRS complex has a normal shape and duration. -Sinus bradycardia may be a normal sinus rhythm in aerobically trained athletes and in some people during sleep. -It also occurs in response to parasympathetic nerve stimulation, carotid sinus massage, Valsalva maneuver, hypothermia, increased intraocular pressure, vagal stimulation, and certain drugs (e.g., β-adrenergic blockers [β-blockers] , calcium channel blockers). -Common disease states associated with sinus bradycardia are hypothyroidism, increased intracranial pressure, and inferior myocardial infarction (MI). Clinical Manifestations: -The clinical significance of sinus bradycardia depends on how the patient tolerates it. -Symptomatic bradycardia refers to an HR that is less than 60 beats/minute and is inadequate for the patient's condition. -This causes the patient to experience symptoms (e.g., fatigue, dizziness, chest pain, syncope). -Signs of symptomatic bradycardia can include pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath. Treatment: -Treatment consists of administration of atropine (an anticholinergic drug) for the patient with symptoms. •Atropine is given to increase atrial contraction; increases heart rate -Pacemaker therapy may be required. -If bradycardia is due to drugs, these may need to be held, discontinued, or reduced.

mitral valve regurgitation

-Mitral valve function depends on intact mitral leaflets, mitral annulus, chordae tendineae, papillary muscles, left atrium, and left ventricle. -A defect in any of these structures can result in regurgitation. -Damage to valve caused by MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and IE. -MI with left ventricular failure increases the risk for rupture of the chordae tendineae and acute MR. -MR allows blood to flow backward from the left ventricle to the left atrium due to incomplete valve closure during systole. -Both the left ventricle and left atrium must work harder to preserve an adequate CO. -In acute MR, the sudden increase in pressure and volume transmits to the pulmonary bed. This results in pulmonary edema and if not treated, cardiogenic shock. -In chronic MR, the additional volume results in left atrial enlargement, left ventricular dilation and hypertrophy, and finally a decrease in CO. -IE = infective endocarditis Acute Clinical Manifestations: -The clinical course of MR is determined by the nature of its onset. -Patients with acute MR will have thready, peripheral pulses and cool, clammy extremities. -A low CO may mask a new systolic murmur. -Rapid assessment (e.g., heart catheterization) and intervention (e.g., valve repair or replacement) are critical. Chronic Clinical Manifestations: -Patients with chronic MR may remain asymptomatic for many years until development of some degree of left ventricular failure. -Early symptoms of left ventricular failure may include weakness, fatigue, palpitations, and dyspnea. These gradually progress to orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema. -Increased left ventricular volume leads to an audible third heart sound (S3), even with normal left ventricular function. The murmur is a loud holosystolic murmur at the apex radiating to the left axilla. -Patients with asymptomatic MR must be monitored carefully. -Surgery (valve repair or replacement) should be considered before significant left ventricular failure or pulmonary hypertension develops.

mitral valve stenosis

-Most cases of adult mitral value stenosis result from rheumatic heart disease. -Rheumatic mitral stenosis is widespread in underdeveloped countries. Less common causes are congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus. •Rheumatoid factor is used to test for rheumatoid arthritis -Rheumatic endocarditis causes scarring of the valve leaflets and the chordae tendineae. -Contractures and adhesions develop between the commissures (the junctional areas). -These deformities block the blood flow and create a pressure difference between the left atrium and the left ventricle during diastole. -As a result, left atrial pressure and volume increase causing higher pulmonary vasculature pressure. -The overloaded left atrium places the patient at risk for the development of atrial fibrillation. -The stenotic mitral valve takes on a "fish mouth" shape because of the thickening and shortening of the mitral valve structures. Clinical Manifestations: -The primary symptom of mitral stenosis is exertional dyspnea due to reduced lung compliance. -Heart sounds include a loud first heart sound and a low-pitched, diastolic murmur (best heard at the apex with the stethoscope). -Fatigue and palpitations from atrial fibrillation may also occur. -Emboli can arise from blood stasis in the left atrium secondary to atrial fibrillation. -Less often, patients may have hoarseness (from atrial enlargement pressing on the laryngeal nerve), hemoptysis (from pulmonary hypertension), and chest pain (from decreased CO and coronary perfusion). -Emboli can form in the left atrium secondary to atrial fibrillation causing a stroke. -Seizures may also occur

left-sided heart failure

-Most common form of HF -Left-sided HF results from left ventricular dysfunction. -This prevents normal, forward blood flow and causes blood to back up into the left atrium and pulmonary veins. -The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. -This manifests as pulmonary congestion and edema. -Results from inability of LV to: •Empty adequately during systole •Fill adequately during diastole -Further classified as: •Systolic •Diastolic •Mixed systolic and diastolic -Blood backs up into left atrium and pulmonary veins -Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema Pathophysiology: -HFrEF: HF with reduced EF -Inability to pump blood forward -Caused by: •Impaired contractile function •Increased afterload •Cardiomyopathy •Mechanical abnormalities -Decreased LV ejection fraction (EF)

pulseless electrical activity

-Pulseless electrical activity (PEA) is a situation in which organized, electrical activity is seen on the ECG, but there is no mechanical heart activity and the patient has no pulse. -Prognosis is poor unless the underlying cause is quickly identified and treated. -Electrical path is going across, but the patient is dead -Can be any shape or rhythm, even NSR: start CPR -The most common causes of PEA can be easily remembered by thinking of your Hs and Ts: •Hypovolemia, hypoxia, hydrogen ion (metabolic acidosis), hyper/hypokalemia, hypoglycemia, hypothermia •Toxins (e.g., drug overdose), cardiac tamponade, thrombosis (e.g., MI, pulmonary embolus), tension pneumothorax, and trauma. -Treatment begins with CPR followed by drug therapy (e.g., epinephrine) and intubation. -Correcting the underlying cause is critical to prognosis.

right-sided heart failure

-Right-sided HF occurs when the right ventricle (RV) fails to pump effectively. -When the RV fails, fluid backs up into the venous system. -This causes movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention). -The most common cause of right-sided HF is left-sided HF. -As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. -The RV has to work harder to push blood to the pulmonary system. -Over time, this increased workload weakens the RV and gradually it fails. -Other causes of right-sided HF (independent of the function of the LV) include RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease).

synchronized cardioversion

-Synchronized cardioversion is the therapy of choice for the patient with ventricular (e.g., VT with a pulse) or supraventricular tachydysrhythmias (e.g., atrial fibrillation with a rapid ventricular response). -A synchronized circuit in the defibrillator delivers a shock that is programmed to occur on the R wave of the QRS complex of the ECG. -Used for atrial fib with rapid ventricular response, PVST that did not respond to adenosine, stable V-tach -The procedure for synchronized cardioversion is the same as for defibrillation with the following exceptions: •The synchronizer switch must be turned on when cardioversion is planned. •If synchronized cardioversion is done on a nonemergency basis (i.e., the patient is awake and hemodynamically stable), the patient is sedated (e.g., IV midazolam [Versed]) before the procedure. Strict attention to maintaining the patient's airway is critical. •Start the initial energy for synchronized cardioversion at 50 to 100 joules (biphasic defibrillator) and 100 joules (monophasic defibrillator) and increase if needed. •If the patient becomes pulseless or the rhythm changes to VF, turn the synchronizer switch off and perform defibrillation.

syncope

-Syncope, a brief lapse in consciousness accompanied by a loss in postural tone (fainting), is a common diagnosis of patients coming into the emergency department. -The causes of syncope can be cardiovascular or noncardiovascular. -Noncardiovascular causes vary and include stress, hypoglycemia, dehydration, stroke, and seizure. -The most common cause of syncope is cardioneurogenic syncope or "vasovagal" syncope (e.g., carotid sinus sensitivity). -Other cardiovascular causes relate to dysrhythmias (e.g., tachycardias, bradycardias), prosthetic valve malfunction, pulmonary emboli, and HF. Diagnostic Studies: -A diagnostic workup for a patient with syncope from a suspected cardiac cause begins with ruling out structural and/or ischemic heart disease. -This is done with echocardiography and stress testing. -In the older patient, who is more likely to have ischemic and structural heart disease, ElectroPhysiology Studies (EPS) is used to diagnose atrial and ventricular tachydysrhythmias, as well as conduction disturbances causing bradydysrhythmias, all of which can cause syncope. -These problems can be treated with antidysrhythmia drug therapy, pacemakers, ICDs, and/or catheter ablation therapy. -In patients without structural heart disease or in whom EPS testing is not diagnostic, the head-up tilt-test may be performed to assess for cardioneurogenic syncope

sinus tachycardia

-The conduction pathway is the same in sinus tachycardia as that in normal sinus rhythm. The sinus rate is 101 to 200 beats/minute -The P wave is normal, precedes each QRS complex, and has a normal shape and duration. -The PR interval is normal, and the QRS complex has a normal shape and duration. -The discharge rate from the sinus node increases because of vagal inhibition or sympathetic stimulation. -Sinus tachycardia is associated with physiologic and psychologic stressors such as exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. -It can also be an effect of drugs such as epinephrine (EpiPen), norepinephrine (Levophed), atropine (AtroPen), caffeine, theophylline (Theo-Dur), or hydralazine (Apresoline). -In addition, many over-the-counter cold remedies have active ingredients (e.g., pseudoephedrine [Sudafed]) that can cause tachycardia. Treatment: -The underlying cause of tachycardia guides the treatment. -For example, for the patient who is experiencing tachycardia from pain, effective pain management is important to treat the tachycardia. -In patients who are clinically stable, vagal maneuvers can be attempted. -In addition, IV β-blockers (e.g., metoprolol [Lopressor]) can be given to reduce HR and decrease myocardial oxygen consumption. -Cardizem is also given

changes associated with myocardial ischemia

-The isoelectric line is flat and represents those normal times in the cardiac cycle when the ECG is not recording any electrical activity in the heart. -These times are as follows: (1) from the end of the P wave to the start of the QRS complex, (2) during the entire ST segment, and (3) from the end of the T wave to the start of the next P wave.

heart transplantation

-The transfer of a healthy donor heart to a patient with a diseased heart. This surgery is used to treat a variety of terminal or end-stage heart conditions. -Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy -3,000 on list; average 2,000 available -Survival rate of 85%-90% at 1year; 75% at 3 -Selection process identifies patients who would most benefit from a new heart -The United Network for Organ Sharing (UNOS) is in charge of a system that gives organs fairly to people. -Once a person meets the criteria for heart transplantation, a complete physical examination and diagnostic workup are done. -In addition, the patient and caregiver undergo a comprehensive psychologic evaluation. -This includes assessing coping skills, support systems, and commitment to follow the rigorous regimen that is essential to a successful transplantation. -The complexity of the transplant process may be overwhelming to a patient with inadequate support systems and a poor understanding of the lifestyle changes needed after transplant. -Retransplantation (i.e., a second or third heart transplant) is also done. Postoperative Monitoring: -A variety of complications can occur after the transplant, including a risk for SCD. -Acute rejection is an immediate posttransplant complication, and immunosuppressive therapy is the key in posttransplant management. -In the first year after transplantation, the major causes of death are acute rejection and infection. -Later on, malignancy (especially lymphoma) and cardiac vasculopathy (accelerated CAD) are major causes of death. -Most immunosuppressive regimens include corticosteroids, calcineurin inhibitors (cyclosporine [Sandimmune, Neoral], tacrolimus [Prograf]), and antiproliferative drugs (mycophenolate mofetil [CellCept]). -Because of the use of immunosuppression therapy, infection is a primary complication after transplant surgery. -On a long-term basis, immunosuppressive therapy increases the risk for cancer. -To detect rejection, an EMB is obtained on a weekly basis for the first month, monthly for the following 6 months, and yearly thereafter. -In this procedure, a catheter is inserted into the jugular vein and moved into the right ventricle. -The catheter uses a bioptome, a device with two small cups that can be closed, to remove small samples of heart muscle. Nursing Care Focuses On: -Promoting patient adaptation to the transplant process -Monitoring cardiac function -Managing lifestyle changes -Providing ongoing teaching to the patient and caregiver

wearable artificial kidney (WAK)

-The wearable artificial kidney (WAK) has recently been developed and is approved for use to improve the quality of life of an ESRD patient. -The WAK is a miniaturized dialysis machine that can be worn on the body. The carrier resembles a tool belt. -The device connects to a patient via a catheter. -Like conventional dialysis machines, it is designed to filter the blood of ESRD patients. -Unlike current portable or stationary dialysis machines, it can run continuously on batteries and is not plugged into an electrical outlet or attached to a water pipe. -The present version weighs about 10 pounds, but future modifications could make it lighter and more streamlined.

third-degree AV heart block

-Third-degree AV block, or complete heart block, constitutes one form of AV dissociation in which no impulses from the atria are conducted to the ventricles. -The atria are stimulated and contract independently of the ventricles. -The ventricular rhythm is an escape rhythm, and the ectopic pacemaker may be above or below the bifurcation of the bundle of His. -The atrial rate is usually a sinus rate of 60 to 100 beats/minute. -The ventricular rate depends on the site of the block. -If it is in the AV node, the rate is 40 to 60 beats/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute. -Atrial and ventricular rhythms are regular but unrelated to each other. -The P wave has a normal shape. -The PR interval is variable, and there is no relationship between the P wave and the QRS complex. -The QRS complex is normal if an escape rhythm is initiated at the bundle of His or above. -It is widened if an escape rhythm is initiated below the bundle of His. -Third-degree AV block is associated with severe heart disease, including CAD, MI, myocarditis, cardiomyopathy, and some systemic diseases, such as amyloidosis and progressive systemic sclerosis (scleroderma). -Some drugs can also cause third-degree AV block, such as digoxin, β-blockers, and calcium channel blockers. -Third-degree AV block usually results in reduced CO with subsequent ischemia, HF, and shock. -Syncope from third-degree AV block may result from severe bradycardia or even periods of asystole. -For symptomatic patients, a transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted. -The use of drugs such as dopamine (Intropin), and epinephrine is a temporary measure to increase HR and support blood pressure until temporary pacing is started. -Patients will need a permanent pacemaker as soon as possible. -Atropine is not an effective drug for this dysrhythmia.

12-lead ECG

-Typically, an ECG consists of 12 leads (or views) of the heart's activity. -A lead consists of a positive and a negative electrode, with the positive electrode being the "seeing eye." -Activity coming toward the positive electrode produces an upward deflection on the EKG paper, and one going away from the seeing eye produces a downward deflection (this is the reason for lead tracings looking different). -Six of the leads measure electrical forces in the frontal plane. These are bipolar (positive and negative) leads I, II, and III (left column of tracings); and unipolar (positive) leads aVr, aVl, and aVf. -The remaining six unipolar leads (V1 through V6) measure the electrical forces in the horizontal plane (precordial leads). -The 12-lead ECG may show changes suggesting structural changes, conduction disturbances, damage (e.g., ischemia, infarction), electrolyte imbalance, or drug toxicity. -Obtaining 12 ECG views of the heart is also helpful in the assessment of dysrhythmias. Nursing Considerations: -Clip excessive hair on chest wall -Rub skin with dry gauze -May need to use alcohol for oily skin -Apply electrode pad -Artifact-movement or poor lead contact

unstable angina

-Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or with less effort than the patient's chronic stable angina pattern. -The pain typically lasts 10 minutes or more. -Prompt treatment is needed for patients suspected of having UA. -The patient with previously diagnosed chronic stable angina will describe a significant change in the pattern of angina. -It will occur with increasing frequency and is easily provoked by minimal or no exertion, during sleep, or even at rest. -Unlike chronic stable angina, UA is unpredictable and must be treated immediately. -Despite efforts to increase awareness, women's symptoms continue to be under-recognized as heart related. •These include fatigue, shortness of breath, indigestion, and anxiety. •Fatigue is the most prominent symptom. •However, all these symptoms can relate to many different diseases and syndromes. •It is because of these reasons that women often present with UA before CAD is diagnosed.

ventricular fibrillation

-Ventricular fibrillation (VF) is a severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude. -This represents the firing of multiple ectopic foci in the ventricle. -Mechanically the ventricle is simply "quivering," with no effective contraction, and consequently no CO occurs. -VF is a lethal dysrhythmia. -HR is not measurable. -Rhythm is irregular and chaotic. -The P wave is not visible, and the PR interval and the QRS interval are not measurable. -VF occurs in acute MI and myocardial ischemia and in chronic diseases such as HF and cardiomyopathy. -It may occur during cardiac pacing or cardiac catheterization procedures because of catheter stimulation of the ventricle. -It may also occur with coronary reperfusion after thrombolytic therapy. -Other clinical associations are electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity. -VF results in an unresponsive, pulseless, and apneic state. -If not rapidly treated, the patient will die. -Treatment consists of immediate initiation of CPR and advanced cardiac life support (ACLS) with the use of defibrillation and definitive drug therapy (e.g., epinephrine, vasopressin [Pitressin]). -There should be no delay in using a defibrillator once available.

assessment of heart rhythm

-When assessing the heart rhythm, make an accurate interpretation and immediately assess the clinical status of the patient. -Assess the patient's hemodynamic response to any change in rhythm. -This information will guide the selection of your interventions. -Determination of the cause of dysrhythmias is a priority. For example, tachycardias may be the result of fever and may cause a decrease in cardiac output (CO) and hypotension. -Electrolyte disturbances can cause dysrhythmias and, if not treated, can lead to life-threatening dysrhythmias. -At all times, assess and treat the patient, not the "monitor," when a dysrhythmia is noted. Assessment Approach: 1. Look for the presence of the P wave. Is it upright or inverted? Is there one for every QRS complex or more than one? Are there atrial fibrillatory or flutter waves present? 2. Evaluate the atrial rhythm. Is it regular or irregular? 3. Calculate the atrial rate. 4. Measure the duration of the PR interval. Is it normal duration or prolonged? 5. Evaluate the ventricular rhythm. Is it regular or irregular? 6. Calculate the ventricular rate. 7. Measure the duration of the QRS complex. Is it normal duration or prolonged? 8. Assess the ST segment. Is it isoelectric (flat), elevated, or depressed? 9. Measure the duration of the QT interval. Is it normal duration or prolonged? 10. Note the T wave. Is it upright or inverted? Another Approach: 1. Atrial and ventricular rates 2. Regularity of rhythm 3. Measurement of PR, QRS, and QT/QTc intervals 4. Shape of waveforms and their consistency 5. Identification of underlying rhythm and dysrhythmias 6. Patient tolerance of rhythm 7. Clinical implication of the rhythm Additional Questions: 1. What is the dominant or underlying rhythm and/or dysrhythmia? 2. What is the clinical significance of your findings? 3. What is the treatment for the particular rhythm?

premature ventricular contractions

-A premature ventricular contraction (PVC) is a contraction coming from an ectopic focus in the ventricles. -It is the premature (early) occurrence of a QRS complex. -A PVC is wide and distorted in shape compared to a QRS complex coming down the normal conduction pathway. -PVCs that arise from different foci appear different in shape from each other and are called multifocal PVCs. -PVCs that have the same shape are called unifocal PVCs. -When every other beat is a PVC, the rhythm is called ventricular bigeminy. -When every third beat is a PVC, it is called ventricular trigeminy. -Two consecutive PVCs are called a couplet. -Ventricular tachycardia occurs when there are three or more consecutive PVCs. -R-on-T phenomenon occurs when a PVC falls on the T wave of a preceding beat. -This is especially dangerous because the PVC is firing during the relative refractory phase of ventricular repolarization. -Excitability of the heart cells increases during this time, and the risk for the PVC to start ventricular tachycardia or ventricular fibrillation is great. -HR varies according to intrinsic rate and number of PVCs. -Rhythm is irregular because of premature beats. -The P wave is rarely visible and is usually lost in the QRS complex of the PVC. -Retrograde conduction may occur, and the P wave may be seen following the ectopic beat. -The PR interval is not measurable. -The QRS complex is wide and distorted in shape, lasting more than 0.12 second. -The T wave is generally large and opposite in direction to the major direction of the QRS complex Terms: -Unifocal: single site -Multifocal or polymorphic: multiple sites -Couplet: 2 in a row -Trigeminy: pattern of 2 regular and 1 vent. -Bigeminy: pattern of 1 regular and 1 vent. -Run of VT: 3 vent. in a row Causes: -Fever -Pain -Medications -Potassium levels -Oxygen levels -PVCs are associated with stimulants such as caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin. -They are also associated with electrolyte imbalances, hypoxia, fever, exercise, and emotional stress. -Disease states associated with PVCs include MI, mitral valve prolapse, HF, cardiomyopathy, and CAD. -PVCs are usually not harmful in a patient with a normal heart. -In heart disease, PVCs may reduce the CO and lead to angina and HF depending on frequency. -Because PVCs in CAD or acute MI indicate ventricular irritability, assess the patient's physiologic response to PVCs. -Obtain the patient's apical-radial pulse rate as PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit. -6 PVCs per minute are too many Treatment: -Treatment relates to the cause of the PVCs (e.g., oxygen therapy for hypoxia, electrolyte replacement). -Assessment of the patient's hemodynamic status is important to determine whether treatment with drug therapy is needed. -Drug therapy includes β-blockers, procainamide (Pronestyl), or amiodarone.

pulmonic valve stenosis

-Almost always congenital -Causes right ventricular hypertension and hypertrophy -Clinical manifestations: fatigue, loud murmur

ventricular tachycardia

-A run of three or more PVCs defines ventricular tachycardia (VT). -Ventricular rate is 150 to 250 beats/minute. -Rhythm may be regular or irregular. -AV dissociation may be present, with P waves occurring independently of the QRS complex. -The atria may be depolarized by the ventricles in a retrograde fashion. -The P wave is usually buried in the QRS complex, and the PR interval is not measurable. -The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration). -The T wave is in the opposite direction of the QRS complex. -Ventricular tachycardia occurs when an ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker. -Different forms of VT exist, depending on QRS configuration. -Monomorphic VT has QRS complexes that are the same in shape, size, and direction. -Polymorphic VT occurs when the QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats. -VT may be sustained (longer than 30 seconds) or nonsustained (less than 30 seconds). -The development of VT is an ominous sign. It is a life-threatening dysrhythmia because of decreased CO and the possibility of development of ventricular fibrillation, which is a lethal dysrhythmia. -VT is associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, long QT syndrome, drug toxicity, and central nervous system disorders. -This dysrhythmia can be seen in patients who have no evidence of heart disease. -VT can be stable (patient has a pulse) or unstable (patient is pulseless). -Sustained VT causes a severe decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction. -This results in hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest. -The dysrhythmia must be treated quickly, even if it occurs only briefly and stops abruptly. -Episodes may recur if prophylactic treatment is not started. -Ventricular fibrillation may also develop. Treatment: -Important to assess your client -Precipitating causes must be identified and treated (e.g., electrolyte imbalances, ischemia, hypoxia). -VT with pulse (hemodynamically stable) is treated with antidysrhythmic. -If the VT is monomorphic and the patient is hemodynamically stable (i.e., pulse is present) and has preserved left ventricular function, IV procainamide, sotalol, or amiodarone is used. -If the VT is polymorphic with a normal baseline QT interval, any one of the following drugs is used: β-adrenergic blockers, amiodarone, procainamide, or sotalol. -Polymorphic VT with a prolonged baseline QT interval is treated with IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing -Drugs that prolong the QT interval (e.g., dofetilide [Tikosyn]) should be discontinued. -Cardioversion is used if drug therapy is ineffective. -VT without a pulse is a life-threatening situation. -It is treated in the same manner as ventricular fibrillation. -Cardiopulmonary resuscitation (CPR) and rapid defibrillation are the first lines of treatment, followed by the administration of vasopressors (e.g., epinephrine) and antidysrhythmics (e.g., amiodarone) if defibrillation is unsuccessful.

atrial fibrillation

-Atrial fibrillation is characterized by a total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction. -During atrial fibrillation, the atrial rate may be as high as 350 to 600 beats/minute. -P waves are replaced by chaotic, fibrillatory waves. -Ventricular rate varies and the rhythm is usually irregular. -When the ventricular rate is between 60 and 100 beats/minute, it is atrial fibrillation with a controlled ventricular response. -Atrial fibrillation with a ventricular rate greater than 100 beats/minute is atrial fibrillation with a rapid (or uncontrolled) ventricular response. -The PR interval is not measurable, and the QRS complex usually has a normal shape and duration. -At times, atrial flutter and atrial fibrillation may coexist -The dysrhythmia may be paroxysmal (i.e., begins and ends spontaneously) or persistent (lasting more than 7 days). -Atrial fibrillation is the most common, clinically significant dysrhythmia with respect to morbidity and mortality rates, and economic impact. -Its prevalence increases with age. -Atrial fibrillation usually occurs in a patient with underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis. -It often develops acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and heart surgery. -Atrial fibrillation results in a decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response. -Thrombi (clots) form in the atria because of blood stasis. -An embolized clot may develop and pass to the brain, causing a stroke. -Atrial fibrillation accounts for as many as 17% of all strokes. Treatment: -The goals of treatment of atrial fibrillation include a decrease in ventricular response (to less than 100 beats/minute), prevention of stroke, and conversion to sinus rhythm, if possible. -Ventricular rate control is a priority for patients with atrial fibrillation. -Drugs used for rate control include calcium channel blockers (e.g., diltiazem), β-blockers (e.g., metoprolol), digoxin (Lanoxin), and dronedarone. -For some patients, drug or electrical conversion of atrial fibrillation to a normal sinus rhythm may be considered (e.g., reduced exercise tolerance with rate control drugs, contraindications to warfarin). -The most common antidysrhythmia drugs used for conversion to and maintenance of sinus rhythm include amiodarone and ibutilide. -Electrical cardioversion may convert atrial fibrillation to a normal sinus rhythm. -If a patient is in atrial fibrillation for longer than 48 hours, anticoagulation therapy with warfarin is needed for 3 to 4 weeks before the cardioversion and for several weeks after successful cardioversion. -Anticoagulation therapy is necessary because the procedure can cause the clots to dislodge. This places the patient at risk for stroke. -A transesophageal echocardiogram may be performed to rule out the presence of clots in the atria. -If no clots are present, anticoagulation therapy may not be needed before the cardioversion. -If drugs or cardioversion do not convert atrial fibrillation to normal sinus rhythm, long-term anticoagulation therapy is needed. -Warfarin is the drug of choice, and patients are monitored for therapeutic levels (e.g., international normalized ratio [INR]). -For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion and remain symptomatic, radiofrequency catheter ablation (similar to the procedure for atrial flutter) and the Maze procedure are further options. -The Maze procedure is a surgical intervention that stops atrial fibrillation by interrupting the ectopic foci that are responsible for the dysrhythmia. -Incisions are made in both atria, and cryoablation (cold therapy) is used to stop the formation and conduction of these signals and restore normal sinus rhythm.

infective endocarditis

-Disease of the endocardial layer of the heart, including the heart valves -IE most often affects the aortic and mitral valves -40,000 to 50,000 new cases each year -By cause: IV drug use (IVDA IE), fungal -By site of involvement: prosthetic valve endocarditis (PVE) -Subacute form affects those with preexisting valve disease -Acute form affects those with healthy valves Causative Agents/Risk Factors: -Bacterial most common: •Staphylococcus aureus (about 30%) •Streptococcus viridans •Coagulase negative Staphylococci -Viruses -Fungi -Categories of high, moderate, and low risk of developing IE -Principal risk factors: •Prosthetic valves •Hemodialysis •IV drug abuse (IVDA) Stages of Infective Endocarditis: -Occurs in three stages: •Bacteremia •Adhesion •Vegetation -Vegetation: •Fibrin, leukocytes, platelets, and microbes •Stick to the valve or endocardium •Parts break off and enter circulation (embolization) •Left-sided vegetation can move to brain, kidneys, spleen •Right-sided vegetation can move to lungs (PE) Manifestations: -Nonspecific: •Fever •Chills •Weakness •Malaise •Fatigue •Anorexia -Subacute form: •Arthralgias •Myalgias •Back pain •Abdominal discomfort •Weight loss •Headache •Clubbing of fingers -Vascular: •Petechiae (indicative of endocarditis spreading to the lungs) •Splinter hemorrhage in nail beds •Oslers' nodes on fingers •Roth spots •New or worsening systolic murmur •Heart failure •Septic emboli Nursing Assessment: -Health history: •Valvular, congenital, or syphilitic heart disease •Previous endocarditis •Staph or strep infection -Drugs—immunosuppressive therapy -Recent surgeries and procedures -IVDA -Alcohol abuse -Weight changes -Chills -Hematuria -Exercise intolerance, weakness, fatigue -Cough, DOE, orthopnea, palpitations -Night sweats -Pain, headache, joint, or muscle tenderness -Arthralgia and myalgias -Petechiae, purpura -Osler's nodes -Splinter hemorrhage -Janeway's lesions Diagnostics: -History -Laboratory tests: •Blood cultures •CBC with differential •ESR, C-reactive protein (CRP) -Echocardiography -Chest x-ray -ECG -Duke criteria Interprofessional Care: -Prophylactic antibiotic treatment for select patients having: •Certain dental procedures •Respiratory tract incisions •Tonsillectomy and adenoidectomy •Surgical procedures involving infected skin, skin structures, or musculoskeletal tissue -Accurate identification of organism -IV antibiotics (long-term) -Repeat blood cultures -Valve replacement if needed -Antipyretics -Fluids -Rest

coronary artery disease (CAD)

-Coronary artery disease is a type of blood vessel disorder that is included in the general category of atherosclerosis. -Consequently, it is common to refer to atherosclerosis as "hardening of the arteries." -Although this disease can occur in any artery in the body, the atheromas (fatty deposits) prefer the coronary arteries. -The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary heart disease, and CAD all describe this disease process. -Atherosclerosis is the major cause of CAD. -It is characterized by deposits of lipids within the intima of the artery. -Endothelial injury and inflammation play a central role in the development of atherosclerosis. Etiology and Pathophysiology: -Normally some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation. -Two factors contribute to the growth and extent of collateral circulation: (1) inherited predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic ischemia. -When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic, increased collateral circulation develops. -When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of collateral circulation developing, and the heart muscle may still receive an adequate amount of blood and oxygen. -However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or coronary spasm, time is inadequate for collateral development. -Consequently, a reduced blood flow results in a more severe ischemia or infarction. Clinical Manifestations: -CAD is a chronic and progressive disease. -Patients may be asymptomatic for many years or they may develop chronic stable chest pain. -When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen, myocardial ischemia occurs. -Angina, or chest pain, is the clinical manifestation of myocardial ischemia. It is caused by either an increased demand for oxygen or a decreased supply of oxygen. -The most common reason for angina to develop is narrowing of one or more coronary arteries by atherosclerosis. -This leads to insufficient blood flow to the heart muscle. -For ischemia secondary to atherosclerotic plaque to occur, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery). Nursing and Interprofessional Care: -An estimated 31.9 million American adults have cholesterol levels greater than or equal to 240 mg/dL (6.2 mmol/L). -Guidelines for treatment of high cholesterol focus on LDL cholesterol. -A complete lipid profile is recommended every 5 years beginning at age 20. -Guidelines recommend the following groups of people receive statin therapy: (1) patients with known CVD, (2) patients with primary elevations of LDL cholesterol levels greater than or equal to 190 mg/dL (e.g., familial hypercholesterolemia), (3) patients between 40 and 75 years old with diabetes and LDL cholesterol levels between 70 and 189 mg/dL, and (4) patients between 40 and 75 years old with LDL cholesterol levels between 70 and 189 mg/dL and a 10-year risk for CVD of at least 7.5%. -Treatment also includes weight loss (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity. -Serum lipid levels should be reassessed after 6 weeks of therapy. If they remain elevated, additional dietary options and drug therapy may be considered. -Several classifications of drugs are used to decrease serum lipids. -Drugs that Restrict Lipoprotein Production: •The statin drugs are the most widely used lipid-lowering drugs. •These drugs inhibit the synthesis of cholesterol in the liver. •An unexplained result of the inhibition of cholesterol synthesis is an increase in hepatic LDL receptors. Consequently, the liver is able to remove more LDLs from the blood. •In addition, statins produce a small increase in HDLs and lower CRP levels. •Serious adverse effects of these drugs are rare and include liver damage and myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle). •Liver enzymes (e.g., aspartate aminotransferase, alanine aminotransferase) are initially monitored and rechecked with any increase in dosage. years and high-risk women (i.e., those with a calculated 10-year CAD risk of >20%) unless contraindicated. •For high-risk women who are intolerant of aspirin, clopidogrel (Plavix) can be substituted. •In healthy women 65 years or older, aspirin therapy may be considered if BP is controlled and the benefit for MI prevention outweighs the risk of GI bleed or hemorrhagic stroke. -Drugs that Restrict Lipoprotein Production: •Niacin (Niaspan), a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. •Niacin also increases HDL levels better than many other lipid-lowering drugs. •Unfortunately, side effects of this drug are common and may include severe flushing, pruritus, gastrointestinal (GI) symptoms, and orthostatic hypotension. -The fibric acid derivatives work by aiding the removal of VLDLs and increasing the production of apolipoproteins A-I and A-II. -They are the most effective drugs for lowering triglycerides and increasing HDL levels. -They have no effect on LDLs. -Although most patients tolerate the drugs well, complaints may include GI irritability. -Antiplatelet therapy-ASA: Clopidogrel (Plavix) -A stent is an expandable meshlike structure designed to keep the vessel open after balloon angioplasty. -Because stents are thrombogenic, many different types of drugs are used to prevent platelet aggregation within the stent. -Drugs commonly used during PCI are unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]). -After PCI, the patient is treated with dual antiplatelet drugs (e.g., aspirin [indefinitely] and clopidogrel) up to 12 months or longer, until the intimal lining grows over the stent and provides a smooth vascular surface. -There are two types of stents: bare metal stents (BMS) and drug-eluting stents (DES). DESs are coated with a drug (e.g., paclitaxel, sirolimus) to reduce the risk of overgrowth of the intimal lining (neointimal hyperplasia) within the stent. -This is the primary cause of in-stent restenosis (ISR). Following DES placement, dual antiplatelet drugs are taken to prevent thrombus formation within the stent (stent thrombosis) for a minimum of 12 months or longer. -The duration of dual antiplatelet drugs for patients with BMS is a minimum of 1 month but ideally one full year after PCI. -The most serious complications from stent placement are abrupt closure from coronary artery dissection and vascular injury at the artery access site (femoral or radial), acute MI, stent embolization, coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal), infection, stroke and emergent coronary artery bypass graft (CABG) surgery. -The possibility of dysrhythmias during and after the procedure is always present.

hemodialysis

Vascular Access Sites: -Obtaining vascular access is one of most difficult problems -Types of access: •Arteriovenous fistulas and grafts: subcutaneous, usually created in the forearm or upper arm with an anastomosis between an artery and a vein (usually cephalic or basilic) •Temporary vascular access: in some situations when immediate vascular access is required, percutaneous cannulation of the internal jugular or femoral vein is performed. Arteriovenous Fistula: -Arteriovenous fistula created by anastomosing an artery and vein. -A subcutaneous AVF is most commonly created in the forearm with an anastomosis between an artery and a vein (usually cephalic). -The fistula allows arterial blood to flow through the vein. -The vein becomes "arterialized" increasing in size and developing thicker walls. -The arterial blood flow is essential to provide the rapid blood flow required for HD. -As the fistula matures, it is more amenable to repeated venipunctures. -Maturation may take 6 weeks to months. -AVF should be placed at least 3 months before the need to initiate HD. -The fistula is the preferred access for HD. -Normally, a thrill (buzzing sensation) can be felt by palpating the fistula, and a bruit (rushing sound) can be heard with a stethoscope. -The thrill and bruit are created by arterial blood moving at a high velocity through the vein. HeRO Graft (Hemodialysis Reliable Outflow): -Special bridge access -Used when other access options are exhausted -Two pieces: •Reinforced tube to bypass blockages in veins •Dialysis graft anastomosed to an artery to be accessed for HD -The HeRO graft is placed under the skin, like both a fistula and standard graft. -The HeRO Graft bypasses the venous system to provide blood flow directly from a target artery to the heart. Dialyzers: -Plastic cartridges that contain thousands of parallel hollow tubes or fibers -Fibers are semipermeable membranes -The blood is pumped into the top of the cartridge and is dispersed into all of the fibers. -Dialysis fluid (dialysate) is pumped into the bottom of the cartridge and bathes the outside of the fibers. -When the dialyzed blood reaches the end of the thousands of semipermeable fibers, it converges into a single tube that returns it to the patient. Procedure: -The needles used for HD are large bore, usually 14- to 16-gauge, and are inserted into the fistula or graft to obtain vascular access. -Two needles placed in fistula or graft: •One needle is placed to pull blood from circulation to HD machine •Other needle is used to return dialyzed blood to the patient -When blood comes in contact with a foreign material (such as the dialyzer) it has a tendency to clot -Heparin is added to prevent clotting -Dialyzer/blood lines primed with saline solution to eliminate air -Terminated by flushing with saline to return all blood to patient -Needles removed and firm pressure applied -To terminate the treatment, a saline solution is used to return the blood in the extracorporeal circuit back to the patient through the vascular access. -The needles are removed from the patient, and firm pressure is applied to the venipuncture sites until the bleeding stops. -Before beginning treatment, assess fluid status (weight, BP, peripheral edema, lung and heart sounds), condition of vascular access, and temperature. -The difference between the last postdialysis weight and the present predialysis weight determines the ultrafiltration or the amount of weight (from fluid) to be removed. -During treatment, take vital signs every 30 to 60 minutes Complications/ Effectiveness: -Hypotension that occurs during HD results primarily from rapid removal of vascular volume (hypovolemia), decreased cardiac output, and decreased systemic intravascular resistance. -Factors associated with the development of muscle cramps include hypotension, hypovolemia, high ultrafiltration rate (large interdialytic weight gain), and low-sodium dialysis solution. -Blood loss may result from blood not being completely rinsed from the dialyzer, accidental separation of blood tubing, dialysis membrane rupture, or bleeding after the removal of needles at the end of HD. -At one time, hepatitis B had an unusually high prevalence in dialysis recipients, but the incidence today is low. -Currently, hepatitis C virus (HCV) is responsible for the majority of cases of hepatitis in dialysis recipients. -Dialysis cannot fully replace normal functions of kidneys -It can ease many of the symptoms -Can also prevent certain complications

continual renal replacement therapy (CRRT)

-Method for treating AKI -Means by which uremic toxins and fluids are removed -The principle of CRRT is to dialyze patients in a more physiologic way (over 24 hours), just like the kidneys. -Acid-base status/electrolyte are adjusted slowly and continuously -Can be used in conjunction with HD -Contraindication: •Patient has life-threatening manifestations of uremia (hyperkalemia, pericarditis) that require rapid treatment -Vascular access for CRRT is achieved through the use of a double-lumen catheter (as used in HD) placed in the jugular or femoral vein. Types of CRRT: -Continuous venovenous hemofiltration (CVVH): removes both fluid and solutes; replacement fluid required -Slow continuous ultrafiltration (SCUF): simplified version of CVVH; removes fluid; no fluid replacement required -Continuous venovenous hemodialysis (CVVHD): removes both fluids and solutes; requires both dialysate and replacement fluid -Continuous venovenous hemodiafiltration (CVVHDF): removes both fluids and solutes; requires both dialysate and replacement fluid Continuous Venovenous Therapies: -A blood pump propels blood through the circuit. -A highly permeable, hollow-fiber hemofilter removes plasma water and nonprotein solutes, which are collectively termed ultrafiltrate. -The ultrafiltration rate (UFR) may range from 0 to 500 mL/hr. -Under the influence of hydrostatic pressure and osmotic pressure, water and nonprotein solutes pass out of the filter into the extracapillary space and drain through the ultrafiltrate port into a collection device (drainage bag). -The remaining fluid continues through the filter and returns to the patient via the return port of the double-lumen catheter. -As ultrafiltrate drains out of the hemofilter, fluid and electrolyte replacements can be infused through a port located before or after the filter as the blood returns to the patient. -Replacement fluid is designed to replace volume and solutes such as sodium, chloride, bicarbonate, and glucose. -Replacement fluid infused into the infusion port before the hemofilter allows for greater clearance of urea and can decrease filter clotting. -Infusion of replacement fluid determined by degree of fluid and electrolyte imbalance -The use of the infusion port located after the filter dilutes intravascular fluid, decreasing the concentration of unwanted solutes such as BUN, creatinine, and potassium. -Anticoagulants are needed to prevent blood clotting and may be infused as a bolus at the initiation of CRRT or through an infusion port before the hemofilter. CRRT vs. HD: -Continuous rather than intermittent -Fluid volume can be removed over days versus hours -Solute removal by convection (no dialysate required) in addition to osmosis and diffusion -Less hemodynamic instability -Does not require constant monitoring by HD nurse but requires a trained ICU nurse -Does not require complicated HD equipment, but a blood pump is needed for venovenous therapies -Can be continued as long as 30 to 40 days -Hemofilter should be changed every 24 to 48 hours -Ultrafiltrate should be clear yellow Nursing Interventions: -Obtain weights -Monitor and document laboratory values daily Assess hourly: •Intake and output •Vital signs •Hemodynamic status -Assess and maintain the patency of the CRRT system. -Care for vascular access site to prevent infection -Although reductions in central venous pressure and pulmonary artery pressure are expected, there should be little change in mean arterial pressure or cardiac output. -Once the patient's AKI is resolved or there is a decision to withdraw treatment, CRRT is discontinued and the needle(s) removed.

kidney transplant

-More than 100,000 patients are currently awaiting kidney transplants -Only 17,000 transplants take place every year -Very successful -One-year graft survival rate: •Deceased donor transplants: 90% •Live donor transplants: 95% -Advances include organ procurement and preservation, surgical techniques, tissue typing and matching, immunosuppressant therapy, and prevention and treatment of graft rejection. -You have to be tissue matched to donate a kidney: if not tissue matched, the recipient may reject the kidney -Advantages of kidney transplant: •Reverses many of pathophysiologic changes associated with renal disease •Eliminates dependence on dialysis •Less expensive than dialysis after first year -Kidneys for transplant may be obtained from compatible blood-type deceased donors, blood relatives, emotionally related (close and distant) living donors (e.g., spouses, distant cousins, etc.), and altruistic living donors who are known (friends) or unknown to the recipient. -Paired organ donation occurs when one donor/recipient pair who are incompatible or poorly matched with each other find another donor/recipient pairs with whom they can exchange kidneys. -Paired organ donation is the practice of matching biologically incompatible donor/recipient pairs to permit transplant in both candidates with a well-matched organ. Contraindications to Recipient Selection: -Disseminated malignancies -Refractory/ untreated cardiac disease -Chronic respiratory failure -Extensive vascular disease -Chronic infection -Unresolved psychosocial disorders -Being HIV-positive or having hepatitis B or C is not a contraindication to transplant. -Some transplant programs exclude patients who are morbidly obese or who continue to smoke (despite smoking cessation interventions). -Certain patients, particularly those with CV disease and diabetes mellitus, are considered high risk and must be carefully evaluated and then monitored closely after transplant. -For a small number of patients who are approaching ESRD, preemptive transplant (before dialysis is required) is possible if a living donor is available. -VRE, MRSA, valley fever are examples of chronic infection -Unresolved psychosocial disorders: recipient feels too guilty about someone having to die so they could have a kidney, or that their loved one is in pain from giving them a kidney Surgical Procedures Before Transplant: -Coronary artery bypass or coronary angioplasty may be indicated for advanced coronary artery disease. -Cholecystectomy may be necessary for patients with a history of gallstones, biliary obstruction, or cholecystitis. -On rare occasions, bilateral nephrectomies may be necessary for patients with refractory hypertension, recurrent urinary tract infections, or kidneys that are grossly enlarged as a result of polycystic kidney disease. Donor Sources: -Live Donors: •Extensive interprofessional evaluation •Crossmatches are done at the time of the evaluation and about a week before the transplant to ensure that no antibodies to the donor are present or that the antibody titer is below the allowed level. •Laboratory studies •24-hour urine •Creatinine clearance •Total protein •Complete blood count •Chemistry and electrolyte profiles •Hepatitis B and C, HIV, CMV testing •An ECG and chest x-ray are also done. •A renal ultrasound and renal arteriogram or three-dimensional CT scan is performed to ensure that the blood vessels supplying each kidney are adequate and that no anomalies exist and to determine selection of the kidney to be used in the transplant. •A transplant psychologist or social worker determines if the individual is emotionally stable and able to deal with the issues related to organ donation. -Advantages: •Better patient and graft survival rates •Immediate organ availability •Immediate function/minimal cold time •Opportunity to have recipient in best possible medical condition -Live Donor Surgical Procedure: •Begins 1 or 2 hours before the recipient's surgery is started •Recipient is surgically prepared in a nearby operating room •Laparoscopic donor nephrectomy: -Most common approach for removing kidney in living donor -Minimally invasive -Fewer risks, shorter recovery time -The laparoscopic approach significantly decreases the hospital stay, pain, operative blood loss, debilitation, and length of time off work. -For these reasons, the number of people willing to donate a kidney has increased significantly. •Open (conventional) nephrectomy: -The donor is placed in the lateral decubitus position on the operating table so that the flank is exposed laterally. -An incision is made at the level of the eleventh rib. -The rib may have to be removed to provide adequate visualization of the kidney. •Donors must be healthy, but they have a longer healing process than the recipient: taking a healthy person and making them sick, and taking a chronically sick person and making them feel better •Ensure that live donor's remaining kidney supports their body enough -Deceased Donor: •Deceased (cadaver) kidney donors are relatively healthy individuals •Have suffered an irreversible brain injury and are declared brain dead •The brain-dead donor must have effective CV function and be supported on a ventilator to preserve the organs. •Even if the donor carried a signed donor card, permission from the donor's legal next of kin is still requested after brain death is determined. •In deceased kidney donation, the kidneys are removed and preserved for up to 72 hours, but most transplant surgeons prefer to transplant kidneys before the cold time (time outside of the body when being transported from the deceased donor to the recipient) reaches 24 hours. •The United Network for Organ Sharing (UNOS) distributes deceased donor kidneys using an objective computerized point system. The ABO group, HLA typing, age, antibody level, and length of time waiting are entered into the national computer for each candidate. •Cold time: put donor kidney in a cooler and transport it to recipient (time is tissue death, important to minimize transfer time) •Make sure recipient is in OR ready for transplant by the time the recipient gets there •Data and testing for extensive cross matching •When a donor becomes available, the donor's key information is compared with the data of all patients awaiting transplant locally and nationwide. •Points are given for how close the HLA match is, how long the patient has been waiting, if the antibody level is unusually high, and if the recipient is younger than 19 years old. •Extra points are given for high antibody levels because this can severely limit the number of donors with whom the patient will not have a positive crossmatch. •The kidney is offered to the recipient with the most points in the local area. If no patients in the local area are suitable, the organ is then offered in the region and then in the nation. •When a kidney arrives at the recipient's transplant center, a final crossmatch is done and must be negative for the deceased donor transplant to proceed. •The only exception to the previous plan is if a patient needs an emergency transplant or if a donor and recipient match on all six HLA antigens (zero antigen mismatch). •The patient meeting either one of these criteria goes to the top of the list. •Emergency transplants are given priority because the patient is facing imminent death if not transplanted. Preoperative Care: -Emotional and physical preparation -Because the patient and caregiver may have been waiting years for the kidney transplant, a review of the operative procedure and what can be expected in the immediate postoperative recovery period is necessary. -Stress that there is a chance the kidney may not function immediately, and dialysis may be required for days to weeks. -Review the need for immunosuppressive drugs and measures to prevent infection (such as cyclosporins, proton pump inhibitors, and steroids). -Monitor ECG, chest X-ray, laboratory studies -Foley catheter with antibiotic solution -Dialysis may be required before surgery for fluid overload or hyperkalemia. -A patient on PD must empty the peritoneal cavity of all dialysate solution. -The vascular access extremity should be labeled "dialysis access, no procedures" to prevent use of the affected extremity for BP measurement, blood drawing, or IV infusions before the patient undergoes surgery. -New kidney gets put in the right lower abdomen, and it comes with a ureter (size is important) -Can cut down a ureter from a 6'9" donor to fit a 5'1" donor, but can't stretch the ureter from a shorter person to fit a taller person's body -New kidney and ureter gets connected to bladder, and the recipient is given a lot of IV fluids: insert a drainage catheter and watch for urine Live Donor Postoperative Care: •Care is similar to that for open or laparoscopic nephrectomy •Closely monitor renal function •Closely monitor hematocrit •Donors usually experience more pain than recipient •Donors who have had an open surgical approach may experience more pain than when a laparoscopic approach is used. •Donors who have had an open surgical approach are usually discharged from the hospital in 4 or 5 days and return to work in 6 to 8 weeks. •With the laparoscopic approach, donors are discharged from the hospital in 2 to 4 days and can return to work in 4 to 6 weeks. •The donor is seen by the surgeon 1 to 2 weeks after discharge. Recipient Postoperative Care: -Maintenance of fluid and electrolyte balance is first priority -Large volumes of urine may be produced soon after transplanted kidney placed due to: •New kidney's ability to filter BUN •Abundance of fluids during operation •Initial renal tubular dysfunction -Urine output during this phase may be as high as 1 L/hr and gradually decreases as the BUN and serum creatinine levels return toward normal. -Urine output is replaced with fluids milliliter for milliliter hourly for the first 12 to 24 hours. -Central venous pressure readings are essential for monitoring postoperative fluid status. -Dehydration must be avoided to prevent subsequent renal hypoperfusion and renal tubular damage. -Electrolyte monitoring to assess for the hyponatremia and hypokalemia often associated with rapid diuresis is critical. -Treatment with potassium supplements or infusion of 0.9% normal saline may be indicated. -IV sodium bicarbonate may also be required if the patient develops metabolic acidosis from a delay in the return of kidney function. -Acute tubular necrosis (ATN) in the transplanted kidney can occur because of prolonged cold times causing ischemic damage and the use of marginal cadaveric donors (those who are medically suboptimal). -While the patient is in ATN, dialysis is required to maintain fluid and electrolyte balance. -A sudden decrease in urine output in the early postoperative period is a cause for concern. -It may be due to dehydration, rejection, a urine leak, or obstruction. -A common cause of early obstruction is a blood clot in the urinary catheter. -Catheter patency must be maintained, since the catheter remains in the bladder for 3 to 5 days to allow the ureter-bladder anastomosis to heal. -ATN can occur because of prolonged cold ischemic times and the use of marginal cadaveric donors (those who are medically suboptimal). -Postoperative teaching should include the prevention and treatment of rejection, infection, and complications of surgery and the purpose and side effects of immunosuppression. Goals of Immunosuppressive Therapy: -Adequately suppress immune response -Lifelong therapy: •Calcineurins: cyclosporine and tacrolimus (avoid grapefruit and other acidic foods because they increase toxicity CYP450 competitive) •Corticosteriods: prednisone, methylprednisolone •Cytotoxic: azathioprine, mycophenolate, sirolimus -Maintain sufficient immunity to prevent overwhelming infection: be up to date their vaccines Rejection: -Hyperacute (antibody-mediated, humoral) rejection: occurs minutes to hours (24hrs) after transplant -Acute rejection: occurs days to first 6 months after transplant -Chronic rejection: fibrosis and scarring; process occurs over months or years and is irreversible -Assess BUN, creatinine, GFR, how much the patient is peeing, how much water they have been drinking -When patients are discharged, give them a diary so they can track their water intake Infection: -Most common infections observed in first month: •Pneumonia •Wound infections •IV line and drain infections •Urinary tract infections -Fungal infections: •Candida •Cryptococcus •Aspergillus •Pneumocystis jiroveci -Underlying systemic illness such as diabetes mellitus or systemic lupus erythematosus, malnutrition, and older age can further compound the negative effects on the immune response. -Fungal and viral infections are common because of the patient's immunosuppressed state. -Fungal infections are difficult to treat, necessitate prolonged treatment periods, and often involve the administration of nephrotoxic drugs. -Transplant recipients usually receive prophylactic antifungal drugs, such as clotrimazole (Mycelex), fluconazole (Diflucan), and trimethoprim/sulfamethoxazole (Bactrim), to prevent these infections. -Send out a UA and culture and sensitivity test to check for UTI -Aspergillus: if urine smells like lavender, the patient may be infected with this Viral infections: •CMV: one of most common •Epstein-Barr virus •Herpes simplex virus (HSV) •Varicella-zoster virus •Polyomavirus (e.g., BK virus) -Primary infections occur as new infections after transplant from an exogenous source, such as the donated organ or a blood transfusion. -Reactivation occurs when a virus exists in a patient and becomes reactivated because of immunosuppression. -If a recipient has never had CMV and receives an organ from a donor with a history of CMV, antiviral prophylaxis will be administered (e.g., ganciclovir [Cytovene], valganciclovir [Valcyte]). -To prevent HSV infections, oral acyclovir (Zovirax) is given for several months after the transplant. -CMV: big virus that goes everywhere, cats carry it in their feces so these patients should not have a cat or empty litterboxes Cardiovascular Disease: -Transplant recipients have increased incidence of atherosclerotic vascular disease -Immunosuppressants can worsen hypertension, dyslipidemia, and hyperlipidemia -Patients need to adhere to antihypertensive regimen -CV disease is the leading cause of death after renal transplantation. -Hypertension, dyslipidemia, diabetes mellitus, smoking, rejection, infections, and increased homocysteine levels (many of which existed prior to the transplant) can all contribute to CV disease. -Teach the patient to control risk factors such as elevated cholesterol, triglyceride, and blood glucose levels and weight gain. -Don't want a mean arterial pressure (MAP) of greater than 60 Malignancies: -Primary cause is immunosuppressive therapy -Regular screening is important -The overall incidence of malignancy is greater in kidney transplant recipients than in the general population. -The most common types of cancer after transplant are •Skin cancers: basal and squamous cell carcinoma and melanoma •Post-transplant lymphoproliferative disorder (PTLD). -The majority on PTLD are B-cell origin, associated with Epstein-Barr virus (EBV), and cause aggressive lymphomas (Hodgkin's and non-Hodgkin's lymphoma). -Patients are also at risk for cancers of the colorectal, breast, cervical, liver, stomach, oropharynx, anus, vulva, and penis. -Preventive care: protective clothing and sunscreen Recurrence of Original Kidney Disease: -Glomerulonephritis -IgA nephropathy -Diabetic nephropathy -Focal segmental sclerosis -Patients must be advised before transplantation if they have a disease known to recur. Corticosteroid-Related Complications: -Aseptic necrosis of hips, knees, and other joints -Peptic ulcer disease -Glucose intolerance and diabetes -Dyslipidemia -Cataracts -Infection -Malignancies -In the first year after transplant, corticosteroid doses are usually decreased to 5 to 10 mg/day. -The use of tacrolimus and cyclosporine has allowed the corticosteroid doses to be much lower than they were in the past. -Many transplant programs have initiated corticosteroid-free drug regimens because of the problems associated with long-term corticosteroid use. -Other centers withdraw patients from corticosteroids after transplantation. -For patients who remain on corticosteroids, vigilant monitoring for side effects and early treatment are essential.