1. Anatomy and Physiology of the Heart

2. Anatomy Chambers – Two upper atria (right and left) – Two lower ventricles (right and left) Muscle layers – Endocardium, myocardium, and epicardium Valves – Atrioventricular valves Mitral and tricuspid – Semilunar valves Aortic and pulmonic

3. Heart Sounds The first heart sound (S 1 ), referred to as lub, occurs when the ventricles contract during systole and when the mitral and tricuspid valves close The second heart sound (S 2 ), called dub, occurs during ventricular relaxation or diastole and is caused by the closing of the aortic and pulmonic valves

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5. Coronary Blood Flow Left coronary artery and the right coronary artery – Left coronary artery branches into the left anterior descending and circumflex arteries – Right coronary artery branches to supply the sinoatrial (SA) and the atrioventricular (AV) nodes, the RA and RV, and the inferior part of the LV

6. Coronary Blood Flow Venous system parallels the arterial system: the great cardiac vein follows the left anterior descending artery and the small cardiac vein follows right coronary artery Veins meet to form the coronary sinus (largest coronary vein), which returns deoxygenated blood from the myocardium to the right atrium

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9. Conduction SA node, called the pacemaker, initiates the impulse The impulse is carried throughout the atria to the AV node, located on the floor of the RA Impulse is delayed in the AV node, then transmitted to the ventricles through the bundle of His The bundle is made up of Purkinje cells and is located where the atrial and ventricular septa meet Bundle of His divides into left and right bundle branches Left branch divides into anterior and posterior branches: fascicles Terminal ends of right and left branches: the Purkinje fibers When impulse reaches Purkinje fibers, ventricles contract

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11. Conduction Cardiac innervation – Heart innervated by sympathetic and parasympathetic fibers of the autonomic nervous system Sympathetic fibers distributed throughout the heart Sympathetic stimulation results in increased heart rate, increased speed of conduction through the AV node, and more forceful contractions Parasympathetic fibers (part of the vagus nerve) found primarily in the SA and AV nodes and the atrial tissue Parasympathetic stimulation results in slowing of heart rate, slowing of conduction through the AV node, and decreased strength of contraction

12. Cardiac Function Cardiac cycle – Contraction and relaxation of the heart make up one heartbeat Cardiac output – Amount of blood (in liters) ejected per minute – Factors that affect stroke volume: preload, contractility, and afterload Myocardial oxygen consumption – Myocardial tissue routinely needs 70% to 75% of the oxygen delivered to it by the coronary arteries

13. Age-Related Changes Heart – Increased density of connective tissue and decreased elasticity – Number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in the ventricles Blood vessels – Changes in connective tissue and elastic fibres in arteries cause them to become stiffer. – Veins stretch and dilate, leading to venous stasis and sometimes impaired venous return.

14. Coronary Artery Disease (CAD) Arteriosclerosis – Abnormal thickening, hardening, loss of elasticity of arterial walls Atherosclerosis – Form of arteriosclerosis; inflammatory disease that begins with endothelial injury and progresses to the complicated lesion seen in advanced stages of the disease process

16. Coronary Artery Disease (CAD) Risk factors – Nonmodifiable Age, gender, heredity, and race – Modifiable Increased serum lipids, high blood pressure, cigarette smoking (nicotine), diabetes mellitus with elevated blood glucose, obesity, sedentary lifestyle – Other factors Stress, sex hormones, birth control pills, excessive alcohol intake, high homocysteine levels

18. Progression of lesions Fatty streak Fibrous plaque Complicated lesions Collateral circulation Branches grow from existing arteries; provide increased blood flow

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20. http://www.youtube.com/watch?v=SjRPxGNOt jM

21. Angina Pectoris The most common symptom of CAD Demand for oxygen by myocardial cells exceeds supply Stable angina – Occurs with exercise or activity and usually subsides with rest Unstable angina – Pain more severe, occurs at rest or with minimal exertion, is often not relieved by NTG or requires more frequent NTG administration, and is not predictable

22. Variant angina Caused by coronary artery spasm; may not be associated with CAD Unpredictable and often occurs at rest

23. Angina Pectoris Medical treatment – Initial therapy for patients with angina A Aspirin and antianginal therapy B Beta-blocker and blood pressure C Cigarette smoking and cholesterol D Diet and diabetes E Education and exercise

24. Acute Myocardial Infarction Risk factors for AMI – Obesity, smoking, a high-fat diet, hypertension, family history, male gender, diabetes mellitus, sedentary lifestyle, and excessive stress

25. Acute Myocardial Infarction Pathophysiology – Begins with occlusion of a coronary artery – Over 4-6 hours, ischemia, injury, infarction develop – Ischemia results from a lack of blood and oxygen to a portion of the heart muscle – If ischemia is not reversed, injury occurs – Deprived of blood and oxygen, the affected tissue becomes soft and loses its normal color – Continued ischemia: infarction of myocardial tissue – Ischemia lasting 20 minutes or more is sufficient to produce irreversible tissue damage

26. Acute Myocardial Infarction Complications – Heart failure, cardiogenic shock, thromboembolism, and ventricular aneurysm/rupture Signs and symptoms Pain Heavy or constrictive pain located below or behind sternum May radiate to the arms, back, neck, or jaw – Patient becomes diaphoretic and lightheaded and may experience nausea, vomiting, and dyspnea – The skin is frequently cold and clammy – Patient experiences great anxiety; feeling of impending doom

27. Acute Myocardial Infarction Medical diagnosis – History and the physical signs and symptoms – Laboratory evidence and ECG changes Cardiac markers – Troponin, myoglobin, and cardiac enzymes Electrocardiogram – Ischemia: ST segment depressed; T wave is inverted – If there has been total occlusion of a coronary artery, the ECG will show ST elevation (STEMI) – Following infarction, another change often seen on the ECG waveforms is a significant Q wave

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29. Acute Myocardial Infarction Medical treatment – Drug therapy Sublingual or intravenous nitroglycerin Morphine or Demerol Oxygen Fibrinolytic therapy Aspirin and beta-adrenergic blockers – Percutaneous coronary intervention (PCI) Intracoronary stents Coronary atherectomy Laser angioplasty Radiation therapy – Coronary artery bypass graft surgery

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31. http://www.youtube.com/watch?v=S9AqBd4R Exk

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34. Acute Myocardial Infarction Assessment – Ask patient to describe the pain, including type, location, duration, and severity Interventions – Pain – Decreased cardiac output – Anxiety Cardiac rehabilitation

35. Heart Failure Etiology and risk factors – Two types Disorders that increase the workload of the heart Disorders that interfere with heart’s pumping ability – Patients at risk for HF: those with CAD, AMI, cardiomyopathy, hypertension, COPD, pulmonary hypertension, anemia, disease of the heart valves, and fluid volume overload

36. Heart Failure Pathophysiology – The LV, RV, or both fail as pumps – Usually left side of heart fails first; right side fails as a result of the left-sided failure Compensation – Sympathetic compensation – Renal compensation – Natriuretic peptides – Ventricular hypertrophy

37. Heart Failure: Signs and Symptoms Left-sided heart failure – Anxious, pale, and tachycardic – Consecutive blood pressure readings may show a downward trend – Auscultation of the lung fields reveals crackles, wheezes, dyspnea, and cough – S 3 and S 4 heart sounds heard

38. Heart Failure: Signs and Symptoms Right-sided heart failure – Increased central venous pressure, jugular venous distention, abdominal engorgement, and dependent edema – Anorexia, nausea, and vomiting from the abdominal engorgement – Fatigue, weight gain, decreased urinary output

39. http://www.youtube.com/watch?v=JXA6LjmKs aU

40. Heart Failure Medical diagnosis – History, physical examination, radiographs, and laboratory test results

41. Heart Failure Medical treatment – Drug therapy ACE inhibitors, diuretics, beta-adrenergic blockers, inotropic agents, cardiac glycosides, and nitrates. In addition, certain patients will benefit from B-type natriuretic peptide – Intra-aortic balloon pump (IABP) – Ventricular assist devices (VADs) – Biventricular pacing – Surgery Coronary artery bypass grafting, valve repair or replacement, partial left ventriculectomy, and cardiac transplantation

42. Heart Failure Assessment – Heart sounds, rate, and rhythm – Jugular vein distention – Baseline respiratory assessment of rate, rhythm, and breath sounds is vital – Measure weight and blood pressure accurately – Inspect skin and palpate for turgor and edema – Intake and output records and daily weights

43. Heart Failure Interventions – Decreased Cardiac Output – Impaired Gas Exchange – Fluid Volume Excess – Activity Intolerance – Anxiety

44. Infective Endocarditis Etiology and risk factors – Primarily affect the valves – Incidence has decreased with the use of antibiotics, but there has been a resurgence of the problem in intravenous drug abusers – Patients with valvular disease also at risk

45. Infective Endocarditis Pathophysiology – Pathogens, usually bacteria, enter the bloodstream by any of the previously mentioned means – The pathogen accumulates on the heart valves and/or the endocardium and forms vegetations

46. Infective Endocarditis Complications – Heart failure and embolization Signs and symptoms – Fever, chills, malaise, fatigue, and weight loss – Chest or abdominal pain; may indicate embolization – Petechiae inside the mouth and on the ankles, feet, and antecubital areas – Osler’s nodes on the patient’s fingertips or toes

47. Infective Endocarditis Medical diagnosis – History, physical examination, results of lab studies – Echocardiography – Serial blood cultures; elevated WBC Medical treatment – Antimicrobials, rest, limitation of activities – Prophylactic anticoagulants – Surgery to replace an infected prosthetic valve

48. Infective Endocarditis Assessment – Review patient’s history for risk factors, recent invasive procedures, pathologic cardiac conditions, and onset of symptoms – Assess for temperature elevation, heart murmur, evidence of HF (cough, peripheral edema), and embolization

49. Infective Endocarditis Interventions – Administer prescribed antibiotics – Assess cardiac output and monitor for complications – Teach patient about the medications prescribed and any restrictions imposed – Encourage adequate rest

50. Pericarditis Etiology and risk factors – Inflammation of the pericardium – May be primary disease or associated with another inflammatory process – The disease may be acute or chronic Acute pericarditis caused by viruses, bacteria, fungi, chemotherapy, or AMI (Dressler’s syndrome) Chronic pericarditis caused by tuberculosis, radiation, or metastases

52. Pericarditis Pathophysiology – In acute pericarditis, inflammatory process increases amount of pericardial fluid and inflammation of the pericardial membranes – In chronic pericarditis, scarring of the pericardium fuses the visceral and parietal pericardia together – Loss of elasticity results from the scarring – Constrictive process prevents adequate ventricular filling

53. Pericarditis Complications – Pericardial effusion or accumulation of fluid in the pericardial space May lead to cardiac tamponade Signs and symptoms – Chest pain Most severe on inspiration Sharp and stabbing but may be described as dull or burning Relieved by sitting up and leaning forward – Dyspnea, chills, and fever

54. Pericarditis Medical diagnosis – Serial ECGs – Echocardiogram – CPK-MB – Blood cultures Medical treatment – Analgesics, antipyretics, anti-inflammatory agents, and antibiotics – Surgical creation of a pericardial window for chronic pericarditis with effusion

55. Pericarditis Assessment – Assessment of heart sounds especially important Interventions – Rest and reduction of activity – Administer and teach patient about medications – Emotional support – Vital signs; auscultate for pericardial friction rub – Note pain characteristics and response to analgesics and anti-inflammatory agents – Monitor the ECG for dysrhythmias

56. Cardiomyopathy Disease of the heart muscle Cause often unknown; may be secondary to another disease process Usually leads to heart failure Three types: dilated, hypertrophic, and restrictive Risk factors with dilated CMP are excessive use of alcohol, pregnancy, and infections Hypertrophic CMP: common in younger individuals Amyloidosis, sarcoidosis, and other immunosuppressive disorders may predispose individuals to restrictive cardiomyopathy

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58. Cardiomyopathy Pathophysiology – Dilated cardiomyopathy: dilation of the ventricle and severely impaired systolic function – Hypertrophic cardiomyopathy: LV hypertrophies and there is thickening of the ventricular septum – Restrictive cardiomyopathy: the myocardium becomes rigid and noncompliant

59. Cardiomyopathy Signs and symptoms – Dilated cardiomyopathy: dyspnea, fatigue, left-sided heart failure, and moderate-to- severe cardiomegaly – Hypertrophic cardiomyopathy: dyspnea, orthopnea, angina, fatigue, syncope, palpitations, ankle edema, and S 4 sounds – Restrictive cardiomyopathy: dyspnea, fatigue, right-sided HF, S 3 and S 4 sounds, and mitral valve regurgitation

60. Cardiomyopathy Medical diagnosis – Echocardiography – Chest radiography http://www.youtube.com/watch?v=TwA0LM5 _1dE

61. Cardiomyopathy Medical treatment – Dilated cardiomyopathy: positive inotropic drugs, diuretics, ACE inhibitors and vasodilators; heart transplant – Hypertrophic cardiomyopathy: antidysrhythmics, antibiotics, anticoagulants, calcium channel blockers, beta-blockers; surgical interventions; implantable cardioverter-defibrillator – Restrictive cardiomyopathy: similar to that of HF therapy. Heart transplantation may be considered

62. Cardiomyopathy Assessment – Primarily for heart failure – Be alert for dyspnea, cough, edema, dysrhythmias, and decreased cardiac output Interventions – Similar to that of patients with HF – A hopeful atmosphere and careful explanation of care requirements – Encourage the family to support the patient – Guide the patient to make lifestyle changes – Encourage patient to make decisions and choices

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64. Sudden Cardiac Death When heart activity and respirations cease abruptly Most common reason is coronary heart disease Often preceded by ventricular tachycardia or ventricular fibrillation and occasionally by severe bradydysrhythmias Sudden cardiac death may be the first indication of CAD Other causes: left ventricular dysfunction, cardiomyopathy, hypokalemia, antidysrhythmics, liquid protein diets, and high alcohol consumption Those who survive sudden cardiac death need extensive testing to determine its nature and cause

65. Sudden Cardiac Death Implantable cardioverter/defibrillator – For patients with life-threatening recurrent ventricular fibrillation who are unresponsive to medications or pacemakers – The device senses heart rate, diagnoses rhythm changes, and treats ventricular dysrhythmias

66. Nursing Care Promote psychosocial adaptation – Body image change and a fear of shocks Patients and families need teaching and support Family instructed in CPR ID bracelet and a card with instructions about the ICD setting carried at all times Advise to avoid strong magnetic fields

67. Valvular Disease Mitral stenosis: narrowing of the opening in the mitral valve that impedes blood flow from the LA into the LV Mitral regurgitation: allows blood to flow back into the LA during diastole Mitral valve prolapse: one or both leaflets enlarges and protrudes into the LA during systole Aortic stenosis: valve cusps become fibrotic and calcify Aortic regurgitation: fibrosis and thickening of the aortic cusps progress until the valve no longer maintains unidirectional blood flow

69. Cardiac Transplantation The first heart transplantation was performed in 1967 in South Africa by Dr. Christiaan Barnard Today in the United States, approximately 2500 are done annually for end-stage heart disease Donor must meet the criteria for brain death, have no malignancies outside the central nervous system, be free of infection, and not have experienced severe chest trauma

70. Cardiac Transplantation Donor and recipient organs carefully matched Recipient must be free of infection at the time of transplantation – Patient prepped as any open-heart procedure – Cardiopulmonary bypass initiated; recipient’s heart is removed except for the posterior portions of the atria – Donor heart trimmed and anastomosed to the remaining native heart – Patient removed from bypass, heart restarted, and chest is closed

71. Cardiac Transplantation Aftercare similar to that of coronary artery bypass surgery – Hemodynamic monitoring, ventilation, cardiac assessment, care of chest tubes, and accurate intake and output measurements are vital Modified protective isolation used Patients and families taught sign/symptoms of infection, to avoid crowds and others with infections Lifelong immunosuppression Rejection monitored by endomyocardial biopsies

72. Electrocardiogram Monitoring 12-lead electrocardiogram – Looks at heart from 12 directions or perspectives – Permits more precise evaluation of the heart’s electrical activity Continuous ECG monitoring – Most units that perform continuous monitoring use the five-lead system with four limb electrodes and a chest electrode

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74. Electrocardiogram Monitoring Interpretation of electrocardiograms – Heart’s electrical activity represented by deflections, positive and negative, from the baseline P wave, QRS complex, and T wave – Criteria for interpreting electrocardiograms Rate calculation Rhythm P waves PR interval QRS complex T waves QT interval

75. Electrocardiogram Monitoring Interpretation of electrocardiograms – Normal sinus rhythm The most common cardiac rhythm is sinus in origin because the impulse originates in the SA node; is conducted normally – Common dysrhythmias (rhythm disturbance from problem in the conduction system) Atrial dysrhythmias Junctional or escape rhythms Ventricular dysrhythmias

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88. Hemodynamic Monitoring Central venous catheter – Placed through the skin, into a venous access (brachial, femoral, subclavian, or jugular sites), and threaded into the RA – Catheter may have 1 to 3 lumens – Mixed venous oxygen saturation

89. Hemodynamic Monitoring Pulmonary artery catheter – Swan-Ganz catheter – Longer than the central venous catheter – Inserted like the central venous catheter and is threaded through the RA, tricuspid valve, RV, pulmonic valve, and into pulmonary artery – Cardiac output Measured continuously or by thermodilution

90. Hemodynamic Monitoring Arterial line – Provides a direct measurement of systolic and diastolic blood pressures