NCLEX Review Course

NCLEX Review Course

NCLEX RN Preparation Program Cardiovascular Disorders Module 5, Part 2 of 3 1 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) http://www.nhlbi.nih.gov/health/dci/Diseases/arr/arr_howheartwork.html 2 Gross Structure of the Heart Layers: Pericardium

Fibrous Serous Pericardium Epicardium Myocardium Endocardium 3 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 4 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 5 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 6

Valves of the Heart Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program 7 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. 8 Conduction system Photo Source: St. Francis Hospitals & Health Centers, http:// www.stfrancishospitals.org/De sktopDefault.aspx?tabid =72&Class=Test&pageid =P07973 9 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 10 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. 11 Autonomic Nervous System Control Cardiac Muscle Sympathetic (Adrenergic) Parasympathetic (Cholinergic)

Systemic blood Vessels Sympathetic vasoconstriction Parasympathetic vasodilation 12 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. 13 Other Chemical Controls of Blood Pressure Kidney

Adrenal cortex - aldosterone Renin-angiotensin system Antidiuretic hormone (vasopressin) 14 System Assessment Evaluate Patients History

Pain Dyspnea Cyanosis Fatigue Palpitations Syncope Hemoptysis Edema Condition of

Extremities 15 Evaluate veins and arterial pulses through inspection/palpation Veins Neck veins Arm and hand veins

Leg and foot veins Arteries Central Peripheral pulses 16 Auscultate lung sounds Lungs

Listen for bibasilar crackles if present, suspect Congestive Heart Failure (CHF) Photo Source, Wikimedia Commons, Creative Commons, http://commons.wikimedia.org/wiki/Image:Xray_lung_consolidation.jpg 17 Auscultate heart sounds Heart sounds frequency, pitch, intensity, duration Murmurs

Systolic Diastolic Pericardial friction rubs 18 Other parameters to assess

Arterial pressure Carotid blood vessels for bruit Palpate and percuss thorax Evaluate chest x-rays Assess lung sounds 19 Diagnostic Tests & Procedures Laboratory Studies Cardiac Enzymes

CK-MB LDH Troponin Myoglobin BNP

Calcium Phosphorus Magnesium BUN Blood glucose CBC Blood coagulation factors Serum lipids Electrolytes

K, Na 20 Diagnostic Procedures Electrocardiogram Central Venous Monitoring Cardiac Catheterization Echocardiography

Angiography Chest x-rays 21 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), http:// www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html 22 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 23 Myocardial Ischemia / Angina Pectoris

Decreased oxygen to heart Exercise-induced chest pain Unstable angina Other risk factors 24 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) 25 Coronary Ischemia/Angina Silent angina - no symptoms, but EKG changes. Often occurs in diabetic patients with CAD. 26 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 27 Unstable Angina

Oxygen: 2-4L nasal cannula Nitroglycerin Morphine Aspirin Baseline vital signs 12 lead EKG Monitor for dysrhythmias, heart failure 28 Myocardial Infarction Photo Source: National Heart, Lung and Blood Institute (NHLBI), http:// www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html

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

30 12-lead EKG Normal Ischemia Injury Acute infarct

Old infarct 31 LABS Myoglobin non specific Troponin CK-MB BNP = CHF 32

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? 33 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 34 Reperfusion Strategies

Thrombolytics Percutaneous Transluminal Coronary Angioplasty (PTCA) Stent Procedure Photo Source: National Heart, Lung and Blood Institute (NHLBI), http:// www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html 35 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 36

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 37 Rehabilitation Diet Progressive exercise

Change modifiable risk factors Weight loss Stress reduction Lipid-lowering drugs Anti-hypertensives Aspirin 38 Coronary Artery Bypass Graft (CABG)

Bypass grafts sewn from aorta to below area of blockage Fluid overload Pacemaker? Bleeding Atrial fibrillation 39 Nursing Management Control pain

Early ambulation Incentive spirometer Change dressings: watch for infection Monitor: VS, lungs, heart, weight, I&O, labs, EKG 40 Complications Stroke Tamponade: pulsus paradoxus

Bleeding Dysrhythmias Post-cardiotomy syndrome 41 Cardiac Dysrhythmias Normal Sinus Rhythm/Regular Sinus Rhythm Rhythm originates from the SA node Atrial and ventricular rhythms are regular Rates are : 60- 100 beats per minute.

42 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.

43 A-V block: 2nd Degree Mobitz I 44 AV Block: 2nd Degree Mobitz II 45 A-V Block: 3rd Degree 46 Supraventricular Tachycardia

47 Atrial Fibrillation 48 Premature Ventricular Contractions (PVCs) 49 Ventricular Tachycardia 50 Ventricular Fibrillation

51 Defibrillation Options Paddles AED ICD Photo Source: Wikimedia Commons (Creative Commons), http://commons.wikimedia.org/wiki/Image:Defibrillator_Monitor.jpg 52 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 53 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. 54

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

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 56 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. 57 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 58 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. 59 CHF: Collaborative Mgmt Vasodilators: Nitrates Positive inotropes: increase contraction

Digoxin (Lanoxin) Beta blockers (though some contractility & are contraindicated) ACE inhibitors Diuretics 60 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. 61 Cardiac Valve Disorders Mitral stenosis Mitral prolapse Aortic stenosis Aortic regurgitation

Photo Source: National Heart, Lung and Blood Institute (NHLBI), http:// www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html 62 Cardiac Valve Disorders Clinical Manifestations: Heart murmur Left ventricular hypertrophy seen on EKG 63 Congestive Heart Failure Photo Source: Lippincott, Williams, &

Wilkins Connection Image Bank, http://connection.lww.com/products/sm eltzer9e/imagebank.asp 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 65 CHF Management (continued) Treat heart failure if present Atrial fibrillation? Antibiotic prophylaxis

Weigh daily 66 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 67

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

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 70

Infective Endocarditis Valves infected, spreads to endothelium Leaflets deform, leak High risk: elderly, prosthetic valves, IV drug abusers, immunosuppressed 71 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 72 Management

IV antimicrobials based on cultures Teach prevention Monitor: sepsis, new murmur, stroke, meningitis, CHF 73 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. 74 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 75 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. 76 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

77 Hypertension Nursing Management TEACH: weight loss, stress management, rationale for medications prescribed & their importance. Low-sodium, low-fat, lowcholesterol 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. 78 Classification Category Normal Systolic <120 mmHg Diastolic <80 mmHg Pre-HTN

120-139 or 80-89 Stage 1 140-159 or 90-99 Stage 2 160 or 100

79 Hypertensive Crisis Assessment Diastolic pressure > 120 mm Hg. Headache Drowsiness Confusion Changes in LOC

Tachycardia and tachypnea Dyspnea/cyanosis/seizure 80 Hypertensive Crisis: Mgmt Lower BP slowly IV nitrates (nitroglycerin)

Nitroprusside (Nipride) Enalapril (Vasotec) Beta blockers Diuretics Monitor rhythm, vital signs 81 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 82 Peripheral Arterial Disease

Stage I: Stage II: Stage III: Stage IV: Asymptomatic Claudication Rest pain Necrosis 83 PVD: Management

Medications Control hypertension Angioplasty, bypasses Exercises Position Vasodilation Avoid vasoconstriction 84 Arterial Bypass

Monitor for graft occlusion Promote graft patency Monitor for compartment syndrome 85 Peripheral Venous Insufficiency

Stasis dermatitis lower legs Edema Ulcers over malleoli Anterior leg ulcers if arterial flow impaired 86 Peripheral Vascular Disease Compression stockings

Sequential compression pump Manage ulcers Elevate legs Avoid prolonged sitting or standing No compression of legs 87 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) 88 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), http:// www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html 89 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 90 Manage Abdominal Aneurysm Non-surgical:

Modify risk factors Monitor BP Regular exams for size, pulsation Report: chest/back pain, SOB, Difficulty swallowing, hoarseness 91 Thoracic Aortic Aneurysm

Pain: neck, shoulders, lower back or abdomen Syncope Dyspnea Tachycardia Cyanosis Weakness 92 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 93 Photo Acknowledgement: All unmarked photos and clip art

contained in this module were obtained from the 2003 Microsoft Office Clip Art Gallery. 94

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