UNIT 2

With clinically evident atherosclerotic CVD With primary low-density lipoprotein (LDL) cholesterol levels of at least 190 mg/dL With type-1 or type-2 diabetes (ages 40 to 75 years) and an LDL cholesterol level of 70 mg/dL or higher, without clinically evident atherosclerotic CVD Without clinically evident atherosclerotic CVD or diabetes with an LDL cholesterol level range of 70 to 189 mg/dL and an estimated 10-year risk of atherosclerotic CVD of at least 7.5% (Note: A downloadable spreadsheet enabling estimation of 10-year and lifetime risk for atherosclerotic CVD and a web-based calculator are available at

The groups who would benefit from statin therapy (cholesterol lowering medications) are those:

ischemia injury necrosis and infarction

ST-segment depression is seen with______ ST-segment elevation is seen with ____ Q waves are seen with _____

Heart failure (HF)

is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. In the past, HF was often referred to as congestive heart failure (CHF), because many patients experience pulmonary or peripheral congestion. Currently HF is recognized as a clinical syndrome characterized by signs and symptoms of fluid overload or of inadequate tissue perfusion. Fluid overload and decreased tissue perfusion result when the heart cannot generate a cardiac output (CO) sufficient to meet the body's demands The term heart failure indicates myocardial disease in which there is a problem with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) that may or may not cause pulmonary or systemic congestion. Some cases of HF are reversible, depending on the cause. Most often, HF is a progressive, lifelong diagnosis that is managed with lifestyle changes and medications to prevent acute congestive episodes. HF results from a variety of cardiovascular (CV) conditions (including chronic hypertension [HTN], CAD, valvular disease, congenital heart defects, and arrhythmias) as well as from conditions such as diabetes mellitus, fever, infection, thyrotoxicosis, iron overload, hypoxia, anemia, and pulmonary embolus Systolic HF results in a decrease in the volume of blood being ejected from the ventricle. The decreased ventricular stretch is sensed by baroreceptors (sensors in blood vessels that respond to perfusion pressure of blood flow) in the aortic and carotid bodies.The sympathetic nervous system is stimulated to release epinephrine and norepinephrine. Sympathetic stimulation causes vasoconstriction of the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the kidney. Renin promotes the formation of angiotensin I, a benign, inactive substance. Angiotensin-converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload (see alert below). Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in retention of sodium and fluid, excretion of potassium (K+) by the renal tubules, and stimulation of the thirst center. This leads to the fluid volume overload commonly seen in HF. Angiotensin, aldosterone, and other neurohormones (e.g., endothelin, prostacyclin) lead to an increase in preload (see alert below) and afterload, which increases stress on the ventricular wall, causing an increase in the workload of the heart. As the heart's workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in end-diastolic blood volume (preload) in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricle (ventricular dilation). The increased size of the ventricle further increases the stress on the ventricular wall, adding to the workload of the heart. One way the heart compensates for the increased workload is to increase the thickness of the heart muscle (ventricular hypertrophy). However, hypertrophy results in an abnormal proliferation of myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones (e.g., angiotensin II), large myocardial cells are produced that are dysfunctional and die early, leaving the other normal myocardial cells to struggle to maintain CO

Pericardial effusion

(accumulation of fluid in the pericardial sac) may accompany pericarditis, advanced HF, metastatic carcinoma, chemotherapy, cardiac surgery, or trauma. Pathophysiology An increase in pericardial fluid raises the pressure within the pericardial sac and compresses the heart. This has the following effects: Increased right ventricular end-diastolic pressure (RVEDP) and left ventricular end-diastolic pressure (LVEDP) Decreased venous return Inability of the ventricles to distend and fill adequately Clinical Manifestations and Assessment feeling of fullness within the chest or may have substantial or ill-defined pain. venous pressure tends to increase, as evidenced by engorged neck veins during inspiration. This rise in venous pressure and vein distension during inspiration is known as Kussmaul sign dyspnea, cough, labile or low blood pressure. Systolic blood pressure that is markedly lower during inhalation is called pulsus paradoxus. Pulsus paradoxus exceeding 10 mm Hg is abnormal. pericardial friction rub The cardinal signs of cardiac tamponade are falling systolic blood pressure, narrowing pulse pressure (difference between the systolic and diastolic pressure, should normally be above 40 mm Hg), rising venous pressure (increased JVD) during inspiration, and distant (muffled) heart sounds (Fig. 15-4). If untreated, shock and death can result.

Unstable angina

(also called preinfarction angina or crescendo angina): Symptoms occur more frequently and last longer than in stable angina. The threshold for pain is lower, and pain may occur at rest.

Transtelephonic monitoring (TTM)

, a form of outpatient ECG monitoring, transmits ECG signals via the telephone. Chest electrodes are connected to a transmitter box. To send the ECG, the telephone mouthpiece is placed over the transmitter box, and the ECG is evaluated at another location. This method is used for diagnosing arrhythmias and evaluating permanent cardiac pacemakers. It is a patient-activated recording that can be sent directly over the phone line and captures data when symptoms present during activities of daily living.

Metabolic syndrome

A diagnosis of this syndrome includes any combination of three of the following conditions: Insulin resistance (fasting glucose greater than 110 mg/dL or abnormal glucose tolerance test) (Har, 2016) Abdominal obesity (waist circumference greater than 35 inches in women, greater than 40 inches in men) Dyslipidemia (triglycerides greater than 150 mg/dL; HDL less than 50 mg/dL in women, less than 40 mg/dL in men) HTN (at least 130/85 mm Hg) (Har, 2016) Proinflammatory state (high levels of C-reactive protein [CRP]) Prothrombotic state (high fibrinogen)

new guidelines for the definition of elevated blood pressure : (Systolic 120 to 129 mm Hg and diastolic <80 mm Hg) Hypertension: (Stage 1 is defined as Systolic 130 to 139 mm Hg or diastolic 80 to 89 mm Hg), and Stage 2 is a Systolic at least 140 mm Hg or diastolic at least 90 mm Hg).

classifications of bp for adults 18 and older

Coronary Artery Stent

After PCI, the area that has been treated may potentially close off partially or completely, a process called restenosis. The intima of the coronary artery has been injured and responds by initiating an acute inflammatory process. This process may include release of mediators that lead to vasoconstriction, clotting, and scar tissue formation. A coronary artery stent is placed to overcome these risks. Restenosis happens in 10% to 50% of patients with PCI after balloon angioplasty without stenting, usually within 6 months (Teirstein & Lytle, 2016). A stent is a metal mesh that provides structural support to a vessel at risk of acute closure. Either bare metal or "drug eluting" stents are used; there are guidelines in place to aid in determining which the cardiologist should choose. Stents have been shown to improve long-term outcomes of PCI (Grossman & Porth, 2014). The stent is positioned over the angioplasty balloon. When the balloon is inflated, the mesh expands and presses against the vessel wall, holding the artery open. The balloon is withdrawn, but the stent is left permanently in place within the artery; eventually endothelium covers the stent, and it is incorporated into the vessel wall. Because of the risk of thrombus formation in the stent, the patient receives antiplatelet medications (examples are clopidogrel [Plavix] and aspirin). These medications are routinely continued for at least 3 to 6 months to decrease the risk of thrombus formation.

heredity, obesity, sleep apnea, advancing age, renal changes, ethnicity/race. diabetes, type A personality, smoking, sedentary lifestyle, Hypothyroidism increased sympathetic nervous system activity increased renal reabsorption of sodium, chloride, and water. increased activity of the renin-angiotensin-aldosterone system,

Associated factors for essential hypertension include

Chest pain that occurs suddenly and continues despite rest and medication Electrocardiogram T-wave inversion, ST-segment elevation, abnormal Q wave The first ECG signs of an acute MI occur as a result of myocardial ischemia and injury. As the area becomes ischemic, myocardial repolarization is delayed, causing the T wave (representing ventricular depolarization) to invert. The ischemic region may remain depolarized while adjacent areas of the myocardium return to the resting state. As ischemia progresses to injury, the T wave becomes enlarged and symmetric. ST segment may rise at least 1 mm above the isoelectric line (area between the T wave and the next P wave is used as the reference for the isoelectric line), or there may be non-ST-segment elevation. Cardiac muscle injury causes elevation of the ST segment and tall, symmetrical T waves. Later, Q waves develop because of the absence of depolarization current from the necrotic tissue and opposing currents from other parts of the heart.

CLINICAL MANIFESTATIONS OF MI

CABG may result in complications such as MI, arrhythmias, hemorrhage, kidney dysfunction. Potential Complications of Cardiac Surgery Decreased Cardiac Output Hypovolemia (most common cause of decreased cardiac output after cardiac surgery) Net loss of blood and intravascular volume Surgical hypothermia (as the reduced body temperature rises after surgery, blood vessels dilate and more volume is needed to fill the vessels). IV fluid loss to the interstitial spaces because surgery and anesthesia make capillary beds more permeable. Increased heart rate, arterial hypotension, low pulmonary artery wedge pressure (PAWP), and low central venous pressures (CVP) often are seen. Fluid replacement may be prescribed. Replacement fluids include: Colloid (albumin, heta-starch), packed red blood cells, or crystalloid solution (normal saline, lactated Ringer's solution). Persistent bleeding Cardiopulmonary bypass may cause platelet dysfunction, and hypothermia alters clotting mechanisms. Surgical trauma causing tissues and blood vessels to ooze bloody drainage. Intraoperative anticoagulant (heparin) therapy Postoperative coagulopathy may also result from liver dysfunction and depletion of clotting components. Accurate measurement of wound bleeding and chest tube blood is essential. Bloody drainage should not exceed 200 mL/hr for the first 4 to 6 hours. Drainage should decrease and stop within a few days, while progressing from sanguineous to seros anguineous and serous drainage. Protamine sulfate may be administered to neutralize unfractionated heparin; vitamin K and blood products may be used to treat hematologic deficiencies. If bleeding persists, the patient may return to the operating room. Cardiac tamponade Fluid and clots accumulate in the pericardial sac, which compresses the heart, preventing blood from filling the ventricles. Signs and symptoms include arterial hypotension, tachycardia, muffled heart sounds, decreasing urine output, and ↑ CVP. Additional signs and symptoms: arterial pressure waveform demonstrating a pulsus paradoxus (decrease of more than 10 mm Hg during inspiration) and decreased chest tube drainage (suggesting that the drainage is trapped or clotted in the mediastinum). The chest drainage system is checked to eliminate possible kinks or obstructions in the tubing. Patency of the tubing in the chest drainage system must be maintained, the nurse can facilitate movement of the fluid by adjusting the position of the tubing therefore helping with forward flow. Chest x-ray may show a widening mediastinum. Emergency medical management is required; may include pericardiocentesis or return to surgery. Fluid overload High PAWP, CVP, and pulmonary artery diastolic pressures, as well as crackles indicate fluid overload. Diuretics are prescribed and the rate of IV fluid administration is reduced. Alternative treatments include continuous renal replacement therapy and dialysis. Hypothermia Low body temperature leads to vasoconstriction, shivering, and arterial hypertension. Patient is rewarmed gradually after surgery, decreasing vasoconstriction. Hypertension Results from postoperative vasoconstriction. It may stretch suture lines and cause postoperative bleeding. The condition may be transient. Vasodilators (nitroglycerin [Tridil], nitroprusside [Nipride, Nitropress]) may be used to treat hypertension. Administer cautiously to avoid hypotension. Tachyarrhythmias Increased heart rate is common with perioperative volume changes. Uncontrolled atrial fibrillation commonly occurs during the first few days postoperatively. If a tachyarrhythmia is the primary problem, the heart rhythm is assessed and medications (e.g., adenosine [Adenocard, Adenoscan], amiodarone [Cordarone], digoxin [Lanoxin], diltiazem [Cardizem], esmolol [Brevibloc], lidocaine [Xylocaine], procainamide [Pronestyl]), may be prescribed. Patients may be prescribed antiarrhythmics before coronary artery bypass graft (CABG) to minimize the risk of postoperative tachyarrhythmias. Carotid massage may be performed by a provider to assist with diagnosing or treating the arrhythmia. Cardioversion and defibrillation are alternatives for symptomatic tachyarrhythmias. For patients who cannot attain normal sinus rhythm, an alternate goal may be to establish a stable rhythm that produces a sufficient cardiac output. Bradycardias Decreased heart rate Many postoperative patients will have temporary pacer wires that can be attached to a pulse generator (pacemaker) to stimulate the heart to beat faster. Less commonly, atropine, epinephrine, or isoproterenol may be used to increase heart rate. Cardiac failure (decreased cardiac output) Myocardial contractility may be decreased perioperatively. The nurse observes for and reports falling mean arterial pressure; rising PAWP, pulmonary artery diastolic pressure, and CVP; increasing tachycardia; restlessness and agitation; peripheral cyanosis; venous distention; labored respirations; and edema. Medical management includes diuretics, digoxin, and IV inotropic agents. MI (may occur intraoperatively or postoperatively) Portion of the cardiac muscle dies; therefore, contractility decreases. Impaired ventricular wall motion further decreases cardiac output. Symptoms may be masked by the postoperative surgical discomfort or the anesthesia-analgesia regimen. Careful assessment to determine the type of pain the patient is experiencing; myocardial infarction (MI) suspected if the mean blood pressure is low with normal preload. Serial electrocardiograms (ECGs) and cardiac biomarkers assist in making the diagnosis (alterations may be due to the surgical intervention). Analgesics are prescribed in small amounts while the patient's blood pressure and respiratory rate are monitored (because vasodilation secondary to analgesics or decreasing pain may occur and compound the hypotension). Activity progression depends on the patient's activity tolerance. Impaired gas exchange During and after anesthesia, patients require mechanical assistance to breathe. Potential exists for postoperative atelectasis. Anesthetic agents stimulate production of mucus, and chest incision pain may decrease the effectiveness of ventilation. Pulmonary complications are often detected during assessment of breath sounds, oxygen saturation levels, arterial blood gases, and when monitoring peak pressure and exhaled tidal volumes on the ventilator. Extended periods of mechanical ventilation may be required while complications are treated. Hemorrhage Untoward and excessive bleeding may be life-threatening. Serial hemoglobin, hematocrit, and coagulation studies are performed to guide therapy. Administration of fluids, colloids, and blood products: packed red blood cells, fresh frozen plasma, platelet concentrate. Administration of aprotinin (Trasylol) perioperatively to reduce blood transfusion needs. Administration of desmopressin acetate (DDAVP) to enhance platelet function. Neurologic changes; stroke Inability to follow simple commands within 6 hours of recovery from anesthetic; different capabilities on right or left side of body Neurologically, most patients begin to recover from anesthesia in the operating room. Patients who are elderly or who have kidney or hepatic failure may take longer to recover. Patient should be evaluated for stroke when neurologic changes are evident. Kidney failure Usually acute and resolves within 3 months but may become chronic and require ongoing dialysis May respond to diuretics or may require continuous renal replacement therapy (CRRT) or dialysis Acute kidney Injury Often results from hypoperfusion of the kidneys or from injury to the renal tubules by nephrotoxic medications Fluids, electrolytes, BUN, creatinine, and urine output are monitored frequently. Follow your medical center's protocol for postprocedure hydration Electrolyte imbalance Postoperative imbalances in potassium, magnesium, sodium, calcium, and blood glucose are related to surgical losses, metabolic changes, and the administration of medications and IV fluids. Monitor electrolytes and basic metabolic studies frequently. Implement treatment to correct electrolyte imbalance promptly Hepatic failure Most common in patients with cirrhosis, hepatitis, or prolonged right-sided heart failure Use of medications metabolized by the liver must be minimized. Bilirubin, albumin, and amylase levels are monitored, and nutritional support must be provided. Infection Surgery and anesthesia alter the patient's immune system. Many invasive devices are used to monitor and support the patient's recovery and may serve as a source of infection. The following must be monitored to detect signs of possible infection: body temperature, white blood cell (WBC) counts and differential counts, incision and puncture sites, cardiac output and systemic vascular resistance, urine (clarity, color, and odor), bilateral breath sounds, sputum (color, odor, amount), as well as nasogastric secretions. Antibiotic therapy may be expanded or modified as necessary. Invasive devices must be discontinued as soon as they are no longer required. Institutional protocols for maintaining and replacing invasive lines and devices must be followed to minimize the patient's risk for infection

COMPLICATIONS OF CABG/ CARDIAC SURGERY

CONTINUOUS MONITORING

Class I: indicated for all patients such as those who have been resuscitated from cardiac arrest Class II: possibly indicated, but not essential, which includes patients who are post-acute myocardial infarction (MI) for 24 to 48 hours for ECG monitoring of arrhythmia, ST-segment ischemia, and/or QTc interval, and Class III: not indicated because risk is so low for patients such as those who have permanent, rate-controlled atrial fibrillation (AF).

Cardiogenic shock

Clinical Manifestations and Assessment cerebral hypoxia (restlessness, confusion, agitation), low blood pressure, rapid and weak pulse, cold and clammy skin, tachypnea with respiratory crackles, decreased urinary output. The pulmonary artery wedge pressure (indirect estimate of left atrial pressure or left ventricular preload) is elevated and the CO is decreased as the left ventricle loses its ability to pump. The systemic vascular resistance is elevated because of the sympathetic nervous system stimulation that occurs as a compensatory response to the decrease in blood pressure. The decreased blood flow to the kidneys causes a hormonal response (i.e., activation of the renin-angiotensin-aldosterone system) that causes fluid retention and further vasoconstriction. Increases in HR, circulating volume, and vasoconstriction occur to maintain circulation to the brain, heart, kidneys, and lungs but at a cost: an increase in the workload of the heart. When the cellular oxygen needs cannot be met, anaerobic metabolism and buildup of lactic acid occur. As a result, ABGs would reveal metabolic acidosis. Continuous central venous oximetry and measurement of blood lactic acid levels may help assess the severity of the shock as well as the effectiveness of treatment. Refer to Chapter 55 for further discussion on lactic acid levels. Continued cellular hypoperfusion eventually results in organ failure. The patient becomes unresponsive, severe hypotension ensues, and the patient develops shallow respirations and cold, cyanotic or mottled skin. Laboratory tests results indicate organ dysfunction.

Bleeding or hematoma Expanding mass surrounding puncture site; hard lump or bluish tinge at sheath insertion site Anticoagulant therapy, coughing, vomiting, bending leg or hip, obesity, bladder distention, high blood pressure Keep the patient on bed rest. Apply manual pressure at site of sheath insertion. Outline extent of hematoma with a marking pen. Monitor results of complete blood cell count and vital signs. If bleeding does not stop, notify physician or nurse practitioner. Anticipate interruption of anticoagulant and antiplatelet therapies. Blood transfusion may be indicated. Lost or weakened pulse distal to sheath insertion site Extremity cool, cyanotic, pale, or painful Arterial thrombus or embolus Assess peripheral circulation by comparing bilateral pulses; note temperature, capillary refill, sensation, and movement, as well as color of the affected extremity. Notify physician or nurse practitioner. Anticipate surgery and anticoagulation or thrombolytic therapy. Pseudoaneurysm and arteriovenous fistula; if they rupture, sudden massive swelling and severe pain will be seen. A large painful pulsatile mass felt or bruit heard near sheath insertion site Vessel trauma during procedure Notify physician or nurse practitioner. Anticipate ultrasound-guided compression. If the pseudoaneurysm is small (less than 2 cm), it may be observed and monitored clinically. Assess circulation, sensation, and motility of involved extremity. Prepare patient for surgery to close fistula if indicated. Retroperitoneal bleeding (blood collecting in the retroperitoneal space may not produce obvious swelling or skin color changes) Back or flank pain Unexplained hypotension Tachycardia Restlessness and agitation Decreased hemoglobin/hematocrit Cullen sign (bluish to purplish periumbilical discoloration) and Grey Turner sign (flank discoloration) may be noted with retroperitoneal bleed Arterial tear causing bleeding into flank area Notify physician or nurse practitioner immediately. Stop any anticoagulation medication. Anticipate need for IV fluids and/or administration of blood. Acute kidney failure Decreased urine output, elevated blood urea nitrogen (BUN), creatinine Nephrotoxic contrast agent Provide hydration to promote excretion of contrast material. Monitor urine output. Monitor BUN and creatinine. Administer renal protective agents (e.g., acetylcysteine [Mucomyst] before and after procedure as prescribed. Allergic reaction Urticaria, hives, sneezing, and bronchospasm Allergic reaction to dye is higher in patients allergic to penicillin or shellfish and in those with known prior reaction to contrast material. Anticipate administering prednisone, antihistamines, and H2 blockers before the coronary procedure for patients with known prior reaction to contrast material or shellfish. If anaphylaxis occurs, the nurse anticipates administering epinephrine and IV saline for hydration. Cardiac tamponade Tachypnea, tachycardia, hypotension, jugular venous distention, and muffled heart sounds; cool extremities from hypoperfusion in some patients Most common cause is perforation due to rupture of a coronary artery. Anticipate a pericardiocentesis in patients with compromised hemodynamic status. Chest pain/acute ischemic event/spasm Complaints of chest pain Benign stent sensation, acute stent thrombosis, abrupt vessel closure, transient coronary spasms, side branch occlusion, and distal embolization of debris Notify the provider when patient complains of chest pain. Monitor vital signs, O2 sat, and lung and cardiac sounds. Assess peripheral perfusion. Monitor electrocardiogram (ECG). Perform serial tests for cardiac markers. Measure troponin. Obtain a 12-lead ECG with any episodes of chest pain.

Complications After Percutaneous Coronary Intervention (PCI)

MI

Coronary occlusion, heart attack, and MI are terms used synonymously, but the preferred term is MI. Pathophysiology In an MI, an area of the myocardium is permanently destroyed. MI is usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. In unstable angina, the plaque ruptures, but the artery is not completely occluded. Because unstable angina and acute MI are considered to be the same process but occurring at different points along a continuum, the term acute coronary syndrome (ACS) may be used in lieu of these diagnoses. Other causes of MI include vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (e.g., from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (e.g., from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine). In each case, a profound imbalance exists between myocardial oxygen supply and demand. Various descriptions are used to further identify an MI: the type of MI (ST-segment elevation, non-ST-segment elevation), the location of the injury to the ventricular wall (anterior, inferior, posterior, or lateral wall), the point in time within the process of infarction (acute, evolving, or old), and the extent of the damage to the myocardium caused by the MI (partial or full thickness). Partial infarcts are associated with severely narrow coronary arteries and present as non-ST-segment elevation, while full-thickness infarcts commonly occur with obstruction of a single coronary artery and present as ST elevation on ECG readings

Large-box Method

Count the number of large boxes between two consecutive R waves (ventricular rate) or P waves (atrial rate) and divide into 300. If, for example, there are four large boxes between two R waves, the heart rate is 300/4, or 75.

Small-box Method

Count the number of small boxes between two consecutive R (ventricular rate) or P waves (atrial rate) waves and divide into 1,500. If, for example, there are 10 small boxes between two R waves, the heart rate is 1500/10, or 150 (see Fig. 17-4). The normal heart rate is between 60 and 100. The term bradycardia is used when the heart rate is below 60, whereas tachycardia refers to rates above 100.

Monitor one limb lead or one limb lead plus one chest lead Monitor ST segments (ST-segment depression is a marker of myocardial ischemia; ST-segment elevation provides evidence of an evolving MI) Monitor QT segments for prolongation Provide graded visual and audible alarms (based on priority, asystole would be highest) Provide computerized rhythm monitoring (arrhythmias are interpreted and stored in the memory of the monitoring system) Produce a graphical recording Interface with the electronic medical record (as applicable)

ECG monitoring systems vary in sophistication but, in general, can do the following:

Ultrafiltration (UF)

Eases symptoms for patients in decompensated HF and can help some patients to respond again to conventional drug therapy; it is a low-volume extracorporeal process that removes fluid from the intravascular compartment. Recent studies show inconsistent findings on the benefit of UF vs. standard diuretic therapy (Mehra, 2015; Marenzi, Kazory, & Agostoni, 2015). Uses a mechanical pump and a hemofilter to remove a specified amount of fluid with each treatment, alleviating the patient's symptoms. Treatment time varies depending on patient needs. During treatment, the intravascular fluid volume remains stable, since fluid shifts from the interstitial space to replace fluid lost in treatment, which reduces edema and third-spacing. Typically, patients do not become hypotensive or hypovolemic with this treatment (Klein, 2014).

Systolic Failure

Impaired ventricular pumping of blood during systole Characterized by reduced stroke volume, incomplete ventricular emptying, cardiac dilation, and elevated left ventricular diastolic pressure Reduced cardiac output evokes compensatory neurohormonal responses that increase heart rate, sodium and water retention, and vasoconstriction Usually caused by ischemic or idiopathic dilated cardiomyopathy, when the left ventricle cannot adequately contract or squeeze out its contents, so that preload increases and stroke volume decreases

Diastolic Failure

Impaired ventricular relaxation filling during diastole Characterized by a stiffened left ventricle that cannot relax and fill sufficiently at normal diastolic pressure The result is either decreased left ventricular end-diastolic volume (leading to decreased cardiac output) or a compensatory rise in left ventricular filling pressure, which can lead to pulmonary venous hypertension Usually caused by hypertensive, hypertrophic, or restrictive cardiomyopathy

Heart transplant

For some patients with end-stage HF, cardiac transplantation is the only option for long-term survival. Some of these patients require mechanical circulatory assistance with an implanted ventricular assist device as a bridge therapy to cardiac transplantation. Research continues toward perfection of a totally implantable artificial heart that may be used as an alternative to transplantation. Heart transplantation involves replacing a person's diseased heart with a donor heart. This is an option for advanced HF patients when all other therapies have failed (Ammirate et al., 2014).

Wireless Mobile Cardiac Monitoring Systems

This outpatient monitoring system, mobile cardiac telemetry (MCT), uses a small sensing device worn by the patient; it transmits the ECG signal to a monitor. When an arrhythmia is detected, the system transmits the ECG to a monitoring center via a telephone line or a wireless communication system. This system enhances detection and early treatment of arrhythmias.

Time and rate are measured on the horizontal axis of the graph, amplitude or voltage is measured on the vertical axis. Each small block on the graph paper equals 0.04 second, and five small blocks form a large block, which equals 0.2 second. When an ECG waveform moves toward the top of the paper, it is called a positive deflection. When it moves toward the bottom of the paper, it is called a negative deflection.

INTERPRETING THE ELECTROCARDIOGRAM

Pericardiocentesis

If cardiac function becomes seriously impaired as a result of pericardial effusion, pericardiocentesis (puncture of the pericardial sac to aspirate pericardial fluid) is performed to remove fluid from the pericardial sac (Fig. 15-5). The major goal of this procedure is to prevent cardiac tamponade, which restricts normal heart filling and contraction. During the procedure, vital signs, oxygen saturation, ECG and, if applicable, hemodynamic pressures are measured. Emergency resuscitation equipment should be readily available. The head of the bed is elevated to 45 to 60 degrees, placing the heart in proximity to the chest wall so that the needle can be inserted into the pericardial sac more easily. If a peripheral IV line is not already in place, one is inserted, and a slow IV infusion is started in case it becomes necessary to administer emergency medications or blood products.

Cardiac resynchronization therapy (CRT)

In the patient with HF who does not improve with standard therapy, CRT may be beneficial. CRT involves the use of a biventricular pacemaker to treat electrical conduction defects. Left bundle branch block is a feature of delayed conduction that is frequently seen in patients with HF that results in dyssynchronous conduction and contraction of the right and left ventricles, which can further decrease EF (Yancy et al., 2013). Use of a pacing device with leads placed in the right atrium, right ventricle, and left ventricular can synchronize the contractions of the right and left ventricles. This intervention has been shown to improve cardiac output, optimize myocardial energy consumption, reduce mitral regurgitation, and slow the ventricular remodeling process. For selected patients, this results in fewer symptoms and increased functional status (Yancy et al., 2013; Krishnamoorthy & Felker, 2014). For patients who require CRT and an implantable cardiac defibrillator (ICD), combination devices are available.

Six-second Method

Locate the 3-second markers along the top or bottom of the ECG paper. Count the number of R waves (ventricular rate) or P waves (atrial rate) occurring between two 3-second markers (thus total time is 6 seconds) and multiply by 10 (thus, 60 seconds or 1 minute).

Alleviation of angina that cannot be controlled with medication or PCI Treatment of multivessel CAD and complicated lesions Prevention and treatment of MI, arrhythmias, or heart failure Treatment for complications from an unsuccessful PCI

MAJOR INDICATIONS FOR CABG

Silent ischemia:

Objective evidence of ischemia (such as electrocardiogram changes with a stress test), but patient reports no symptoms

The patient with suspected MI is given aspirin, nitroglycerin, morphine, beta-blocker, Also on discharge, there needs to be documentation that the patient was discharged on a statin, an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin-receptor blocking agent (ARB), and aspirin. These are "quality indicators" for ACS treatment and are now publicly reported measures. Remember SAAB: statin, ace or arb, aspirin, beta-blocker. If any of these are not prescribed, clear documentation as to why not must be provided. Analgesics The analgesic of choice for acute MI is morphine sulfate

PHARMACOLOGIC THERAPY FOR MI

Variant angina (also called Prinzmetal's angina):

Pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm

ABNORMAL VENTRICULAR CONDUCTION (BBB)

Pathophysiology If there is a delay or defect in the conduction system within the ventricles (right and left bundle branches), the QRS complex will be prolonged or widened (greater than 0.12 second). A BBB may be described as right or left and complete or incomplete. They may occasionally be present in otherwise healthy individuals; however, they may also be caused by ventricular enlargement (ventricular hypertrophy or cardiomyopathy) or anteroseptal myocardial ischemia or infarction. A BBB may be clinically insignificant, though it can be serious when associated with an acute MI.

SINUS BRADYCARDIA

Pathophysiology Sinus bradycardia occurs when the sinus node creates an impulse at a slower-than-normal rate. The causes include lower metabolic needs (e.g., sleep, athletic training, hypothyroidism), vagal stimulation (e.g., from vomiting, suctioning, severe pain, extreme emotions), medications (e.g., calcium-channel blockers, amiodarone, beta blockers), increased intracranial pressure (ICP), and MI specifically the inferior wall (10% to 15% of patients with inferior MIs develop sinus bradycardia) (Olgin & Zipes, 2015). Clinical Manifestations and Assessment ECG characteristics are: Rate: Less than 60 beats per minute (bpm) Rhythm: Regular P wave: Present before each QRS and consistent in size and shape PR interval: Normal QRS duration: Normal Medical and Nursing Management Only bradycardias that cause serious signs and symptoms (altered mental status, ongoing chest pain, hypotension, or shock) require immediate treatment. transcutaneous pacing and atropine. If pacing is unavailable or ineffective, a dopamine or epinephrine infusion may be considered If significant bradycardia is due to medications, the medications should be withheld while their necessity is re-evaluated.

VENTRICULAR TACHYCARDIA

Pathophysiology Ventricular tachycardia is defined as three or more consecutive ventricular beats occurring at a rate exceeding 100 bpm. The causes are similar to those of PVCs. Ultimately, those causes will determine the course of treatment with consideration to the underlying disease; the projected, associated risk; the period of time that the risk exists; and the benefits and risks as well as tolerance of the planned treatment. VT is usually associated with ACS but can also occur in specific clinical conditions: after an MI, with inherited primary arrhythmia syndromes, such as long QT syndrome, with electrolyte imbalances, cardiomyopathies, structural heart disease, and due to proarrhythmic medications that may precede ventricular fibrillation. Untreated VT can deteriorate into ventricular fibrillation, a lethal arrhythmia and sudden cardiac death. Clinical Manifestations and Assessment The patient can experience a range of symptoms related to decreased cardiac output, such as hypotension or syncope, pulselessness, and unresponsiveness. In contrast, some patients may be initially asymptomatic but usually will decompensate hemodynamically. ECG characteristics are: Rate: 100 to 250 bpm Rhythm: Regular P wave: Usually not visible; if visible are not associated with the QRS complex (called dissociation) PR interval: None QRS duration: Greater than 0.12 second Medical and Nursing Management epinephrine alone should be considered to establish a rhythm that can be treated in the event that the initial rhythm is a nonshockable one. Amiodarone administered IV is often the antiarrhythmic medication of choice for a stable patient with VT. Cardioversion is the treatment of choice for monophasic VT in a symptomatic patient.

Implantable cardiac defibrillators (ICDs)

Patients with HF are at high risk for arrhythmias. In patients with life-threatening arrhythmias, placement of an ICD can prevent sudden cardiac death and extend survival. ICDs can provide a range of therapies that include cardioversion, defibrillation, and pacing. A lead or leads are placed in the appropriate chamber's endocardium and attached to a generator box that can be implanted in the right or left side of the chest, under the clavicle. Wearable cardioverter defibrillators have recently been used as a bridge to implantable defibrillators (Chung, 2014).

Ventricular access devices/destination therapy

Patients with end-stage HF may require a ventricular assist device (VAD) for greater support for the failing ventricle(s). A VAD can reduce myocardial ischemia and workload, limit permanent cardiac damage, and restore adequate organ perfusion. Indications for use include: as a bridge to myocardial recovery in acute ventricular failure (e.g., shock, acute MI, etc.), as a bridge to heart transplantation in chronic ventricular failure, and for permanent therapy for end-stage chronic HF. VADs are also known as destination therapy. VADs are mechanical blood pumps that work by augmenting or replacing the function of either the left or right ventricle. There are currently four FDA-approved devices that are used as bridges to transplantation in adults. One of the four is also approved for use as destination therapy or as long-term mechanical support of the heart. The devises may be pulsatile or continuous flow (nonpulsatile) (Sunagawa et al., 2017). All shares a common problem with infectious complications, risk for thromboembolic complications, and possibility of mechanical failure common to any machine.

Cardiac rehabilitation is categorized in three phases.

Phase I begins with the diagnosis of atherosclerosis, which may occur when the patient is admitted to the hospital for ACS (e.g., unstable angina or acute MI). It includes any postprocedural activity that occurs during the hospitalization. Phase I consists of low-level activities and initial education for the patient and family. Phase II occurs after the patient has been discharged. It usually lasts for 4 to 6 weeks but may extend to 6 months. This outpatient program consists of supervised, often ECG-monitored, exercise training that is individualized based on the results of an exercise stress test. Phase III focuses on maintaining cardiovascular stability and long-term conditioning. The patient is usually self-directed during this phase and does not require a supervised program, although it may be offered. The goals of each phase build on the accomplishments of the previous phase.

Stable angina:

Predictable and consistent pain that occurs on exertion and is relieved by rest

Left-Sided HF

Pulmonary congestion from impaired left ventricle (LV) function LV cannot pump blood out of the ventricle effectively into the aorta and the systemic circulation Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary interstitial edema and impaired gas exchange Dyspnea, orthopnea, PND Cough Pulmonary crackles (rales) Decrease O2 saturation levels S3 ventricular gallop Oliguria, if kidney perfusion is diminished (Note: Nocturia may occur when perfusion improves with sleeping due to improved perfusion at rest.) Decreased perfusion to other systemic organs (advanced failure): Sluggish GI motility Dizziness, lightheadedness, confusion, restlessness Anxiety Skin cool and clammy Decrease in EF Tachycardia and/or weak/thready pulse Fatigue or activity intolerance

Pericardiotomy

Recurrent pericardial effusions, usually associated with neoplastic disease, may be treated by a pericardiotomy (pericardial window). Under general anesthesia, a portion of the pericardium is excised to permit the pericardial fluid to drain continuously into the mediastinum and is reabsorbed via lymphatics (Imazio, 2014). The nursing care is the same as that for other cardiac surgery

RIGHT SIDED HF

Right ventricle pump failure leading to congestion in the peripheral tissues and the viscera Right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the venous circulation Increased venous pressure leads to jugular vein distension (JVD) and increased hydrostatic pressure throughout the venous system. Normal central venous pressure (CVP) is 2-8 mm Hg. A CVP greater than 8 mm Hg associated with hypervolemia (excessive fluid circulating in the body) or right-sided HF Hepatomegaly, hepatojugular reflux, and ascites can occur with venous congestion due to right-sided HF. Recall with right-sided HF, there is accumulation of fluid in the systemic venous circulation. Lower extremity dependent edema (dependent edema is swelling that follows the position of the body): Legs and feet May progress to thighs, external genitalia, lower trunk, abdomen, and sacral edema (in a bed-bound patient) Pitting edema (indentations in the skin remain even after slight compression with the fingertips) Hepatomegaly (enlargement of the liver) Ascites (accumulation of fluid in the peritoneal cavity) Anorexia and nausea Weight gain due to retention of fluid Weakness/fatigue from reduced CO and impaired cognition Decreased perfusion to other systemic organs (advanced failure)

Clinical Manifestations and Assessment Ischemia of the heart muscle may produce pain or other symptoms, varying in severity from mild indigestion to a choking or heavy sensation in the upper chest that ranges from discomfort to agonizing pain accompanied by severe apprehension and a feeling of impending death. Typically, the pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm. The patient often feels tightness or a heavy, choking, or strangling sensation that has a vise-like, insistent quality. The patient with diabetes mellitus may not have severe pain with angina because diabetic neuropathy can dull the perception of pain. A woman may have different symptoms than a man, because coronary disease in women tends to be more diffuse and affects long segments of the artery rather than discrete segments. Table 14-2 discusses anginal pain. The nurse is alert for complaints of unusual fatigue; weakness or numbness in the arms, wrists, and hands; SOB; pallor; diaphoresis; anxiety; dizziness or lightheadedness; and nausea and vomiting that may accompany the pain (called associated signs and symptoms). Angina may subside with rest or nitroglycerin. In many patients, anginal symptoms follow a stable, predictable pattern. The diagnosis of angina begins with the patient's history related to the clinical manifestations of ischemia. A 12-lead electrocardiogram (ECG) and blood laboratory biomarker values help in making the diagnosis. The patient may undergo an exercise or pharmacologic stress test in which the heart is monitored by ECG, echocardiogram, or both. The patient may also be referred for a nuclear scan or invasive procedure (e.g., cardiac catheterization, coronary artery angiography). Medical Management The objectives of the medical management of CAD and angina are to decrease the oxygen demand of the myocardium and to increase the oxygen supply. Medically, these objectives are met through pharmacologic therapy and control of risk factors. Alternatively, reperfusion procedures may be used to restore the blood supply to the myocardium. These include PCI procedures (e.g., percutaneous transluminal coronary angioplasty [PTCA] with intracoronary stent placement, atherectomy) CABG.

SIGNS AND SYMPTOMS DIAGNOSIS TREATMENT OF ANGINA

Positive inotrope: A medication that increases myocardial contractility (force of contraction) Negative inotrope: A medication that decreases myocardial contractility Positive chronotrope: A medication that increases heart rate Negative chronotrope: A medication that decreases heart rate Nitrates Beta-Adrenergic Blocking Agents Calcium-Channel Blocking Agents Antiplatelet and Anticoagulant Medications Oxygen Administration

Several types of drugs are used to treat coronary vascular disease:

Intractable or refractory angina:

Severe incapacitating chest pain

Respiratory Tachypnea, shortness of breath (SOB), orthopnea, dyspnea on exertion (DOE), hypoxemia, crackles on lung auscultation, wheeze, dry or productive cough Cardiac and peripheral vascular Edema, jugular vein distention (JVD), displaced point of maximum impulse (PMI), S3 gallop rhythm, tricuspid and/or mitral regurgitation murmurs, hypotension, decreased mean arterial pressure (MAP), narrow pulse pressure, cool skin and extremities, delayed capillary refill, tachycardia Renal Decreased urinary output, oliguria, rising creatinine Gastrointestinal Abdominal distention, ascites, liver engorgement, positive abdominojugular reflex Central nervous Dizziness, decreased sensorium, syncope, fatigue Behavioral/emotional Anxiety, restlessness

Signs and Symptoms of Decreased Cardiac Output

0.10 0.10

The normal QRS interval is less than ___second (2.5 small boxes). QRS duration of more than ___is termed "wide QRS" and is indicative of abnormal ventricular conduction, such as BBBs or ventricular tachycardia.

STEMI:

The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. In this type of MI, significant damage to the myocardium occurs.

Unstable angina:

The patient has clinical manifestations of coronary ischemia, but ECG or cardiac biomarkers show no evidence of acute MI.

Non-STEMI:

The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI.

"off pump" CABG or "OPCAB."

The potential benefits of OPCAB include a decrease in the incidence of stroke and other neurologic complications, reduced blood usage, less kidney failure, and fewer cardiac rhythm disturbances. Also done today is the "MIDCAB," or minimally invasive coronary artery bypass surgery. The MIDCAB is performed on a beating heart via a thoracotomy incision and is only suitable for certain lesions that are located in the arteries on the anterior portions of the heart. Patients undergoing any type of CABG surgery will go to the intensive care unit for approximately 24 hours, and then transfer to the step-down unit. The average overall hospital stay for CABG surgery is anticipated at 5 days

CPB (i.e., extracorporeal circulation)

The procedure mechanically circulates and oxygenates blood for the body while bypassing the heart and lungs. CPB maintains perfusion to body organs and tissues, and allows the surgeon to complete the anastomoses in a motionless, bloodless surgical field. CPB is accomplished by placing a cannula in the right atrium, vena cava, or femoral vein to withdraw blood from the body. The cannula is connected to tubing filled with an isotonic crystalloid solution (usually 5% dextrose in lactated Ringer's solution). Venous blood removed from the body by the cannula is filtered, oxygenated, cooled or warmed by the machine, and then returned to the body. The cannula used to return the oxygenated blood is usually inserted in the ascending aorta, or it may be inserted in the femoral artery. The heart is stopped by the injection of cardioplegia solution, which is high in potassium, into the coronary arteries. The patient receives heparin to prevent clotting and thrombus formation in the bypass circuit when blood comes in contact with the foreign surfaces of the tubing. At the end of the procedure, when the patient is disconnected from the bypass machine, protamine sulfate is administered to reverse the effects of heparin. During the procedure, hypothermia is maintained, usually 28° to 32°C (82.4° to 89.6°F). The blood is cooled during CPB and returned to the body. The cooled blood slows the body's basal metabolic rate, thereby decreasing the demand for oxygen. Cooled blood usually has a higher viscosity, but the crystalloid solution used to prime the bypass tubing dilutes the blood. When the surgical procedure is completed, the blood is rewarmed as it passes through the CPB circuit. Urine output, arterial blood gases (ABGs), electrolytes, and coagulation studies are monitored to assess the patient's status during CPB.

Troponin,

a protein found in the myocardium, regulates the myocardial contractile process. There are three isomers of troponin: C, I, and T. Troponin C binds calcium to activate muscle contraction, while troponins I and T are specific for cardiac muscle, and are currently recognized as reliable and critical biomarkers of myocardial injury. A normal troponin I level is less than 0.5 ng/mL. An increase in the level of troponin in the serum can be detected within a few hours during acute MI. It remains elevated for a long period, often as long as 3 weeks, and it, therefore, can be used to detect recent myocardial damage.

continuous monitoring,

although limb electrodes are still used, they are positioned on the torso as opposed to the lower legs and arms, as in a 12-lead ECG. This allows for greater patient movement and comfort and reduced interference from skeletal muscle artifact. The four disposable electrodes are positioned in specific locations on the patient's chest, and a cable is connected to the monitor or telemetry device in the following arrangement: the right arm (RA) electrode placed on the right upper chest (below the clavicle) and the RA wire (usually white) attached; the left arm (LA) electrode placed on the left upper chest (below the clavicle) and the LA wire (usually black) attached; the left leg (LL) electrode placed on the left torso below the rib cage and on the left side of the abdomen and the LL wire (usually red) attached; the right leg (RL) electrode placed on the right torso and the RL wire (usually green) attached. A maxim used to recall placement is "white on right (snow over grass [green]) and smoke (black) over fire (red)." The color-coding of wires is not an international standard.

atherosclerosis,

an abnormal accumulation of lipid or fatty substances and fibrous tissue in the lining of arterial blood vessel walls. These substances create blockages and narrow the coronary vessels in a way that reduces blood flow to the myocardium. It is now known that atherosclerosis involves a repetitious inflammatory response to injury to the artery wall and subsequent alteration in the structural and biochemical properties of the arterial walls. Pathophysiology Atherosclerosis begins as fatty streaks of lipids that are deposited in the intima of the arterial wall. These lesions commonly begin early in life, perhaps even in childhood. Genetics and environmental factors influence the progression of these lesions. The continued development of atherosclerosis involves an inflammatory response, which begins with injury to the vascular endothelium. The injury may be initiated by smoking, hypertension (HTN), and other factors. The presence of inflammation has multiple effects on the arterial wall, including the attraction of inflammatory cells (including macrophages or monocytes, white blood cells [WBCs]) The macrophages infiltrate the injured vascular endothelium and ingest lipids, which turns them into what are called "foam cells." These foam cells are present in all stages of atherosclerotic plaque formation Activated macrophages also release biochemical substances that can further damage the endothelium, attracting platelets and initiating clotting. Smooth muscle cells within the vessel wall subsequently proliferate and form a fibrous cap over a center that is filled with lipid and inflammatory infiltrate. These deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lipid core may grow, causing it to rupture, and this ruptured plaque is a focus for thrombus formation. Then the thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI), which is the death of a portion of the heart muscle.

White-coat hypertension

and masked hypertension are two additional types of hypertension with emerging concern for complications (AHA, 2016a). The patient with white-coat hypertension has normal ambulatory BP readings but elevated pressures (greater than 140/90) in a health care office or clinic. Those identified as having white-coat hypertension should have follow-up with ambulatory home blood pressure monitoring to determine if the situation is, indeed, isolated. Ambulatory monitoring will also determine if masked hypertension exists (discussed below) and if systolic hypertension is present; in addition, it will help to prevent overdiagnosis and treatment, which may cause unnecessary side effects

The PP and RR intervals

are measured from the beginning of one P or R wave to the beginning of the next P or R wave. The PP interval is used to determine atrial rate and rhythm. The RR interval is measured from one QRS complex to the next QRS complex. The RR interval is used to determine ventricular rate and rhythm

Two leads

commonly used for continuous monitoring are leads II and V1. Lead II provides the best visualization of atrial depolarization (represented by the P wave) and is preferred for monitoring atrial activity and heart rate. Lead V1 best records ventricular depolarization and is most helpful when monitoring the patient for tachycardias. The AACN Practice Alert for dysrhythmia monitoring and the AHA Practice Standards for ECG monitoring recommend V1 as the preferred lead to monitor for wide QRS complex tachycardia. The next best lead is V6. Monitoring for ST-segment changes is also important in terms of detecting ischemia

MI, heart failure, left ventricular hypertrophy, kidney failure, stroke, impaired vision.

complications of hypertension

Hypertensive urgency

describes a situation in which BP is severely elevated, but there is no evidence of impending or progressive target organ damage (Adams & Urban, 2016). Elevated BPs associated with severe headache, epistaxis, or anxiety are classified as urgencies. Reducing blood pressure can be accomplished by increasing the dose of the patient's current medications or by adding a second medication. Oral medications with rapid onset of action may be used, including clonidine (Catapres), captopril (Capoten), or labetalol (Trandate)

Diagnostic evaluation includes: chest x-ray 12-lead electrocardiogram (ECG) two-dimensional (2D) echocardiogram with Doppler flow study three-dimensional (3D) echocardiogram with strain Cardiac magnetic resonance testing is now considered the gold standard for assessing cardiac function. complete blood cell count, electrolyte levels (including calcium and magnesium), blood urea nitrogen, creatinine, serum glucose, serum albumin, liver function tests, thyroid-stimulating hormone, urinalysis, and BNP levels. A right-sided heart catheterization MEDICAL MANAGEMENT Specific objectives include the following: Eliminate or reduce any etiologic contributory factors, especially those that may be reversible (e.g., atrial fibrillation, excessive alcohol ingestion, uncontrolled HTN). Reduce the workload on the heart by reducing afterload and preload. Optimize all therapeutic regimens. Prevent exacerbations of HF. LIFESTYLE CHANGES restriction of dietary sodium; avoidance of excessive fluid intake, alcohol, REDUCTION smoking; quitting weight reduction when indicated; regular exercise.

diagnostics for heart failure and treatment

Supraventricular tachycardia (SVT)

is a broad term used to describe tachycardias where the atrial and/or the ventricular rates exceed 100 bpm at rest (Page et al., 2016). The mechanism involves an electrical impulse originating above the ventricles, commonly from tissue at the HIS bundle and above (AV node). The heart rate is increases by an abnormal electrical impulse starting in the atria, and the ventricular rate follows the atrial impulse resulting in this "tachy" arrhythmia. Broadly, SVT includes sinus tachycardia, focal and multifocal atrial tachycardias, junctional tachycardias, AV nodal re-entry tachycardia (AVNRT), and various other accessory pathway-mediated reentrant tachycardias. Technically, AF is an SVT, but it is not grouped this way in the AHA guidelines and was addressed separately. SVTs even without AF included are among the most common arrhythmias that require treatment. Conduction abnormalities may occur because of aberrant conduction, a pre-existing BBB, or an accessory pathway that results in pre-excitation Clinical Manifestation reports of palpitations, chest pain, shortness of breath, dizziness, Syncope panic and anxiety, ECG characteristics are: Rate: over 100 bpm Rhythm: Regular P wave: If visible, inverted P waves sometimes seen after the QRS PR interval: Not measurable QRS duration: In paroxysmal SVT, the QRS is normal. Medical and Nursing Management Vagal maneuvers are recommended as a first step to discontinue the rhythm in patients who are hemodynamically stable. adenosine. synchronized cardioversion. Intravenous beta blockers, IV diltiazem, or IV verapamil (class IIa) can also be used to convert the patient's rhythm to NSR (Page et al., 2015). patients are placed on oral beta blockers, diltiazem, or verapamil and taught how to do the vasovagal maneuver.

Angina pectoris

is a clinical syndrome usually characterized by episodes or paroxysms of pain, pressure, or discomfort in the chest, jaw, shoulder, back, or arm that is caused by myocardial ischemia (Ferri, 2016). The cause is insufficient coronary blood flow (usually caused by atherosclerotic disease), resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the demand for oxygen exceeds the supply. The severity of angina is based on the precipitating activity and its effect on activities of daily living. Pathophysiology usually caused by atherosclerotic disease. Almost invariably, angina is associated with a significant obstruction of a major coronary artery. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands. When there is an increase in demand, flow through the coronary arteries needs to be increased. When there is blockage in a coronary artery, flow cannot be increased, and ischemia results. Because angina is a symptom of coronary atherosclerosis, the risk factors are the same.

Ambulatory ECG

is a continuous form of monitoring used in the outpatient setting to identify the etiology of distressing symptoms (pre-syncope, syncope, palpitations) that may be caused by arrhythmias, myocardial ischemia, or pacemaker dysfunction. In addition to monitoring for arrhythmias and evaluation of silent ischemia, ambulatory monitoring is used to evaluate arrhythmia and device therapy as well as prognosis and risk stratification of various cardiac populations. Ambulatory ECG monitoring may also be used in patients who have had a cryptogenic stroke (strokes that cannot be attributable to any specific cause) where paroxysmal AF is suspected

A cardiac catheterization

is a diagnostic procedure carried out in the cardiac catheterization laboratory where a vascular catheter is inserted in an artery (mostly radial or femoral) and threaded through your blood vessels to your heart; dye that is seen on fluoroscopy (x-ray) is then injected, and the structures of the heart and the patency of the coronary arteries are visualized. Coronary vessels with blockages are definitively identified, and often during the same procedure, are opened by a PCI. During PCI, the vascular catheter that is balloon-tipped is used to open blocked coronary arteries. Most often a stent is then deployed to maintain patency of the artery. PCI is used in patients with angina and as an intervention for acute MI. Catheter-based interventions can also be used to open blocked CABGs. Hollow catheters called sheaths are inserted usually via the radial or femoral artery and occasionally the brachial artery. Catheters are then threaded through the sheaths, up through the aorta, and into the coronary arteries. Angiography is performed using injected radiopaque contrast agents (commonly called dye) to identify the location and extent of the blockage. A balloon-tipped dilation catheter is passed through the sheath and positioned over the lesion. The physician determines the catheter position by examining markers on the balloon that can be seen with fluoroscopy. When the catheter is positioned properly, the balloon is inflated with high pressure for several seconds and then deflated. The pressure compresses and possibly "cracks" the atheroma (Fig. 14-5). The media and adventitia of the coronary artery are also stretched. The appropriate stent is then put into place to keep the artery open Because the blood supply to the coronary artery decreases while the balloon is inflated, the patient may complain of chest pain and the ECG may display significant ST-segment changes. Intracoronary stents are usually positioned in the intima of the vessel to maintain patency after the balloon is withdrawn. PCI procedures have a success rate of greater than 95%; the only exception is a chronic total coronary (100%) obstruction of the lumen, where the ability to negotiate a guidewire through the blockage is only about 50% to 90% (and varies substantially with the operator's expertise) (Teirstein & Lytle, 2016). Refer to Table 14-3 for complications after PCI.

The 12-lead ECG

is a diagnostic tool that uses 10 electrodes: one placed on each limb and six placed on the chest (precordial). In combination, these 10 electrodes produce 12 different waveforms (or leads). These 12 leads include three bipolar leads (I, II, III) and nine unipolar leads (aVR, aVL, aVF, V1-V6). Bipolar leads measure electrical activity traveling between a positive and negative electrode, while unipolar leads record electrical activity from a single reference point. Together, the 12 leads show electrical activity in both a frontal plane and a transverse plane. The four limb electrodes are placed on the lower legs, near the ankles, and on the arms, near the wrists. The remaining six electrodes are placed across the left side of the chest. Locating the specific anatomical landmark is critical for correct chest electrode placement (Box 17-2). If the patient needs a series of ECGs, consistency of electrode placement is also important. In some cases, the chest electrodes are left in place or the correct location is marked with an indelible pen to ensure the identical placement for follow-up ECGs.

Myoglobin

is a hemeprotein that helps transport oxygen. Like CK-MB enzyme, myoglobin is found in cardiac and skeletal muscle. A normal level is 5 to 70 ng/mL or 5 to 70 μg/L. The myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results are an excellent parameter for ruling out an acute MI.

premature atrial complex (PAC)

is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node. The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (e.g., as in hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states (e.g., with pregnancy), hypoxemia, or atrial ischemia, injury, or infarction. Clinical Manifestations and Assessment PACs are common ECG findings, often found without cardiac pathology. The patient may report, "My heart skipped a beat"; however, many times the patient is asymptomatic. ECG characteristics are: Rate: Depends on the underlying rhythm Rhythm: Irregular P wave: Size and shape of the P wave associated with the premature beat is different from sinus node-generated P wave PR interval: The PR interval of the premature beat is greater than 0.12 second but shorter than the sinus generated PR interval QRS duration: Normal Medical and Nursing Management If PACs are infrequent, no treatment is necessary since hemodynamic stability is maintained. If they are frequent (more than six per minute), this may be a sign of a worsening condition or the onset of more serious arrhythmias, such as AF, and further work-up may be clinically indicated.

hypertensive emergency

is a situation in which diastolic BP is greater than 120 mm Hg and must be lowered quickly to halt or prevent damage to the target organs (Adams & Urban, 2016;. Conditions associated with hypertensive emergency include eclampsia or preeclampsia, MI, dissecting aortic aneurysm, intracranial hemorrhage, and hyperthyroidism or thyroid storm. In hypertensive emergencies, patients present with severe elevations in blood pressure, accompanied by rapidly progressive target organ dysfunction, such as myocardial or cerebral ischemia or infarction, pulmonary edema, or kidney failure (Victor, 2016). Patient complaints include headaches, confusion, blurred vision, nausea and vomiting, seizures, pulmonary edema, oliguria, and hypertensive retinopathy (Victor, 2016, p. 394). The therapeutic goals are a controlled, gradual reduction of the BP by 10% in the first hour and by an additional 15% during the next 3 to 12 hours to a blood pressure of no less than 160/110 mm Hg (Victor, 2016). Additional gradual reductions are made over the next 48 hours until blood pressure normalizes.

CABG

is a surgical procedure in which a blood vessel is grafted to the occluded coronary artery so that blood can flow beyond the occlusion; it is also called a bypass graft. For a patient to be considered for CABG, the coronary arteries to be bypassed must have approximately a 70% occlusion (60% if in the left main coronary artery). If significant blockage is not present, the flow through the artery will compete with the flow through the bypass, and circulation to the ischemic area of myocardium may not be improved. It is also necessary that the artery be patent beyond the area of blockage or the flow through the bypass will be impeded. Vessels commonly used for CABG are the greater saphenous vein, followed by the lesser saphenous vein (other veins may also be used) as well as the internal thoracic arteries (Fig. 14-7). If a vein is be used, it is removed from its original location and grafted to the ascending aorta and to the coronary artery distal to the lesion. pleural effusions (fluid collection within the pleural space) in the immediate postoperative period (Heffner, 2016), which is associated with a variety of etiologies, including accumulation of pleural fluid because of congestive heart failure, surgical tissue trauma, hemorrhage from harvesting of the IMA, postoperative atelectasis and diaphragmatic dysfunction, or chylothorax (lymphatic fluid in the pleural space) because of unintended thoracic duct injury during the operative event. Signs and symptoms vary based upon the etiology; however, the nurse is alert for dyspnea, cough, orthopnea (SOB when lying flat), splinting, dullness to percussion, decreased breath sounds, and decreased respiratory excursion on the affected side

premature ventricular complex (PVC)

is an impulse that starts in a ventricle and is conducted through the ventricles before the next normal sinus impulse. Premature ventricular contractions can occur in healthy people, especially with intake of caffeine, nicotine, or alcohol. They are also caused by cardiac ischemia or infarction, increased workload on the heart (e.g., exercise, fever, hypervolemia, heart failure, tachycardia), digitalis toxicity, hypoxia, acidosis, or electrolyte imbalances, especially hypokalemia. Clinical Manifestations and Assessment The patient may be asymptomatic or complain that their heart "skipped a beat." Bigeminy is a rhythm in which every other complex is a PVC. In trigeminy, every third complex is a PVC, and in quadrigeminy, every fourth complex is a PVC. PVCs may present singly or in pairs (often referred to as couplets). Three or more successive PVCs are termed ventricular tachycardia (VT) (discussed next). ECG characteristics are: Rate: Depends on the underlying rhythm Rhythm: Regular P wave: Visibility of P wave depends on the timing of the PVC; may be absent (hidden in the QRS or T wave) or in front of the QRS. If the P wave follows the QRS, the shape of the P wave may be different. PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 second. QRS duration: Duration of the QRS in a PVC is 0.12 second or longer (wide); shape is bizarre and abnormal. Medical and Nursing Management Initial treatment is aimed at correcting the cause of the arrhythmia (e.g., treat hypokalemia). Long-term pharmacotherapy for PVCs is not indicated unless the patient is symptomatic. In the absence of disease, PVCs usually are not serious. In the patient with an acute MI or in the context of HF, PVCs may be more frequent and reflect the underlying heart disease or represent an early modifiable risk factor for heart failure

Hypertensive crisis

is defined as a diastolic BP of higher than 180/120 mm Hg. Approximately 1% of individuals with hypertension will have a hypertensive crisis at some point. Hypertensive crises occur when hypertension is untreated or has been poorly controlled as well as in those who have discontinued their medications. These crises are more common in men, older adults, and African Americans (Adams & Urban, 2016). Other causes of hypertensive crises include head injury, pheochromocytoma (a tumor of the adrenal medulla that causes excess secretion of catecholamines), food-drug interactions (such as tyramine combined with a monamine oxidase [MAO] inhibitors), eclampsia or preeclampsia, substance abuse (e.g., cocaine intoxication), and kidney disease

DASH

is low in saturated and trans fats as well as rich in potassium, calcium, magnesium, fiber, and protein. Further, the DASH approach emphasizes vegetables, fruits, and fat-free or low-fat dairy products. It includes whole grains, fish, poultry, beans, seeds, nuts, and vegetable oils and limits sodium, sweets, sugary beverages, and red meats, which not only lowers blood pressure but also prevents cardiovascular disease Consistent with the DASH approach, the target sodium intake should be 2,300 to 2,400 mg daily (1 teaspoon). Those who already have hypertension, diabetes, or CKD as well as African-American individuals and adults aged 51 and over should reduce sodium intake further, to 1,500 mg of sodium daily

the PR interval

is measured from the beginning of the P wave to the beginning of the QRS complex and represents the time needed for sinus node stimulation, atrial depolarization, and conduction through the AV node before ventricular depolarization. In adults, the normal range for the PR is 0.12 to 0.20 second.

Pulmonary edema

is the abnormal accumulation of fluid in the lungs. The fluid may accumulate in the interstitial spaces and in the alveoli. Pulmonary edema can be categorized into two subsets depending on the etiology: cardiogenic noncardiogenic Pathophysiology Myocardial scarring as a result of ischemia can limit the dispensability of the ventricle and render it vulnerable to a sudden increase in workload. With increased resistance to left ventricular filling, blood backs up into the pulmonary circulation. The patient quickly develops pulmonary edema, sometimes called flash pulmonary edema, from the blood volume overload in the lungs. Pulmonary edema can also be caused by noncardiac disorders, such as kidney failure, liver failure, and oncologic conditions that cause the body to retain fluid. The pathophysiology is similar to that seen in HF, in that the left ventricle cannot handle the volume overload, and blood volume and pressure build up in the left atrium. The rapid increase in atrial pressure results in an acute increase in pulmonary venous pressure, which produces an increase in hydrostatic pressure that forces fluid out of the pulmonary capillaries into the interstitial spaces and alveoli. Impaired lymphatic drainage also contributes to the accumulation of fluid in the lung tissues. The fluid within the alveoli mixes with air, creating "bubbles" that are expelled from the mouth and nose, producing the classic symptom of pulmonary edema: frothy sputum; alveoli are flooded with fluid from the capillaries, producing thin secretions containing air bubbles that frequently are colored with hemoglobin Clinical Manifestations and Assessment restless Anxious. sudden onset of breathlessness, sense of suffocation, cough that produces a large amount of frothy sputum (that may be blood tinged), cold and moist skin, cyanotic (bluish) nail beds, a weak and rapid pulse, pulmonary crackles (rales), expiratory wheezing, distended neck veins.

Creatinine kinase-myocardial band (CK-MB)

is the cardiac-specific isoenzyme; CK-MB is found mainly in cardiac cells and, therefore, increases only when there has been damage to these cells. Elevated CK-MB assessed by mass assay is an indicator of acute MI; its level begins to increase within a few hours and peaks within 24 hours of an MI. A normal CK-MB is 0 to 3 ng/mL or 1 to 3 μg/L. If the patient has cardiac complaints and negative CK-MB for more than 48 hours, then etiologies for the symptoms outside of an MI will be assessed.

CO

is the volume of blood being pumped by the heart per minute and is the product of the heart rate (HR) multiplied by the stroke volume (SV), which is the amount of blood pumped out from the ventricles per beat. PVR is related to the diameter of the blood vessel and the viscosity of the blood. The thicker the blood or smaller the radius of the blood vessel, the higher the resistance. Circadian variations in blood pressure occur. Blood pressure tends to be highest shortly after awakening and then decreases throughout the day, reaching the lowest point between 2 AM and 5 AM. Individuals who reflect this pattern are known as dippers; those who reflect a pattern of a flattened 24-hour blood pressure profile are referred to as nondippers. Nondippers may be at higher risk for cardiovascular and kidney disease; however, additional research is needed to determine optimal therapy

echocardiogram

is used to evaluate ventricular function. It may be used to assist in diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect hypokinetic and akinetic wall motion, can determine the ejection fraction, and can also assess valvular function.

Weight reductiom Maintain normal body weight (body mass index 18.5-24.9 kg/m2). 5-20 mm Hg/10 kg Adopt DASH (Dietary Approaches to Stop Hypertension) eating plan Consume a diet rich in fruits, vegetables, fiber, potassium, and low-fat dairy products, and reduce consumption of animal protein, fat, and saturated fat. 8-14 mm Hg Dietary sodium reduction Reduce dietary sodium intake to 2.4-g sodium or 6-g sodium chloride per day. 2-8 mm Hg Physical activity Engage in regular aerobic physical activity such as 30 minutes of brisk walking 3-5 days per week 4-9 mm Hg Moderation of alcohol consumption Limit consumption to no more than two drinks (e.g., 24-oz beer, 10-oz wine, or 3-oz 80-proof whiskey) per day in most men and to no more than one drink per day in women and lighter-weight people. 2-4 mm Hg

lifestyle changes for hypertension

The U wave

may or may not be present and is thought to represent repolarization of the Purkinje fibers; it is, however, sometimes seen in patients with hypokalemia (low potassium levels), hypertension, or heart disease. If present, the U wave follows the T wave and is usually smaller than the P wave. If tall, it may be mistaken for an extra P wave.

The treatment goal for most individuals under 60 years of age with hypertension, regardless of complicating conditions, is a BP of less than 140/90 mm Hg. The aim for individuals with prehypertension and no complicating conditions is to lower BP to normal. JNC8 recommends that people over the age of 60 begin pharmacologic treatment when the blood pressure is greater than 150/90; lifestyle changes should also be emphasized. Health care providers should monitor these patients every 1 to 3 months until their BP goal is reached and then every 3 to 6 months thereafter. While JNC7 recommended those with diabetes or CKD attain a target pressure of less than 130/80 mm Hg, current JNC8 guidelines call for similar treatment goals for all hypertensive populations, maintaining blood pressure less than 140/90 Most recent guidelines recommend a systolic pressure of 130 mm Hg is the upper limit of normal at all ages (ACC/AHA, 2017). In the general population, including those with diabetes but excluding all African Americans, initial antihypertensive treatment should include a thiazide-like diuretic, calcium-channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACEI), or angiotensin-receptor blocker (ARB). In the general African American population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB. In the population aged 18 or older, regardless of race or presence of diabetes, those who have CKD as well as initial or added antihypertensive treatment should include an ACEI or ARB to improve kidney outcome.

medical and nursing management for hypertension

Atrial flutter

occurs in the atrium and creates impulses at a rapid but regular atrial rate between 220 and 350 times per minute. Because the atrial rate is faster than the atrioventricular (AV) node can conduct, not all atrial impulses are conducted into the ventricle. This is an important feature of this arrhythmia because if all atrial impulses were conducted to the ventricle, the ventricular rate would also be 220 to 350, which would result in a life-threatening arrhythmia. Causes include coronary artery disease (CAD), hypertension, mitral or tricuspid valve disease, hyperthyroidism or thyrotoxicosis, chronic lung disease, cor pulmonale (right ventricular failure), pulmonary emboli, previous extensive atrial ablation, and cardiomyopathy. A clinical relationship between atrial flutter and AF can be appreciated often in the same patient post open heart surgery Clinical Manifestations and Assessment Atrial flutter may not cause any symptoms or, instead, may cause serious signs and symptoms, such as fatigue, lightheadedness, chest pain, shortness of breath, and low blood pressure. The risk of mural (wall) emboli forming in the atria increases with this arrhythmia because without a strong atrial contraction, stasis of blood occurs; therefore, the nurse remains alert for signs of pulmonary or systemic emboli. ECG characteristics are: Rate: Atrial rate ranges between 220 and 350 bpm; ventricular rate usually ranges between 75 and 150 depending on AV node conduction Rhythm: Usually regular but may be irregular because of a change in the AV conduction P wave: Flutter waves in a characteristic "sawtooth" pattern PR interval: Not measurable QRS duration: Normal Medical and Nursing Management cardioversion or radiofrequency ablation (discussed later in this chapter) to terminate it and restore NSR (January et al., 2014). If the patient is unstable, urgent electrical cardioversion is usually indicated (discussed later in this chapter). antithrombotic therapy is recommended per the same risk profile used for AF (AHA/ACC/HRS, 2014). flecainide, dofetilide, propafenone, and intravenous ibutilide are useful for pharmacologic cardioversion of AF or atrial flutter, provided there are no contraindications to the selected medication

Cardiogenic shock

occurs when decreased CO leads to inadequate tissue perfusion and initiation of the shock syndrome. Cardiogenic shock may occur following MI, when a large area of myocardium becomes ischemic, necrotic, and hypokinetic (slow or diminished muscle motion). It also can occur as a result of end-stage HF, cardiac tamponade, pulmonary embolism (PE), cardiomyopathy, and arrhythmias. Cardiogenic shock is a life-threatening condition with a high mortality rate. Pathophysiology The heart muscle loses its contractile power, resulting in a marked reduction in SV and CO. The decreased CO, in turn, reduces arterial blood pressure and tissue perfusion in the vital organs (heart, brain, lung, kidneys). Flow to the coronary arteries is reduced, resulting in decreased oxygen supply to the myocardium, which increases ischemia and further reduces the heart's ability to pump. Inadequate emptying of the ventricle also leads to increased pulmonary pressures, pulmonary congestion, and pulmonary edema, exacerbating the hypoxia, causing ischemia of vital organs, and setting a vicious cycle in motion.

Junctional rhythm

occurs when the AV node, instead of the sinus node, becomes the pacemaker of the heart. When the sinus node slows (e.g., from increased vagal tone) or when the impulse cannot be conducted through the AV node (e.g., because of complete heart block), the AV node automatically discharges an impulse. Junctional escape rhythm may be caused by acute coronary syndromes; valvular disease; hypoxia; increased parasympathetic tone; or the effects of medication, including digoxin, beta blockers, and calcium-channel blockers. Clinical Manifestations and Assessment The patient may be asymptomatic or experience signs and symptoms associated with a decreased cardiac output. ECG characteristics are: Rate: 40 to 60 bpm Rhythm: Regular P wave: If visible, may be before, during, or after the QRS PR interval: If a P wave is visible, less than 0.12 second QRS duration: Normal See Figure 17-12. Medical and Nursing Management If the patient is symptomatic, the treatment is the same as for bradycardia; the patient may be paced (temporary or permanent) or is given IV atropine or epinephrine.

Normal sinus rhythm

occurs when the electrical impulse starts at the sinus node and travels through the normal conduction pathway. Normal sinus rhythm serves as a baseline for comparison in identifying all other arrhythmias. ECG characteristics are as follows: Rate: 60 to 100 in the adult Rhythm: Regular P wave: Normal and consistent shape; always in front of the QRS PR interval: Consistent interval between 0.12 and 0.20 second QRS duration: Less than 0.10 second

Cardiac arrest

occurs when the heart ceases to produce an effective pulse and circulate blood. Pathophysiology Cardiac arrest may be caused by a cardiac electrical event such as ventricular fibrillation, progressive profound bradycardia, or when there is no heart rhythm at all (asystole). Cardiac arrest may follow respiratory arrest; it may also occur when electrical activity is present but there is ineffective cardiac contraction or circulating volume, which is called pulseless electrical activity (PEA). PEA can be caused by hypovolemia (e.g., with excessive bleeding), hypoxia, hypothermia, hyperkalemia, massive PE, MI, and medication overdose (e.g., beta blockers, calcium-channel blockers). Clinical Manifestations and Assessment consciousness, pulse, and blood pressure are lost immediately. Ineffective respiratory gasping may occur. The pupils of the eyes begin dilating within 45 seconds. Seizures may or may not occur.

Sinus tachycardia

occurs when the sinus node creates an impulse at a faster-than-normal rate. Causes may include the following: Physiologic or psychological stress (e.g., acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, pulmonary emboli, hypermetabolic states, fever, exercise, anxiety) Medications that stimulate the sympathetic response (e.g., catecholamines, aminophylline, atropine, thyroid medications), stimulants (e.g., caffeine, alcohol, nicotine), and illicit drugs (e.g., amphetamines, cocaine, ecstasy) Clinical Manifestations and Assessment As the heart rate increases, the diastolic filling time decreases, possibly resulting in reduced cardiac output and associated symptoms If the rapid rate persists and the heart can no longer compensate for the decreased ventricular filling, the patient may develop acute pulmonary edema or cardiac ischemia. ECG characteristics are: Rate: Greater than 100 bpm Rhythm: Regular P wave: Present before each QRS and consistent in size and shape PR interval: Normal QRS duration: Normal See Figure 17-7.

Stage 1 hypertension

occurs when the systolic pressure is 140 to 159 mm Hg or greater and/or the diastolic pressure is 90 to 99 mm Hg or greater. Stage 2 hypertension occurs when the systolic pressure is 160 mm Hg or higher, or the diastolic pressure is 100 mm Hg or higher. Severe hypertension is demonstrated with the systolic BP greater than or equals to 180 mm Hg or the diastolic BP greater than or equals to 110 mm Hg

Masked hypertension

presents as normal pressure readings in provider settings but elevated BPs at home or work. Masked hypertension is known to be a precursor of sustained hypertension.

Angina pectoris

refers to chest pain that is brought about by myocardial ischemia. If the decrease in blood supply is significant enough, of long enough duration, or both, death of myocardial cells, or MI, may result. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction.

The P wave

represents the electrical impulse starting in the sinus node and spreading through the atria (atrial depolarization leading to atrial contraction).

The QRS complex

represents ventricular depolarization. Not all QRS complexes have all three waveforms. The Q wave is the first negative deflection after the P wave. The R wave is the first positive deflection after the P wave, and the S wave is the first negative deflection after the R wave. The QRS complex is normally less than 0.10 second in duration (2.5 small boxes).

The T wave

represents ventricular repolarization or electrical recovery. It follows the QRS complex and is usually in the same direction as the QRS complex. Atrial repolarization also occurs but is not visible on the ECG because it occurs at the same time as the QRS.

Risk Factors for CAD Age (men over 45 years old, women over 55 years old) Gender (in people less than 55 years of age, men are at a greater risk; after 55 years of age, men and women have the same risk; or women under 55 years of age who have premature menopause without estrogen replacement therapy) Race (African Americans, Mexican Americans, Native Americans, and some Asian Americans demonstrate increased risk) Family history of first-degree relative with premature diagnosis of heart disease metabolic syndrome increased body mass index (BMI), chronic kidney disease, chronic infections nonalcoholic fatty liver disease (NAFLD) influenza; sleep apnea, Known modifiable risk factors include diabetes and prediabetes, HTN, smoking, obesity, physical inactivity, high blood cholesterol, unhealthy diet, stress

risk factors for CAD

AF

should be distinguished from atrial flutter. AF causes rapid, disorganized, and uncoordinated electrical activity within the atria. AF may be transient, starting and stopping suddenly and occurring for a very short time (paroxysmal), or it may be persistent, requiring treatment to terminate the rhythm or to control the ventricular rate. Further, AF may be described in terms of duration of episodes, such as long-standing, permanent, or nonvalvular AF. Long-standing persistent AF is continuous or AF lasting longer than 12 months in duration; permanent AF is used when the physician and patient together decide to stop further attempts to restore and maintain NSR. Finally, the term nonvalvular AF is used when AF exists in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair (AHA/ACC/HRS, 2014). The erratic atrial contraction promotes formation of thrombi within the atria, increasing the risk for an embolic event such as stroke (brain attack). In fact, patients with AF have a fivefold increase in the risk for stroke and a twofold increase in mortality Clinical Manifestations and Assessment , there is a rapid ventricular response, which reduces the time for ventricular filling, resulting in a smaller stroke volume. loss of the atrial contraction (sometimes referred to as atrial kick) reduces ventricular filling volume and reduces cardiac output by 25%. This often leads to symptoms of fatigue and malaise. ECG characteristics are: Rate: Atrial rate is 300 to 400, with a variable ventricular response rate (typically rapid) Rhythm: Irregular P wave: No discernible P waves; irregular undulating waves may be seen and are referred to as fibrillatory waves PR interval: Not measurable QRS duration: Normal Medical and Nursing Management Cardioversion of AF can be done either by medication or an electrical shock. Direct-current cardioversion is more effective than pharmacologic cardioversion (Knight, 2013). electrical cardioversion is indicated when a patient with new-onset AF is hemodynamically unstable (Knight, 2013). Shocks are delivered in sync with the QRS wave. Biphasic defibrillators are used more often with less energy required (150 to 200 J) than when using the older, monophasic defibrillators with higher-energy settings. Pharmacologic cardioversion is done with intravenous (IV) ibutilide, procainamide, or amiodarone. For AF episodes shorter than 48 to 72 hours duration, the efficacy of ibutilide is approximately 60% to 70%, whereas amiodarone's efficacy is approximately 40% to 50%, and procainamide's efficacy is 30% to 40% Pacemaker implantation or catheter ablation is sometimes indicated for patients who are unresponsive to medications. Cryoballoon ablation

primary hypertension;

that is, high BP from an unidentified cause . This type of hypertension has also been called essential or idiopathic hypertension. The remainder of this group have secondary hypertension, which is high BP related to an identified cause. These causes include narrowing of the renal arteries or renal artery stenosis, kidney disease, hyperaldosteronism (mineralocorticoid hypertension), medications, pregnancy, and coarctation of the aorta

Five-electrode monitoring systems

use four electrodes placed as above, in the LA, RA, LL, and RL positions, as well as one chest electrode that can be placed in any one of the precordial locations (V1-V6). Monitoring systems with five electrodes permit the nurse to decide which leads will be monitored based on the patient's diagnosis and condition. Five-electrode systems have a display that allows two leads to be monitored simultaneously; typically, the nurse chooses one limb lead and one precordial lead to be viewed. The ability to monitor a limb lead and precordial lead simultaneously is often necessary for accurate identification of many arrhythmias, including arrhythmias with a wide QRS complex (BBBs, ventricular pacemaker rhythms, and wide QRS tachycardias).

The ST segment,

which represents early ventricular repolarization, lasts from the end of the QRS complex to the beginning of the T wave. The beginning of the ST segment is usually identified by a change in the thickness or angle of the terminal portion of the QRS complex and is called the J point. The end of the ST segment may be more difficult to identify because it merges into the T wave. The ST segment is analyzed to identify whether it is above or below the isoelectric line, which may be, among other signs and symptoms, a sign of cardiac ischemia.

The QT interval,

which represents the total time for ventricular depolarization and repolarization, is measured from the beginning of the QRS complex to the end of the T wave. The QT interval varies with heart rate, gender, and age. If the QT interval becomes prolonged, the patient may be at risk for a lethal ventricular arrhythmia called torsade de pointes.

Prehypertension

—blood pressure higher than the normal 120/80 or lower but not yet in the high blood pressure range.