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Key points for cardiac, Lecture notes of Nursing

State Fair Community CollegeNursing

Cardiac key points for nursing

Typology: Lecture notes

2019/2020

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Lewis: Medical-Surgical Nursing, 9th Edition
Chapter 32
Nursing Assessment: Cardiovascular System
KEY POINTS
Structures and Functions of CARDIOVASCULAR SYSTEM
Heart
•The heart
•oHas four chambers: the right and left atrium and right and left ventricles.
•oIs composed of three layers: endocardium, myocardium, and epicardium.
•oIs surrounded by a fibroserous sac called the pericardium.
•oHas four valves: mitral, aortic, tricuspid, and pulmonary. These serve to maintain
the one-way flow of blood.
•The right side of the heart receives venous blood from the body (via the vena cava) and
pumps it to the lungs where it is oxygenated. Blood returns to the left side of the heart (via the
pulmonary veins) and is pumped to the body via the aorta.
•The coronary circulation provides blood to the myocardium (heart muscle). The right and
left coronary arteries are the first two branches off the aorta.
•The conduction system consists of specialized cells that create and transport electrical
impulses. These electrical impulses initiate depolarization of the myocardium. This triggers a
cardiac contraction.
•oEach electrical impulse starts at the SA node (located in the right atrium), travels
to the AV node (located at the atrioventricular junction), through the bundle of His, down
the right and left bundle branches (located in the ventricular septum), and terminating in
the Purkinje fibers.
•oThe electrical activity of the heart is recorded on an electrocardiogram (ECG).
•Contraction of the myocardium, or systole, results in ejection of blood from the
ventricles. Relaxation of the myocardium, or diastole, allows for filling of the ventricles.
•Cardiac output (CO) is the amount of blood pumped by each ventricle in 1 minute. It is
calculated by multiplying the amount of blood ejected from the ventricle with each heartbeat
(stroke volume [SV]) by the heart rate (HR) per minute: CO = SV HR.
•Factors affecting SV are preload, contractility, and afterload. Preload is the volume of
blood in the ventricles at the end of diastole, and afterload represents the systemic resistance
against which the left ventricle must pump.
Regulation of Cardiovascular System
•Stimulation of the sympathetic nervous system increases HR, speed of conduction
through the AV node, and force of atrial and ventricular contractions, whereas stimulation of the
parasympathetic nervous system decreases HR.
•Stimulation of baroreceptors and chemoreceptors, located in the aortic arch and carotid
sinus, can initiate changes in HR and arterial pressure.
•Normal BP is systolic BP less than 120 mm Hg and diastolic BP less than 80 mm Hg.
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Lewis: Medical-Surgical Nursing, 9 th^ Edition

Chapter 32 Nursing Assessment: Cardiovascular System KEY POINTS Structures and Functions of CARDIOVASCULAR SYSTEM Heart

  •  The heart
    • o Has four chambers: the right and left atrium and right and left ventricles.
    • o Is composed of three layers: endocardium, myocardium, and epicardium.
    • o Is surrounded by a fibroserous sac called the pericardium.
    • o Has four valves: mitral, aortic, tricuspid, and pulmonary. These serve to maintain the one-way flow of blood.
  •  The right side of the heart receives venous blood from the body (via the vena cava) and pumps it to the lungs where it is oxygenated. Blood returns to the left side of the heart (via the pulmonary veins) and is pumped to the body via the aorta.
  •  The coronary circulation provides blood to the myocardium (heart muscle). The right and left coronary arteries are the first two branches off the aorta.
  •  The conduction system consists of specialized cells that create and transport electrical impulses. These electrical impulses initiate depolarization of the myocardium. This triggers a cardiac contraction. - o Each electrical impulse starts at the SA node (located in the right atrium), travels to the AV node (located at the atrioventricular junction), through the bundle of His, down the right and left bundle branches (located in the ventricular septum), and terminating in the Purkinje fibers. - o The electrical activity of the heart is recorded on an electrocardiogram (ECG).
  •  Contraction of the myocardium, or systole , results in ejection of blood from the ventricles. Relaxation of the myocardium, or diastole , allows for filling of the ventricles.
  •  Cardiac output (CO) is the amount of blood pumped by each ventricle in 1 minute. It is calculated by multiplying the amount of blood ejected from the ventricle with each heartbeat (stroke volume [SV]) by the heart rate (HR) per minute: CO = SV HR.
  •  Factors affecting SV are preload, contractility, and afterload. Preload is the volume of blood in the ventricles at the end of diastole, and afterload represents the systemic resistance against which the left ventricle must pump. Regulation of Cardiovascular System
  •  Stimulation of the sympathetic nervous system increases HR, speed of conduction through the AV node, and force of atrial and ventricular contractions, whereas stimulation of the parasympathetic nervous system decreases HR.
  •  Stimulation of baroreceptors and chemoreceptors, located in the aortic arch and carotid sinus, can initiate changes in HR and arterial pressure.
  •  Normal BP is systolic BP less than 120 mm Hg and diastolic BP less than 80 mm Hg.
  • o The two main factors influencing BP are cardiac output (CO) and systemic vascular resistance (SVR), which is the force opposing the movement of blood.
  • o BP can be measured by invasive techniques (catheter inserted in an artery) and noninvasive techniques (using a sphygmomanometer and a stethoscope, or an automated noninvasive device).
  •  A mean arterial pressure (MAP) of greater than 60 is necessary to sustain the vital organs of an average person under most conditions. Assessment OF CARDIOVASCULAR SYSTEM Past Health History
  •  A health history for the cardiac system consists of assessment of past health history, medications, surgery or other treatments, family health history, psychosocial history, risk factor identification, and a review of systems using functional health patterns.
  •  Obtain a thorough history of the present illness. Explore and document common signs of cardiac problems (e.g., pain, dyspnea). Describe the course of the patient’s illness, including when it began, the type of symptoms, and factors that alleviate or aggravate these symptoms. Physical Examination
  •  Vital signs, including orthostatic (postural) BPs and HRs, should be obtained prior to the physical examination. During physical examination, the skin, neck veins, capillary refill, thorax, epigastric area, and lungs should be assessed. Auscultate the carotid arteries, abdominal aorta, and femoral arteries.
  •  When listening to the heart sounds, note S 1 , S 2 , and any murmurs, clicks, pericardial friction rubs, or extra heart sounds (S 3 or S 4 ). Diagnostic Studies OF CARDIOVASCULAR SYSTEM Blood Studies
  •  Cardiac-specific troponin and creatine kinase (CK)-MB are sensitive indicators of early myocardial injury and infarction.
  •  Alterations in the lipid profile, cholesterol, triglycerides, and high-density and low- density lipoproteins have been linked to heart disease.
  •  High sensitivity C-reactive protein is an independent risk factor for CAD and may be a predictor of cardiac events.
  •  B-type natriuretic peptide (BNP) has emerged as the marker of choice for differentiating a cardiac or respiratory cause of dyspnea. Other Studies
  •  12-lead electrocardiogram (ECG)
  • o Deviations from the normal sinus rhythm can indicate abnormalities in heart function.
  • o ECGs can be obtained as a one-time recording, or for longer periods of time using ambulatory ECG (Holter monitoring) or event and loop monitors.
  •  Exercise or stress testing is used to evaluate the cardiovascular response to physical stress. Perfusion imaging with exercise testing can differentiate viable myocardial tissue from scar tissue and assess the effectiveness of various therapies.
  •  An echocardiogram provides information about valvular structure and motion, cardiac chamber size and contents, ventricular muscle and septal motion and thickness, pericardial sac, and ejection fraction (EF).
  •  A number of nuclear medicine studies provide information on the structure and function of the heart in determining the presence and extent of heart disease. These include multigated
  • o The PR interval represents the time period for the impulse to spread through the atria, atrioventricular (AV) node, bundle of His, and Purkinje fibers.
  • o The QRS complex represents depolarization of the ventricles (ventricular contraction).
  • o The QRS interval represents the time it takes for depolarization.
  • o The ST segment represents the time between ventricular depolarization and repolarization. This segment should be flat or isoelectric and represents the absence of any electrical activity between these two events.
  • o The T wave represents repolarization of the ventricles.
  • o The QT interval represents the total time for depolarization and repolarization of the ventricles.
  •  Dysrhythmias result from disorders of impulse formation, conduction of impulses, or both. Evaluation of Dysrhythmias
  •  Dysrhythmias result from various abnormalities and disease states, and the cause of a dysrhythmia influences the treatment.
  •  Noninvasive diagnostic tests used to evaluate cardiac dysrhythmias and the effectiveness of antidysrhythmia drug therapy include Holter monitoring, event monitoring (or loop recorder), exercise treadmill testing, and signal-averaged ECG.
  •  An electrophysiologic study (EPS) identifies different mechanisms of tachydysrhythmias, heart blocks, bradydysrhythmias, and causes of syncope. Types of Dysrhythmias
  • Sinus bradycardia has a normal sinus rhythm, but the SA node fires at a rate less than 60 beats per minute. It may be a normal clinical condition. Treatment is only indicated in those with symptoms.
  • Sinus tachycardia has a normal sinus rhythm, but the SA node fires at a rate 101 to 200 beats per minute because of vagal inhibition or sympathetic stimulation.
  • o It is associated with stressors such as exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear. It can also be an effect of certain drugs.
  • o Treatment is based on the underlying cause. -Premature atrial contraction (PAC) is a contraction originating from an ectopic focus in the atrium in a location other than the sinus node. PACs come earlier than the next expected sinus beat. In healthy persons, isolated PACs are not significant. In persons with heart disease, frequent PACs may warn of or initiate more serious dysrhythmias. -Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His. The rate is 150 to 220 beats per minute. - o Prolonged PSVT with HR greater than 180 beats per minute may decrease cardiac output (CO), resulting in hypotension, dyspnea, and angina. - o Treatments for PSVT include vagal stimulation and IV adenosine.
  • Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth- shaped flutter waves that originate from a single ectopic focus in the right atrium.
  • o High ventricular rates (over 100 per minute) and the loss of the atrial “kick” (atrial contraction reflected by a sinus P wave) can decrease CO and cause serious consequences such as chest pain and HF.
  • o Patients with atrial flutter are at increased risk of stroke.
  • o Radiofrequency catheter ablation is the treatment of choice.
  • Atrial fibrillation is characterized by a total disorganization of atrial electrical activity caused by multiple ectopic foci resulting in loss of effective atrial contraction.
  • o Atrial fibrillation usually occurs in the patient with underlying heart disease, such as coronary artery disease (CAD), rheumatic heart disease, and cardiomyopathy.
  • o Atrial fibrillation often results in a decrease in CO and poses an increased risk of stroke because of clot formation, necessitating anticoagulation therapy.
  • o For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion, radiofrequency catheter ablation and the Maze procedure are options.
  • Junctional dysrhythmias refer to dysrhythmias that originate in the area of the AV node, in which the AV node becomes the pacemaker of the heart. Junctional dysrhythmias include junctional premature beats, junctional escape rhythm, accelerated junctional rhythm, and junctional tachycardia. These dysrhythmias are treated according to the type, patient’s tolerance of the rhythm, and patient’s clinical condition.
  •  In first-degree AV block, every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged. First-degree AV block is usually not serious but can be a precursor of higher degrees of AV block. Patients with first-degree AV block are asymptomatic. There is no treatment.
  •  In second-degree AV block, type I (Mobitz I or Wenckebach heart block), there is a gradual lengthening of the PR interval until an atrial impulse is nonconducted and a QRS complex is blocked (missing).
  • o Type I AV block is usually a result of myocardial ischemia or inferior MI. It is almost always transient and is usually well tolerated. However, it may be a warning signal of a more serious AV conduction disturbance.
  • o If the patient is symptomatic, atropine is used to increase HR, or a temporary pacemaker may be needed.
  • Second-degree AV block, type II (Mobitz II heart block), involves a P wave that is nonconducted without progressive antecedent PR lengthening. This almost always occurs when a block in one of the bundle branches is present (e.g., anterior MI).
  • o Type II AV block often progresses to third-degree AV block and is associated with a poor prognosis.
  • o Treatment before the insertion of a permanent pacemaker may be necessary if the patient becomes symptomatic and involves the use of a temporary transvenous or transcutaneous pacemaker.
  •  In third-degree AV block, or complete heart block, no impulses from the atria are conducted to the ventricles.
  • o It almost always results in reduced CO with subsequent ischemia, HF, and shock.
  • o For symptomatic patients, a transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted followed by a permanent pacemaker. -Premature ventricular contraction (PVC) is the premature occurrence of a QRS complex, which is wide and distorted in shape compared with a QRS complex initiated from the normal conduction pathway.
  •  Radiofrequency catheter ablation therapy is used to “burn” or ablate accessory pathways or ectopic sites in the atria, AV node, and ventricles. - o Catheter ablation is the nonpharmacologic treatment of choice for atrial dysrhythmias resulting in rapid ventricular rates and AV nodal reentrant tachycardia refractory to drug therapy. - o Care of the patient following ablation therapy is similar to that of a patient undergoing cardiac catheterization. Pacemakers
  •  The artificial cardiac pacemaker is an electronic device used to pace the heart when the normal conduction pathway is damaged or diseased.
  •  Pacemakers provide antibradycardia, antitachycardia, and overdrive pacing.
  •  A permanent pacemaker is implanted totally within the body.
  •  A specialized type of cardiac pacing is used for the management of HF.
  • o Cardiac resynchronization therapy (CRT) is a pacing technique that resynchronizes the cardiac cycle by pacing both ventricles, thus promoting improvement in ventricular function.
  • o Devices often combine CRT with an ICD for maximum therapy.
  • o A temporary pacemaker is one that has the power source outside the body. There are three types of temporary pacemakers: transvenous, epicardial, and transcutaneous pacemakers.
  •  Patients with temporary or permanent pacemakers will be ECG monitored to evaluate the status of the pacemaker.
  •  Complications of invasive temporary (i.e., transvenous) or permanent pacemaker insertion include infection and hematoma formation at the site of insertion of the pacemaker power source or leads, pneumothorax, failure to sense or capture with possible symptomatic bradycardia, perforation of the atrial or ventricular septum by the pacing lead, and appearance of “end-of-life” battery parameters on testing the pacemaker. ECG CHANGES ASSOCIATED WITH ACUTE CORONARY SYNDROME
  •  The 12-lead ECG is the primary diagnostic tool used to evaluate patients presenting with acute coronary syndrome (ACS).
  •  Definitive ECG changes that occur in response to ischemia, injury, or infarction of myocardial cells can be seen in the leads that face the area of involvement.
  • o Typical changes seen in ischemia include ST-segment depression and/or T-wave inversion.
  • o ST-segment elevation is common with myocardial injury.
  • o ST-segment elevation and pathologic Q wave may be seen on the ECG of a patient with MI.
  •  Patient-monitoring guidelines for patients with suspected ACS include continuous, multilead ECG and ST-segment monitoring. SYNCOPE
  • Syncope is a brief lapse in consciousness accompanied by a loss in postural tone (fainting).
  •  The causes of syncope are categorized as cardiovascular or noncardiovascular:
  • o Common cardiovascular causes of syncope include vasovagal syncope and primary cardiac dysrhythmias.
  • o Noncardiovascular causes can include hypoglycemia, hysteria, seizure, stroke, and transient ischemic attack.
  •  Various diagnostic tests are used to determine the cause of syncope, including echocardiography, stress testing, EPS, head-up tilt-test, Holter monitors, and event/loop recorders.

Lewis: Medical-Surgical Nursing, 9 th^ Edition

Chapter 34 Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome KEY POINTS CORONARY ARTERY DISEASE

  • Coronary artery disease (CAD) is a type of blood vessel disorder included in the general category of atherosclerosis. Atherosclerosis is characterized by the deposit of cholesterol and lipids within the intimal wall of an artery.
  •  CAD is a progressive disease that develops in stages. When it becomes symptomatic, the disease process is usually well advanced. -  Normally some arterial anastomoses or connections, termed collateral circulation, exist within the coronary circulation. Their growth and extent is attributed to the inherited predisposition to develop new blood vessels and the presence of chronic ischemia.
  •  Many risk factors have been associated with CAD. o Nonmodifiable risk factors are age, gender, ethnicity, and genetic inheritance. o Modifiable risk factors include elevated serum lipids, elevated blood pressure, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and homocysteine level. ♣ Elevated serum lipid levels is one of the most firmly established risk factors for CAD. - High-density lipoproteins (HDLs) carry lipids away from arteries and to the liver for metabolism. High serum HDL levels are desirable. - HDL levels are increased by physical activity, moderate alcohol consumption, and estrogen administration. - Elevated low-density lipoprotein (LDL) levels correlate most closely with an increased incidence of atherosclerosis and CAD. o Diabetes, metabolic syndrome, elevated homocysteine levels, and certain psychologic states (i.e., anxiety, anger, depression) have also been found to be contributing risk factors for CAD. NURSING AND COLLABORATIVE MANAGEMENT: CORONARY ARTERY DISEASE
  • • Prevention and early treatment of CAD must involve a multifactorial approach and needs to be ongoing throughout the lifespan.
  • • Prinzmetal’s angina is a rare form of angina that often occurs at rest, usually in response to spasm of a major coronary artery. When spasms occur, the patient experiences angina and transient ST segment elevation.
  • • Tobacco, alcohol, and cocaine use may precipitate coronary artery spasms; Prinzmetal’s angina may also be seen in patients with a history of migraine headaches and Raynaud’s phenomenon.
  • • The pain may be relieved by moderate exercise or it may disappear spontaneously. Calcium channel blockers and/or nitrates are used to control the angina. ACUTE CORONARY SYNDROME
  • • Acute coronary syndrome (ACS) develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina, non–ST-segment- elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI).
  • • Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency. MYOCARDIAL INFARCTION
  • • Myocardial infarction (MI) occurs as a result of sustained ischemia, causing irreversible myocardial cell death. Contractile function of the heart stops in the infarcted area(s).
  • • The acute MI process takes time, evolving over a period of up to 12 hours.
  • • Infarctions are described based on the location of damage.
  • • Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. The pain is usually described as a heaviness, pressure, tightness, burning, constriction, or crushing.
  • • Complications after MI can occur:
  • o Dysrhythmias are the most common complication and the most common cause of death in patients in the prehospital period.
  • o Other complications include heart failure, cardiogenic shock, papillary muscle dysfunction or rupture, ventricular aneurysm, and pericarditis.
  • • Primary diagnostic studies used to determine whether a person has unstable angina (UA) or an MI include an ECG and serum cardiac markers. COLLABORATIVE CARE: ACUTE CORONARY SYNDROME
  • • Rapid diagnosis and treatment for a patient with ACS is necessary to preserve cardiac function.
  • • For patients with STEMI or NSTEMI with positive cardiac markers, reperfusion therapy is the recommended treatment of choice. This can include emergent PCI for STEMI or NSTEMI or thrombolytic (fibrinolytic) therapy for STEMI. - o Cardiac catheterization is used to locate and assess blockage and implement treatment modalities if needed. - o Thrombolytic therapy aims to stop infarction process by dissolving the thrombus in the coronary artery to reperfuse the myocardium.
  • • Coronary revascularization with coronary artery bypass graft (CABG) surgery is recommended for patients who fail medical management, have left main coronary artery or three-vessel (3 different coronary arteries) disease, are not candidates for PCI, have failed PCI with ongoing chest pain, or have diabetes.
  • o Minimally invasive direct CABG surgery can be used for patients requiring one or two bypasses in one or two coronary arteries on the anterior surface of the heart.
  • o Off-pump coronary artery bypass procedure uses full or partial sternotomy to enable access to all coronary vessels.
  • o Transmyocardial laser revascularization is an indirect revascularization procedure used for patients with advanced CAD who are not candidates for traditional bypass surgery and who have persistent angina after maximum medical therapy. Drug Therapy
  • • Initial management of the patient with chest pain includes aspirin, oxygen, IV nitroglycerin, anticoagulation, and morphine sulfate for pain unrelieved by nitroglycerin.
  • • IV antiplatelet and/or direct thrombin inhibitors are also used if PCI is anticipated.
  • • ACE inhibitors, calcium channel blockers, angiotensin receptor blockers, and long-acting nitrates are used in select situations.
  • • Oral -adrenergic blockers are given after day 2 if there are no contraindications.
  • • Stool softeners are given to facilitate and promote the comfort of bowel evacuation. NURSING MANAGEMENT: CHRONIC STABLE ANGINA AND ACUTE CORONARY SYNDROME Nursing Implementation: Chronic Stable Angina
  • • The following nursing measures should be instituted for a patient experiencing angina: (1) position patient upright unless contraindicated and administer supplemental oxygen, (2) assess vital signs, (3) obtain a 12-lead ECG, (4) provide prompt pain relief first with a nitrate followed by an opioid analgesic if needed, and (5) auscultate heart and breath sounds.
  • • Teaching for a patient with angina should include information regarding ACS, managing angina, risk factor reduction, and medication. Nursing Implementation: Acute Coronary Syndrome
  • • Initial treatment of a patient with ACS includes pain assessment and relief, physiologic monitoring, promotion of rest and comfort, alleviation of stress and anxiety, and understanding of the patient’s emotional and behavioral reactions.
  • o Nitroglycerin, morphine sulfate, and supplemental oxygen should be provided as needed to eliminate or reduce chest pain.
  • o Continuous ECG monitoring, frequent vital signs, intake and output, and physical assessment should be done. Included is an assessment of heart and breath sounds and inspection for evidence of early heart failure.
  • o Bed rest may be ordered for the first few days after an MI involving a large portion of the ventricle. A patient with an uncomplicated MI may rest in a chair within 8 to 12 hours after the event.
  • o Anxiety is common following ACS. Your role is to identify the source of anxiety, assist the patient in reducing it, and provide appropriate patient teaching.
  • o It is important to ensure adequate rest periods free from interruption. Comfort measures that can promote rest include frequent oral care, adequate warmth, a quiet atmosphere, use of relaxation therapy (e.g., guided imagery), and assurance that personnel are nearby and responsive to the patient’s needs.
  • • After PCI, your major responsibilities involve (1) monitoring for signs of recurrent angina; (2) frequent assessment of vital signs, including HR and rhythm; (3) evaluation of the insertion site for signs of bleeding; (4) neurovascular assessment of the extremity used; and (5) maintenance of bed rest per institution policy.
  • • The most common approach to preventing a recurrence and improving survival is the use of an implantable cardioverter-defibrillator (ICD) in conjunction with drug therapy.
  • • Survivors of SCD may develop a “time bomb” mentality, fearing the recurrence of cardiac arrest. They and their caregivers often become anxious, angry, hopeless, and depressed. They may need to deal with additional issues such as possible driving restrictions, role reversal, and change in occupation.

Lewis: Medical-Surgical Nursing, 9

th

Edition

Chapter 33 Nursing Management: Hypertension KEY POINTS Normal Regulation of Blood Pressure

  •  Blood pressure (BP) is the force exerted by the blood against the walls of the blood vessel. It must be adequate to maintain tissue perfusion during activity and rest.
  •  Regulation of BP involves nervous, cardiovascular, endothelial, renal, and endocrine functions. HYPERTENSION Classification of Hypertension
  • Hypertension , or high BP, is defined as a persistent systolic BP (SBP) 140 mm Hg, diastolic BP (DBP) 90 mm Hg, or current use of antihypertensive medication.
  •  Hypertension is classified as follows:
  • o Prehypertension is BP 120 to 139 per 80 to 89 mm Hg.
  • o Hypertension, Stage 1 is BP 140 to 159 per 90 to 99 mm Hg.
  • o Hypertension, Stage 2 is systolic BP 160 or diastolic BP 100 mm Hg.
  • o Isolated systolic hypertension (ISH) is average SBP 140 mm Hg coupled with an average DBP less than 90 mm Hg. ♣ ISH is more common in older adults. ♣ Control of ISH decreases the incidence of stroke, heart failure, cardiovascular mortality, and total mortality. Etiology
  • Primary (essential or idiopathic) hypertension is elevated BP without an identified cause. It accounts for 90% to 95% of all cases of hypertension.
  • Secondary hypertension is elevated BP with a specific cause. It accounts for 5% to 10% of hypertension in adults. Pathophysiology of Primary Hypertension
  • The hemodynamic hallmark of hypertension is persistently increased SVR.
  • This persistent elevation in SVR may occur in various ways. Abnormalities of any of the mechanisms involved in the maintenance of normal BP, including sodium intake, the renin-

angiotensin-aldosterone mechanism, and sympathetic nervous system (SNS) stimulation, can result in the development of hypertension.

  • Abnormalities of glucose, insulin, and lipoprotein metabolism are common in primary hypertension.
  • Contributing factors to the development of hypertension include cardiovascular risk factors combined with socioeconomic conditions and gender and ethnic differences. Clinical Manifestations
  • Often called the “ silent killer ” because it is frequently asymptomatic until it becomes severe and target organ disease occurs.
  • Target organ diseases occur in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vessels (peripheral vascular disease), kidney (nephrosclerosis), and eyes (retinopathy).
  • o It is one of the leading causes of end-stage renal disease, especially in African Americans.
  • o Damage to retinal vessels provides an indication of concurrent vessel damage in the heart, brain, and kidney. Manifestations of severe retinal damage include blurring of vision, retinal hemorrhage, and loss of vision.
  • • There is a direct relationship between hypertension and cardiovascular disease (CVD). Hypertension is a major risk factor for coronary artery disease (CAD), stroke, and cerebral atherosclerosis.
  • • Sustained high BP increases the cardiac workload and produces left ventricular hypertrophy (LVH). Progressive LVH, especially in association with CAD, is associated with the development of heart failure. Diagnostic Studies
  • • Basic laboratory studies are performed to (1) identify or rule out causes of secondary hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular risk, or (4) establish baseline levels before initiating therapy.
  • • Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to screen for renal involvement and to provide baseline information about kidney function.
  • • Lipid profile provides information about additional risk factors that predispose to atherosclerosis and cardiovascular disease.
  • • ECG and echocardiography provide information about the cardiac status.
  • • Ambulatory BP monitoring (ABPM) may be used to measure BP at preset intervals over a 24-hour period. Collaborative Care
  • • The goal for treating primary hypertension is BP less than 140/90 mm Hg. A goal of less than 130/80 mm Hg is recommended for patients who are at high risk for CAD as well as for patients with preexisting CAD.
  • • Lifestyle modifications are indicated for all patients with prehypertension and hypertension. These include (1) reducing weight (if appropriate), (2) using the DASH eating plan, (3) restricting dietary sodium and alcohol intake, (4) avoiding tobacco products, (5) participating in physical activity, and (6) reducing psychosocial risk factors that contribute to the risk of developing CVD. Drug Therapy
  • • Drugs currently available for treating hypertension work by (1) decreasing the volume of circulating blood and/or (2) reducing SVR.
  • • In some older people, there is a wide gap between the first Korotkoff sound and subsequent beats ( auscultatory gap ). Failure to inflate the cuff high enough may result in underestimating the SBP.
  • • A goal BP less than 140 per 90 mmHg for people 65 to 79 years of age and an SBP goal of 140 to 145 mmHg for those 80-years-old and older are recommended.
  • • Orthostatic hypotension often occurs in older adults because of impaired baroreceptor reflex mechanisms, volume depletion, and chronic disease states, such as decreased renal and hepatic function or electrolyte imbalance. HYPERTENSIVE CRISIS
  • • Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency. This is determined by the degree of target organ disease and how quickly the BP must be lowered.
  • • Hypertensive urgency develops over days to weeks. The BP is severely elevated but there is no clinical evidence of target organ disease.
  • o Hypertensive urgencies usually do not require IV medications but can be managed with oral agents.
  • o If a patient with hypertensive urgency is not hospitalized, outpatient follow-up should be arranged within 24 hours.
  • • Hypertensive emergencies require hospitalization with intensive care monitoring and the IV administration of antihypertensive drugs, including vasodilators, adrenergic inhibitors, the ACE inhibitor enalaprilat, and the calcium channel blocker clevidipine (Cleviprex). Drugs are titrated based on MAP.
  • • Regular, ongoing assessment (e.g., ECG monitoring, vital signs, urinary output, level of consciousness, visual changes) is essential to evaluate the patient with severe hypertension.

Lewis: Medical-Surgical Nursing, 9

th

Edition

Chapter 37 Nursing Management: Inflammatory and Structural Heart Disorders KEY POINTS INFECTIVE ENDOCARDITIS

  • Infective endocarditis (IE) is an infection of the endocardial surface of the heart that affects the cardiac valves.
  •  IE can be classified by rapidity of onset, cause, or site of involvement. -  The most common causative organisms of IE are Staphylococcus aureus and Streptococcus viridans.
  • o Vegetation, the primary lesion of IE, adheres to the valve surface or endocardium and can embolize to various organs and to the extremities, causing ischemia and infarction.
  • o The infection may spread locally to cause damage to the valves or to their supporting structures resulting in dysrhythmias, valve dysfunction, and eventual invasion of the myocardium, leading to heart failure (HF), sepsis, and heart block.
  •  Clinical findings in IE are nonspecific and can involve multiple organ systems.
  •  Definitive diagnosis of IE exists if two of the following major criteria are present: positive blood cultures, new or changed cardiac murmur, or intracardiac mass or vegetation noted on echocardiography.
  •  Antibiotic prophylaxis is necessary for patients with specific cardiac conditions undergoing certain invasive procedures (e.g., dental work that perforates the oral mucosa).
  •  Accurate identification and eradicating the infecting organism are key to successful treatment of IE.
  • o Drug therapy consists of long-term treatment with IV antibiotic therapy with subsequent blood cultures to evaluate the effectiveness of antibiotic therapy.
  • o Early valve replacement followed by prolonged (6 weeks or longer) drug therapy is recommended for patients with fungal infection and prosthetic valve endocarditis.
  •  The patient with IE has multiple problems that require nursing management.
  • o Patients and caregivers must be taught to recognize signs and symptoms of life- threatening complications of IE, such as stroke, pulmonary edema, and HF.
  • o Fever (chronic or intermittent) is a common early sign that the drug therapy is ineffective. ACUTE PERICARDITIS
  • Pericarditis is caused by inflammation of the pericardial sac (the pericardium).
  • Acute pericarditis most often is idiopathic but can be caused by uremia, viral or bacterial infection, acute myocardial infarction (MI), cardiac surgery, tuberculosis, neoplasm, inflammation caused by radiation to the chest, and trauma.
  •  Pericarditis in the acute MI patient may be described as two distinct syndromes: (1) acute pericarditis (occurs within the initial 48 to 72 hours after an MI) and (2) Dressler syndrome (late pericarditis that appears 4 to 6 weeks after an MI).
  •  Clinical manifestations include the following:
  • o Progressive, frequently severe chest pain that is sharp and pleuritic in nature and worse with deep inspiration and when lying supine. The pain is relieved by sitting up and leaning forward. It can be referred to the shoulder and upper back.
  • o The hallmark finding in acute pericarditis is a pericardial friction rub. -  Complications include pericardial effusion and cardiac tamponade.
  •  Collaborative care includes the following:
  • o Antibiotics
  • o Pain and inflammation are usually treated with nonsteroidal antiinflammatory drugs (NSAIDs) or high-dose salicylates. Cortiocosteroids may be an option in some patients.
  • o Colchicine, an antiinflammatory agent used for gout, may be considered for patients who have recurrent pericarditis. - o Pericardiocentesis or pericardial window is usually performed if accompanied by acute cardiac tamponade, purulent pericarditis, and a high suspicion of a neoplasm.
  • o Rheumatic endocarditis is found primarily in the valves. Vegetation forms and valve leaflets may fuse and become thickened or even calcified, resulting in stenosis or regurgitation. - o Myocardial involvement is characterized by Aschoff’s bodies.
  •  Clinical manifestations of RF include the presence of two major criteria or one major and two minor criteria plus evidence of a preceding group A streptococcal infection.
  • o Major criteria include the following:  Carditis results in three signs: murmurs of mitral or aortic regurgitation, or mitral stenosis; cardiac enlargement and HF; pericarditis  Monoarthritis or polyarthritis  Sydenham’s chorea  Erythema marginatum lesions o Minor criteria include the clinical findings of fever and polyarthralgia and laboratory findings: elevated erythrocyte sedimentation rate (ESR), elevated white blood cells, and elevated C-reactive protein (CRP).  The overall goals for a patient with RF include (1) normal or baseline heart function, (2) resumption of daily activities without joint pain, and (3) verbalization of the ability to manage the disease sequelae.  Health promotion emphasizes prevention of RF by early detection and treatment of group A streptococcal pharyngitis with antibiotics, specifically penicillin.
  • o The success of treatment requires strict adherence to the full course of antibiotic therapy.
  • o The primary goals of managing a patient with RF are to control and eradicate the infecting organism; prevent cardiac complications; and relieve joint pain, fever, and other symptoms with antibiotics, optimal rest, and antipyretics, NSAIDs, and steroids.
  • o Secondary prevention aims at stopping the recurrence of RF with prophylactic antibiotics. Patients with RF without carditis require prophylaxis until age 20 and for a minimum of 5 years. Patients with rheumatic carditis and residual heart disease (e.g., persistent valve disease) will need longer-term and even life-long prophylaxis. VALVULAR HEART DISEASE
  •  Valvular stenosis refers to a constriction or narrowing of the valve opening.
  •  Valvular regurgitation (also called insufficiency) occurs with incomplete closure of the valve leaflets and results in the backward flow of blood. MITRAL VALVE STENOSIS
  •  Most adult mitral valve stenosis results from rheumatic heart disease. Less commonly, it can occur congenitally, from rheumatoid arthritis, and from systemic lupus erythematosus.
  •  Clinical manifestations of mitral stenosis include exertional dyspnea, fatigue, palpitations from atrial fibrillation, and a loud first heart sound and a low-pitched, diastolic murmur. MITRAL VALVE REGURGITATION
  •  Mitral regurgitation (MR) is caused by MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and IE.
  •  In chronic MR, the additional volume load results in atrial enlargement (placing the patient at risk for atrial fibrillation), ventricular dilation, and eventual ventricular hypertrophy.
  •  In acute MR, there is a sudden increase in pressure and volume that is transmitted to the pulmonary bed, resulting in pulmonary edema and life-threatening cardiogenic shock.
  •  Clinical manifestations of acute MR include thready, peripheral pulses; cool, clammy extremities; and a new systolic murmur.
  •  Patients with asymptomatic MR should be monitored carefully, and surgery should be considered before significant left ventricular failure or pulmonary hypertension develops. MITRAL VALVE PROLAPSE
  •  Mitral valve prolapse (MVP) is an abnormality of the mitral valve leaflets and the papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the left atrium during systole. The etiology of MVP is unknown.
  •  In many patients, MVP found by echocardiography is not accompanied by any other clinical manifestations of cardiac disease, and the significance of the finding is unclear. AORTIC VALVE STENOSIS
  •  In older patients, aortic stenosis is a result of rheumatic fever or fibrocalcific degeneration that may have an etiology similar to coronary artery disease.
  •  Aortic stenosis results in left ventricular hypertrophy and increased myocardial oxygen consumption. As the disease progresses, cardiac output (CO) is reduced, leading to decreased tissue perfusion, pulmonary hypertension, and HF.
  •  Clinical manifestations include a systolic murmur and the classic triad of angina, syncope, and exertional dyspnea. AORTIC VALVE REGURGITATION
  •  Acute aortic regurgitation (AR) is caused by IE, trauma, or aortic dissection.
  •  Chronic AR is generally the result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions.
  •  Clinical manifestations of acute AR include severe dyspnea, chest pain, and hypotension indicating left ventricular failure and cardiogenic shock that constitute a medical emergency. -  Clinical manifestations of chronic AR include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea after considerable myocardial dysfunction has occurred. TRICUSPID AND PULMONIC VALVE DISEASE
  •  Diseases of the tricuspid and pulmonic valves are uncommon, with stenosis occurring more frequently than regurgitation. Pulmonary stenosis is almost always congenital.
  •  Tricuspid stenosis occurs almost exclusively in patients with RF or who are IV drug abusers. It results in right atrial enlargement and elevated systemic venous pressures. COLLABORATIVE CARE OF VALVULAR HEART DISEASE
  •  Collaborative care of valvular heart disease includes the prevention of recurrent RF and IE and the prevention of exacerbations of HF, acute pulmonary edema, and thromboembolism.
  •  Anticoagulant therapy is used to prevent and treat systemic or pulmonary embolization.
  •  An alternative treatment for stenotic valvular heart disease is percutaneous transluminal balloon valvuloplasty to split open the fused commissures.
  •  Surgical intervention is based on the clinical state of the patient and depends on the valves involved, the pathology and severity of the disease, and the patient’s clinical condition.
  • o Valve repair, including a valvulotomy, valvuloplasty, or annuloplasty, is typically the surgical procedure of choice.
  • o Valve replacement may be required. A wide variety of prosthetic valves, both mechanical and biologic, are available.