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15 Structural Cardiac Disorders Textbook Readings for Lesson 15: Structural Cardiac Disorders Topics Textbook Pages Review 598–604 Pericarditis 667–669 Cardiomyopathies 669–670 Valvular Dysfunction 670–674 Rheumatic Fever/Rheumatic Heart Disease 674–677 Endocarditis 677–679 Congenital Heart Defects 710–720 Key Terms Vascular Resistance Pressure against which a cardiac chamber must eject blood Resistance varies with the size of the vessel and changes in the opening and closing of channels High resistance impedes blood flow, low encourages blood flow Narrow tube means greater resistance NURS325B04 1 Lesson 15 Oxygen Saturation (SaO2) Percent of available hemoglobin that is bound to oxygen Oxygen Content Normally higher in the left side of the heart-blood is returning from the lungs (about 95%) Normally lower in the right side–venous blood is returning from the body (about 72–80%) Chamber Pressure atria—thin-walled chambers, low pressure, ventricles—thicker walled with high pressure left ventricle has the greatest pressure because it must pump blood into the high-pressure systemic circulation Cardiac Shunt Left to right-oxygenated blood from left side of heart goes into right side of heart Right to left—less oxygenated blood goes from the right side of the heart into the left side or systemic circulation NURS325B04 2 Lesson 15 Cyanosis Bluish discoloration of the skin due to decreased oxygen levels in the arterial blood Murmur A blowing or swishing sound that occurs with turbulent blood flow in the heart or great vessels Fetal Circulation Structures Important for Normal Fetal Circulation Ductus Venosus connects umbilical vein to inferior vena cava. Takes oxygenated blood from the placenta to fetus, closes at birth. Foramen Ovale opening between right & left atria, blood goes through and bypasses fetus lungs closes 15-18 hours after birth. NURS325B04 3 Lesson 15 Ductus Arteriosus joins pulmonary artery to distal aortic arch bypasses fetus lungs; circulates oxygenated blood to body, closes 10-21 days after birth. Congenital Heart Disease Etiology: Multifactorial—drugs, diseases, heredity, environment Acyanotic Heart Disease The 3 "Acyanotic" defects are Atrial Septal Defect, Ventricular Septa Defect, and Coarctation of the aorta. Note that all 3 defects have left-to-right shunts. Blood in the left side of the heart has just been through the lungs where it got oxygenated. So, left-to-right shunts (where oxygenated blood abnormally moves to the right side), do NOT cause low O2 (cyanotic) problems. You should see more problems related to pressure changes. Atrial Septal Defect Left to Right Shunt. An abnormal opening between atria leads to increased pressure and oxygenation in right side of heart. Females 3:1. NURS325B04 4 Lesson 15 Ventricular Septal Defect Left to Right Shunt. An abnormal opening between the ventricles leads to increased pressure and oxygenation in the right side of the heart. Frequently associated with other defects. Most close spontaneously. Left to Right Shunt The failure of the fetal structure to close after birth. Blood shunted from high-pressure aorta to lower pressure pulmonary artery. In premature babies, it may stay open due to low oxygen saturation. Indomethacin given to close PDA. Surgery rarely needed. Females 3:1. Survival Rate: 99–100% on all three types NURS325B04 5 Lesson 15 Coarctation of Aorta Acyanotic heart disease. A localized narrowing of the aorta. 2 types Preductal: between the ductus arteriosus and the subclavian artery Postductal: distal to the ductus arteriosus Increased pressure proximal to the defect causing high blood pressure and bounding pulses in upper extremities and head with dizziness, headaches, fainting and epistaxis Decreased blood supply distal to the defect causing decreased or absent femoral pulses, muscle cramps and coolness in lower extremities. Males 4:1 Survival 99% in older child 83% in infants Diagnosis/Management of Coarctation of Aorta NURS325B04 6 Lesson 15 Echocardiogram and/or cardiac catheterization Surgical correction if needed. Cyanotic Heart Disease (low O2) Two "cyanotic" defects are Tetralogy of Fallot and Transposition of Great Vessels. Note that both of these have right-to-left shunts. Right to Left Shunt: Desaturated venous blood flows into the left side of the heart, bypassing the lungs, because the pressure on the right side is greater than the left, or the vessels are misplaced. Tetralogy of Fallot One of the most common cyanotic heart diseases. Increased pressure in the right ventricle results in hypertrophy, deoxygenated blood is shunted into the overriding aorta and left ventricle because of septal defect and pulmonary stenosis. 4 defects present Ventricular septal defect Pulmonary stenosis Overriding aorta Right ventricular hypertrophy NURS325B04 7 Lesson 15 Manifestation/Management Polycythemia Anoxic spells Decreased physical growth Murmur Treatment Palliative surgery to increase pulmonary blood flow Corrective surgery to correct all of the defects NURS325B04 8 Lesson 15 Survival Rate 95% or better after Neonatal Period Transposition of Great Vessels 2 separate circulations. The pulmonary artery leaves the left ventricle and the aorta leaves the right ventricle. Must have a defect present to allow communication between the 2 circulations in order to have extrauterine life. Associated defects may be an atrial septal defect, ventricular septal defect or patent ductus arteriosus Predominately in males Significant number have history of familial diabetes Congestive heart failure Tachycardia Tachypnea Hepatomegaly Cardiomegaly NURS325B04 9 Lesson 15 Surgery Palliative—to increase pulmonary blood flow Corrective—new procedure switches vessels Survival rates vary with procedure and age—85-90% Manifestations/Management Depends on size and type of associated defects Infections/Inflammation of the Heart Infective Endocarditis Inflammation of the endocardium (inner lining of the heart), especially involves the valve tissues. Etiology Causal agents: Microorganisms. Most commonly streptococcus or staphylococcus, but can be any virus, bacteria, fungus, etc. Pathophysiology The key to understanding the patho of endocarditis is that there needs to be TWO things: Endothelial damage and bugs ( microorganisms). So the main part of the patho is understanding HOW this endothelial damage can occur. After the damage occurs, THEN bugs (microorganisms) have to come along before infective endocarditis develops. Risk Factors— (for endothelial damage of myocardial tissue) 1. Turbulent blood flow —valve disease, prosthetic heart valves 2. Infection risk factors —long term indwelling lines, dental work, GU procedure 3. Autoimmune Diseases —deposition of immune complexes in the tissues 4. HIV—associated cardiac involvement Non-bacterial thrombotic activity—This is an inflammation reaction in response to the endothelial damage. The endothelial damage (remember the examples above NURS325B04 10 Lesson 15 for how this can occur) exposes the basement membrane of the endothelium (which contains a type of collagen that actually attracts platelets). Pathology steps 1. Endocardium must be "prepared" for colonization. The endothelial damage does this—see risk factors above. Remember that you have to have BOTH damage AND bugs.... 2. Colonization. Microorganisms (bugs) circulating in the bloodstream must adhere to the damaged endothelial surface. This is GREATLY facilitated by the non-bacterial thrombotic process described above. 3. Infective vegetation forms (usually on and around the valves). This occurs by: (a.) bacteria stimulating the clotting cascade. This leads to increased fibrin formation around the colonies. (b.) then the bacterial colonies are embedded in these protective fibrin clots. This makes them less accessible to host defenses. Another way to say this is that these bacterial colonies are underneath the clots, which protects them from the person's immune cells. 4. Valve dysfunction occurs due to the infective vegetation. Take a look at some of the website pictures at the end of the lesson. Compare a nice normal valve to one that is all full of vegetation. No wonder the valves don't work well! Vegetation may break off and become embolus- causing other symptoms. 2 types: Subacute Bacterial Endocarditis (SBE)—develops gradually (weeks/months) Acute Bacterial Endocarditis (ABE) More severe develops in days to months Other Risk Factors Heart disease (CAD, rheumatic fever, degenerative, valvular) Cardiac surgery Chronic debilitating diseases Intravenous drug abuse Immunosuppression Manifestations NURS325B04 11 Lesson 15 Splinter hemorrhages (micro-emboli that look like splinters in the nail beds) Osler's Nodes (painful due to inflammation around small infected emboli) Janaway Lesions (flat, small non-tender red spots) Possible Emboli Manifestations in main organs or systems (CNS, Splenic, Renal, Pulmonary, Cardiac) Diagnosis/Management of Endocarditis: Echocardiogram Antibiotics Antimicrobial agents for 4-6 wks Valve replacement Prophylaxis with antibiotics for invasive procedures Use the Web Resources links found at the unit level of your online course for more information on the topics covered in this section. Pericarditis Inflammation of the sac around the heart Acute or chronic (healed form of acute that results in a chronic pericardial dysfunction) Etiology Infections, myocardial injury, hypersensitivity reactions, metabolic disorders, neoplasms NURS325B04 12 Lesson 15 Classifications according to exudate Serous Fibrinous Purulent Hemorrhagic Pathophysiology-Inflammatory process: WBC collect where tissue injury occurred and produces an exudate in the sac around the heart. The accumulating exudate may limit the heart function and thus decrease cardiac output. Manifestations Severe chest pain radiating to the back, presence of a friction rub (pericardial layers rub together during movement) Sysphagia Weakness Malaise Restlessness Weight loss Fever Sinus tachycardia Management Treat underlying cause Symptomatic treatment (ASA, NSAIDs, analgesics) If this is chronic, may have to remove the pericardium NURS325B04 13 Lesson 15 Cardiomyopathies Definition Disease of the myocardium itself—affects the pumping ability of the heart—fibers cannot contract well. Etiology Most are idiopathic! May be secondary to toxins, infections, immunological disorders, nutritional disorders (alcoholism), and genetics. Classes Dilated (congestive)—enlarged heart due to degeneration to the heart fibers. Both RV and LV balloon out. Immense cardiomegaly. You see manifestations of both LV Failure and RV Failure. Hypertrophic—Ventricular SEPTUM and LV hypertrophy leads to altered shape of chambers and poorly coordinated contractions. You see manifestations of LV Failure. Restrictive—This is the clinical picture of constrictive pericaditis. The myocardial muscle becomes INFILTRATED with abnormal substances, causing dysfunction of the ventricles. You see manifestations of both LV Failure and RV Failure. Manifestations LV Failure: Dyspnea on exertion Fatigue Orthopnea Fluid in lungs, crackles RV Failure: Edema Jugular vein distention Liver congestion NURS325B04 14 Lesson 15 Management Treat CHF symptomatically for each type using various drugs Diuretics Beta blockers (decrease hypercontractibility) Calcium channel blockers (to enhance diastolic relaxation) Heart transplant Valvular Disorders Valvular disorders are usually caused by inflammation or infections (remember infective endocarditis and rheumatic fever?), trauma, degeneration and age, or connective tissue disorders. Look at a picture of the valve leaflets or cusps. In order to understand the valve problems, you have absolutely GOT to remember the normal flow of blood through the heart, where the valves are, when they are open, and when they are closed. An absolute MUST to remember this. Stenosis Valve opening (orifice) is narrowed and/or constricted. Therefore the blood flow through the valve is impeded. When the valve should be wide open, it cannot be wide open. This can lead to increased pressure and workload of the chamber that is trying to eject blood through the stenotic valve. Regurgitation or Insufficiency Another word is Incompetence. A regurgitant or insufficient or incompetent valve is one whose leaflets do not close as tightly as they should. During systole blood can leak back through the valves that are supposed to be closed (back into the atria). In essence, this means that the chambers behind and in front of the valve are pumping some of the blood again! So, there is increased volume to pump, and increased workload of both the atria and ventricle. Aortic Valve Stenosis Increased LV pressure and LV hypertrophy and LV workload Narrowed pulse pressure Systolic murmur NURS325B04 15 Lesson 15 Mitral Valve Stenosis Increased LA pressure Pulmonary hypertension, edema, RV Failure Diastolic murmur Aortic Regurgitation Increased LV volume and overload, LV hypertrophy, and LV workload Diastolic murmur Mitral Regurgitation LA and LV hypertrophy to increase cardiac output LV Failure Systolic murmur Management Valve repair or replacement for severe cases. Prophylactic antibiotics before surgery and dental work. Mitral Valve Prolapse Most common valvular disorder in the U.S. Up to 30% of young women have this disorder. Usually asymptomatic and it is suggested that this may be a normal variant. Usually diagnosed incidentally on physical exam. May be associated with connective tissue diseases such as Marfan's Syndrome or scoliosis. May show some symptoms of mitral regurgitation if prolapse is sufficient enough. No treatment is usually necessary. May use prophylactic antibiotics. Acute Rheumatic Fever NURS325B04 16 Lesson 15 Etiology Group A Beta hemolytic streptococcus (after a pharyngeal infection). Risk groups Individuals with either untreated strept throat or those who do not complete the prescribed medications; others living in crowded sub-standard conditions. Pathophysiology Diffuse inflammatory disease involving the heart, joints, subcutaneous tissue, CNS and skin. Usually seen in ages 3-15 yr. Manifestations RF is diagnosed if strept throat and 2 major or 1 major and 2 minor manifestations are present. Major manifestations Carditis or Rheumatic Heart Disease—In app. 10% of cases strept has affinity to endocardium. Bacterial vegetation forms on the valve leaflets— causing swelling—and on the myocardium, causing it to become fibrotic and necrotic (called Aschoff Bodies). Tachycardia is in proportion to the fever. Migratory polyarthritis—Large joints are painful with no permanent disability. Syndenham's Chorea—Largely females, self-limiting, purposeless movements, no permanent disability. Subcutaneous nodules—Small painless nodules on the extensor tendons on knees, knuckles, and elbows. Erythema marginatum—Nonpruretic, transient rash on trunk and proximal extremities NURS325B04 17 Lesson 15 Minor manifestations Fever Documented history of strept throat through screening such as C-reactive protein, ASO titer Arthralgia Increased Sedimentation Rate Management Antibiotics for strept infection ASA or anti-inflammatory agent Bed rest in cardiac involvement Long-term SBE prophylaxis Use the Web Resources links found at the unit level of your online course for more information on the topics covered in this section. When you have completed your assigned textbook readings and the course discussion for this lesson, be sure to complete the Self-Check Test before you begin the next lesson. NURS325B04 18 Lesson 15 NURS325B04, Lesson 15 Self-Check Questions in the online course are randomized to provide a more comprehensive learning experience. The questions listed below are the same ones that you will use in the Lesson 15 Self-Check test of the online course, though the order of the questions and/or answers may be different. Question 1 Which of the following would cause the LEAST amount of hypoxemia? a ductus arteriosus that remains patent months after birth atrial septal defect Tetralogy of Fallot transposition of the great vessels Question 2 The oxygen content of the blood on the LEFT side of the heart is about 75%. decreased due to the high pressure. about 95%. heading to the lungs to become oxygenated. Question 3 Which of the following is considered a cyanotic congenital heart defect? atrial septal ventricular septal patent ductus arteriosus Tetralogy of Fallot Question 4 NURS325B04 19 Lesson 15 Ventricular Septal Defect, an abnormal opening between the ventricles, demonstrates which of the following? cyanotic disorder a localized narrowing of the aorta two separate circulations left to right shunt Question 5 What abnormal heart sound would you auscultate with pericarditis? murmur pericardial friction rub S3 S4 Question 6 Inflammation of the inner lining of the heart is called what? cardiomyopathy endocarditis mitral stenosis pericarditis Question 7 The class of cardiomyopathy that is due to a thickened ventral septum is dilated. congestive. hypertrophic. restrictive. Question 8 Which of the following would confirm the diagnosis of Rheumatic fever? NURS325B04 20 Lesson 15 strept throat, migratory polyarthritis, subcutaneous nodules strept throat, tachycardia, fever Carditis, fever, arthralgia carditis, migratory polyarthritis, increased sedimentation rate Question 9 Which of the following manifestations is most likely for pericarditis? accumulation of fluid in the pericardial sac Osler's nodes emboli formation in the major organ systems vegetation formation on the cardiac valves Question 10 Which of the following would cause the MOST amount of hypoxemia? right to left cardiac shunt mitral valve stenosis a foramen ovale that closes off after birth left to right cardiac shunt NURS325B04 21 Lesson 15
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