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1 NCLEX RN Preparation Program Cardiovascular Disorders Module 5, Part 2 of 3.

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Presentation on theme: "1 NCLEX RN Preparation Program Cardiovascular Disorders Module 5, Part 2 of 3."— Presentation transcript:

1 1 NCLEX RN Preparation Program Cardiovascular Disorders Module 5, Part 2 of 3

2 2 Cardiovascular System Introduction The heart and the circulatory system comprise one of the most essential parts of the body. Failure to function results in death of the organism. Photo Source: National Heart, Lung and Blood Institute (NHLBI)

3 3 Gross Structure of the Heart Layers: Pericardium Fibrous Serous Pericardium Epicardium Myocardium Endocardium

4 4 Chambers of the Heart Heart, a muscular organ divided by a septum into two halves. Right or venous chamber and left or arterial chamber. Right Chambers Right Atrium Right Ventricle Left Chambers Left Atrium Left Ventricle

5 5 Coronary Blood Supply Right Coronary Artery Left Coronary Artery Left anterior descending Circumflex Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program

6 6 Valves of the Heart Valves are strong membranous openings that provide one-way flow of blood. Atrioventricular valves – prevent backflow of blood from ventricles to atria during systole. Tricuspid Mitral Semilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. Pulmonic Aortic

7 7 Valves of the Heart Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program

8 8 Conduction system Specialized tissue that allows rapid transmission of electrical impulses through the myocardium Sinoatrial node – main pacemaker of heart. Normal rhythmic, self-excitatory impulse is generated.

9 9 Conduction system Photo Source: St. Francis Hospitals & Health Centers, rg/DesktopDefault.aspx?tabid= 72&Class=Test&pageid=P rg/DesktopDefault.aspx?tabid= 72&Class=Test&pageid=P079 73

10 10 Gross Structure of Vasculature Arteries: transport blood under high pressure to body tissues Precapillary sphincters Arteriovenous shunts Capillaries – exchanging fluid and nutrients between blood and interstitial space. Veins: acts as conduits for transport of the blood from tissues back to heart

11 11 Physiology of the Heart Contraction – shortening or increase in muscle tension. Utilizes chemical energy to do the work of contraction Cardiac Muscle Principle: Frank Starling Law: the greater the heart is filled during diastole, within physiological limits, the greater the quantity of blood pumped into the aorta and pulmonary artery.

12 12 Autonomic Nervous System Control Cardiac Muscle Sympathetic (Adrenergic) Parasympathetic (Cholinergic) Systemic blood Vessels Sympathetic – vasoconstriction Parasympathetic – vasodilation

13 13 Baroreceptor Reflex (Pressoreceptors) Located in the walls of large systemic arteries Rise in pressure results in baroreceptors transmitting signals to CNS (Central Nervous System) to inhibit sympathetic action Other signals, in turn, sent to circulatory system to reduce pressure back to normal. Result: decreased heart rate, vasodilation, decreased BP.

14 14 Other Chemical Controls of Blood Pressure Kidney Adrenal cortex - aldosterone Renin-angiotensin system Antidiuretic hormone (vasopressin)

15 15 System Assessment Evaluate Patients History Pain Dyspnea Cyanosis Fatigue Palpitations Syncope Hemoptysis Edema Condition of Extremities

16 16 Evaluate veins and arterial pulses through inspection/palpation Veins Neck veins Arm and hand veins Leg and foot veins Arteries Central Peripheral pulses

17 17 Auscultate lung sounds Lungs Listen for bibasilar crackles – if present, suspect Congestive Heart Failure (CHF) Photo Source, Wikimedia Commons, Creative Commons,

18 18 Auscultate heart sounds Heart sounds – frequency, pitch, intensity, duration Murmurs Systolic Diastolic Pericardial friction rubs

19 19 Other parameters to assess Arterial pressure Carotid blood vessels for bruit Palpate and percuss thorax Evaluate chest x-rays Assess lung sounds

20 20 Diagnostic Tests & Procedures Laboratory Studies Cardiac Enzymes CK-MB LDH Troponin Myoglobin BNP CBC Blood coagulation factors Serum lipids Electrolytes K, Na Calcium Phosphorus Magnesium BUN Blood glucose

21 21 Diagnostic Procedures Electrocardiogram Central Venous Monitoring Cardiac Catheterization Echocardiography Angiography Chest x-rays

22 22 Acute Coronary Syndromes Coronary Artery Disease (CAD) Narrowing or obstruction of one or more coronary arteries as a result of atherosclerosis, an accumulation of lipid-containing plaque in the arteries. Photo Source: National Heart, Lung and Blood Institute (NHLBI),

23 23 Pathophysiology Atherosclerosis - fat deposited in intima of arterial wall Inflammatory response begins Macrophages inflitrate area to ingest lipids, then die Smooth muscles cells within the blood vessel cover the area with fiber and plaque is formed. If the plaque is thin, the lipid center may grow, rupture, become a thrombus

24 24 Myocardial Ischemia / Angina Pectoris Decreased oxygen to heart Exercise-induced chest pain Unstable angina Other risk factors

25 25 Coronary Artery Disease Myocardial ischemia CLINICAL MANIFESTATIONS: May be asymptomatic unless ischemia occurs Chest pains or pressure, may radiate to jaw, back, shoulder Palpitations, weakness Dyspnea Syncope Nausea Excessive fatigue EKG changes (T wave inversion)

26 26 Coronary Ischemia/Angina Silent angina - no symptoms, but EKG changes. Often occurs in diabetic patients with CAD.

27 27 Teaching for Angina Rest at onset of chest pain Take one nitroglycerin, repeat 2 more prn No relief by 3rd, call 911 Previous angina with particular activity, take nitroglycerin prior to activity

28 28 Unstable Angina Oxygen: 2-4L nasal cannula Nitroglycerin Morphine Aspirin Baseline vital signs 12 lead EKG Monitor for dysrhythmias, heart failure

29 29 Myocardial Infarction Photo Source: National Heart, Lung and Blood Institute (NHLBI),

30 30 MI: Signs and Symptoms Pain Nausea Impending doom Diaphoresis Dyspnea Dysrhythmias

31 31 12-lead EKG Normal Ischemia Injury Acute infarct Old infarct

32 32 LABS Myoglobin – non specific Troponin CK-MB BNP = CHF

33 33 Collaborative Management Immediate assessment Vital signs with oxygen saturation 12-lead EKG Cardiac enzymes Chest x-ray Electrolytes – K + & Mg ++ Immediate treatment – MONA Beta blockers?

34 34 MONA Acronym from Advanced Cardiac Life Support (ACLS) though order is ONMA. O = Oxygen 2-4 liters per nasal cannula N = Nitroglycerin (if not already tried outside hospital); relieves pain M= Morphine relieves pain, decreases anxiety, increases venous pooling (to reduce cardiac workload) A = Aspirin prevents platelet aggregation at the site of obstruction

35 35 Reperfusion Strategies Thrombolytics Percutaneous Transluminal Coronary Angioplasty (PTCA) Stent Procedure Photo Source: National Heart, Lung and Blood Institute (NHLBI),

36 36 Post-PCTA Care Monitor V/S Assess distal pulses Bed rest with limb straight for 6 – 8 hours Anticoagulants/antiplatelet agents – prevent thrombus formation Monitor IV nitroglycerin – prevent coronary artery spasms ASA once a day permanently Assist planning lifestyle modification

37 37 Acute Myocardial Infarction Bed rest for 24 to 36 hrs Pain control Monitor rhythm Assess for new murmurs Monitor potassium, magnesium Monitor for heart failure Gradual increase of activities

38 38 Rehabilitation Diet Progressive exercise Change modifiable risk factors Weight loss Stress reduction Lipid-lowering drugs Anti-hypertensives Aspirin

39 39 Coronary Artery Bypass Graft (CABG) Bypass grafts sewn from aorta to below area of blockage Fluid overload Pacemaker? Bleeding Atrial fibrillation

40 40 Nursing Management Control pain Early ambulation Incentive spirometer Change dressings: watch for infection Monitor: VS, lungs, heart, weight, I&O, labs, EKG

41 41 Complications Stroke Tamponade: pulsus paradoxus Bleeding Dysrhythmias Post-cardiotomy syndrome

42 42 Cardiac Dysrhythmias Normal Sinus Rhythm/Regular Sinus Rhythm Rhythm originates from the SA node Atrial and ventricular rhythms are regular Rates are : beats per minute.

43 43 Cardiac Dysrhythmias Sinus bradycardia Atrial and ventricular rates below 60 beats per minute Treatment may be necessary if symptomatic Note: low rates may be normal for some patients.

44 44 A-V block: 2 nd Degree Mobitz I

45 45 AV Block: 2 nd Degree Mobitz II

46 46 A-V Block: 3 rd Degree

47 47 Supraventricular Tachycardia

48 48 Atrial Fibrillation

49 49 Premature Ventricular Contractions (PVCs)

50 50 Ventricular Tachycardia

51 51 Ventricular Fibrillation

52 52 Defibrillation Options Paddles AED ICD Photo Source: Wikimedia Commons (Creative Commons),

53 53 Asystole/PEA CPR, epinephrine, vasopressin, atropine Consider 6 Hs, 5 Ts below: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypoglycemia, Hypothermia Toxins, Tamponade (cardiac); Tension pneumothorax; Thrombosis (coronary or pulmonary); Trauma

54 54 Cardiac Pacemaker Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the patients intrinsic pacemaker fails to provide a perfusing rhythm.

55 55 Pacemakers Types of Pacemakers Temporary Transvenous invasive temporary pacing Epicardial invasive temporary Permanent

56 56 Patient Education Programmed rate When to notify MD: Dizziness, weakness, sudden weight gain of 3-5 pounds overnight, persistent hiccups. Check pulse daily, report sudden slowing or increasing of pulse. Signs/symptoms to report: Fever, redness, swelling, drainage from insertion site, dizziness, fatigue, shortness of breath, chest pains, swelling of ankles/legs Pacemaker identification, medic alert Measure pulse daily, keep record

57 57 Patient Education (continued) Wear loose-fitting clothing Avoid contact sports Inform all health care providers of pacemaker Most electrical appliances can be used without any interference with the functioning of the pacemaker. If any unusual feelings occur when near any electrical devices, move 5 to 10 feet away and check pulse.

58 58 Congestive Heart Failure Inability of the heart to maintain adequate circulation to meet the metabolic needs of the body because of impaired pumping actions. Cardiac output diminished and peripheral tissue not adequately perfused Congestion of the lungs and periphery may occur. Classification: Acute and Chronic Types: Right-sided/left-sided heart failures

59 59 Congestive Heart Failure Clinical manifestations Weight gain, I & 0, edema, if severe: ascites Crackles in lungs (especially bibasilar) Dyspnea, orthopnea, urinary frequency, murmurs (if valve problem) S3 heart sound - sign heart beginning to fail & increased blood volume remains in heart after each beat BNP lab test - the higher the number, the worse the CHF is. Can monitor severity of CHF, improvement due to treatment regimen, timely diagnosing of CHF Jugular vein distension, LOC, pulse oximetry.

60 60 CHF: Collaborative Mgmt Vasodilators: Nitrates Positive inotropes: increase contraction Digoxin (Lanoxin) Beta blockers (though some contractility & are contraindicated) ACE inhibitors Diuretics

61 61 CHF: Nursing Management Elevate head of bed Give oxygen Decrease oxygen demand Exacerbation? Identify precipitating factors Teach: low-salt diet, medications and their rationale, weigh daily, exercise but pace activities. Wait 90 min. after meals to exercise. Avoid extremes in weather when exercising.

62 62 Cardiac Valve Disorders Mitral stenosis Mitral prolapse Aortic stenosis Aortic regurgitation Photo Source: National Heart, Lung and Blood Institute (NHLBI),

63 63 Cardiac Valve Disorders Clinical Manifestations: Heart murmur Left ventricular hypertrophy seen on EKG

64 Congestive Heart Failure Photo Source: Lippincott, Williams, & Wilkins Connection Image Bank, eltzer9e/imagebank.asp eltzer9e/imagebank.asp

65 65 Congestive Heart Failure Collaborative Management Digoxin (inotropic) Diuretics (lasix, aldactone) Coreg - beta blocker shown to improve cardiac function in CHF patient Ace inhibitor - shown to improve cardiac function in CHF patient Oxygen, cardiac rehab

66 66 CHF Management (continued) Treat heart failure if present Atrial fibrillation? Antibiotic prophylaxis Weigh daily

67 67 Pericarditis Inflammation of pericardial sac. Can be caused by viral infection, complicaton after cardiac surgery 10 days to 2 months, or after MI Idiopathic cause, or disorder of connective tissue (lupus), cancer, radiation therapy, etc

68 68 Pericarditis: Manifestations Chest pain on inspiration, worse when patient leans forward, lying down or turning Pericardial friction rub Symptoms of right-sided heart failure Mild fever, elevated WBC, ESR Atrial fibrillation common 12 lead EKG may have elevation in ALL leads Can worsen to cardiac tamponade

69 69 Pericarditis Collaborative Management NSAIDs or corticosteroids Pericardiocentesis or surgical pericardial window

70 70 Pericarditis: Nursing Mgmt Position for comfort Monitor for cardiac tamponade (fluid between heart and pericardial sac) that causes heart to be compressed inside the sac leading to decreased blood pressure and shock, distant heart sounds Teach: gradual increases of activity Teach: avoid aspirin, anticoagulants

71 71 Infective Endocarditis Valves infected, spreads to endothelium Leaflets deform, leak High risk: elderly, prosthetic valves, IV drug abusers, immunosuppressed

72 72 Manifestations Slow onset Flu-like symptoms, anorexia, weight loss, joint & back pain, fever, splinter hemorrhages undernails, petechiae, murmur, headache? Major complication: embolus Diagnosis: blood culture, echocardiogram

73 73 Management IV antimicrobials based on cultures Teach prevention Monitor: sepsis, new murmur, stroke, meningitis, CHF

74 74 Hypertension Pathophysiology 90-95% unknown cause 5-10% secondary causes Some genetic tendency, obesity, stress, excess sodium intake Prolonged hypertension eventually damages blood vessels, heart (LVH) and kidneys, eyes, brain.

75 75 Hypertension Clinical manifestations Usually asymptomatic silent killer Some report headache, especially early morning Risk factors Family history Age Diabetes Obesity Heavy alcohol High sodium intake

76 76 Hypertension Goals: reduce BP. Goal: 120/80 Ask for S/S indicative of HTN Obtain BP on both arms Family history, weight, dietary patterns Identify medication therapy Assess cardiac, neuro, renal, diagnostic and lab studies.

77 77 Hypertension Collaborative Management Medications: diuretics, beta blockers, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockers Monitor and routine follow-up with EKG, lipid lower agents if needed

78 78 Hypertension Nursing Management TEACH: weight loss, stress management, rationale for medications prescribed & their importance. Low-sodium, low-fat, low- cholesterol diet. Stop smoking. Limit caffeine, alcohol. Teach how to modify risk factors. Monitor for target-organ problems. Teach potential problems if hypertension untreated. Many people undiagnosed. Promote screening for early detection.

79 79 Classification CategorySystolicDiastolic Normal<120 mmHg<80 mmHg Pre-HTN or80-89 Stage or90-99 Stage or 100

80 80 Hypertensive Crisis… Assessment Diastolic pressure > 120 mm Hg. Headache Drowsiness Confusion Changes in LOC Tachycardia and tachypnea Dyspnea/cyanosis/seizure

81 81 Hypertensive Crisis: Mgmt Lower BP slowly IV nitrates (nitroglycerin) Nitroprusside (Nipride) Enalapril (Vasotec) Beta blockers Diuretics Monitor rhythm, vital signs

82 82 Peripheral Vascular Disease (PVD) Pathophysiology Generalized atherosclerosis (plaque development) or arteriosclerosis (hardening of the arteries) Narrowing of lumen, obstruction by thrombosis Bifurcation or branch areas higher risk of blockage. If have PVD, at risk of having CAD as well

83 83 Peripheral Arterial Disease Stage I: Asymptomatic Stage II: Claudication Stage III: Rest pain Stage IV: Necrosis

84 84 PVD: Management Medications Control hypertension Angioplasty, bypasses Exercises Position Vasodilation Avoid vasoconstriction

85 85 Arterial Bypass Monitor for graft occlusion Promote graft patency Monitor for compartment syndrome

86 86 Peripheral Venous Insufficiency Stasis dermatitis lower legs Edema Ulcers over malleoli Anterior leg ulcers if arterial flow impaired

87 87 Peripheral Vascular Disease Compression stockings Sequential compression pump Manage ulcers Elevate legs Avoid prolonged sitting or standing No compression of legs

88 88 Abdominal Aortic Aneurysm Localized dilatation of the wall of the abdominal aorta caused by congenital weakness, trauma, disease, atherosclerosis Risk factors: smoking, hypertension Progressive weakening and enlarging of area of vessel If a tear develops - medical emergency (rupture)

89 89 Aortic Aneurysms Goal of treatment: limit progression of the condition by modifying risk factors, controlling BP, recognizing symptoms early, and preventing rupture Photo Source: National Heart, Lung and Blood Institute (NHLBI),

90 90 Abdominal Aortic Aneurysm Clinical Manifestations: Can palpate enlarged aorta, possible bruit ausculated If rupture, sudden pain in back or abdomen If tearing, pain in abdominal area or back; can be slowly progressive If rupture-hemorrhage, shock, death unless emergent surgical intervention

91 91 Manage Abdominal Aneurysm Non-surgical: Modify risk factors Monitor BP Regular exams for size, pulsation Report: chest/back pain, SOB, Difficulty swallowing, hoarseness

92 92 Thoracic Aortic Aneurysm Pain: neck, shoulders, lower back or abdomen Syncope Dyspnea Tachycardia Cyanosis Weakness

93 93 Manage Thoracic Aneurysm Monitor V/S Assess for pain – abdominal or back pains. Check peripheral pulses, including temperature and color Observe for signs of rupture Note tenderness/distention of abdomen

94 94 Photo Acknowledgement: All unmarked photos and clip art contained in this module were obtained from the 2003 Microsoft Office Clip Art Gallery.

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