NCLEX RN Preparation Program

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

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)

Gross Structure of the Heart
Layers: Pericardium Fibrous Serous Pericardium Epicardium Myocardium Endocardium The heart is composed of 3 layers: Pericardium- fibrous outer layer Myocardium – middle layer of muscle fibers, creates the pumping action Endocardium - lines the inside of the heart

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 Chambers of the heart: Right Chambers distribute venous blood to the lungs through the pulmonary artery Right Atrium-receives blood returning from the body via the superior vena cava. Contains the SA node, the pacemaker of the heart Right Ventricle-pumps into the lungs through the pulmonic valve Left Chambers distribute oxygenated blood to the body Left Atrium-receives oxygenated blood through lungs Left Ventricle-pumps blood throughout body through aortic valve

Coronary Blood Supply Right Coronary Artery Left Coronary Artery
Left anterior descending Circumflex Coronary vessels lie on outside of heart and provide the heart muscle with oxygenated blood. These vessels serve different areas of the heart. Changes on an electrocardiogram (EKG) identify and predict which coronary vessel has a problem by knowing which area of the heart is served by that vessel and matching it to the area the EKG is looking at. Left main coronary divides into left anterior descending (LAD) and circumflex LAD: most of left ventricle and septum Circumflex: left atrium, lateral & posterior left ventricle, SA node (39% of population) Right coronary artery: right atrium, right ventricle, inferior part of left ventricle, SA (59%) and AV (88%) nodes Photo Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program

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 Valves: 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 has 3 cusps or leaflets. Between right atrium and right ventricle Mitral-has 2 cusps or leaflets. Between left atrium and left ventricle Semilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. Pulmonic-between right ventricle and pulmonary artery Aortic-between left ventricle and aorta

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

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. Conduction system: Specialized tissue that allows rapid transmission of electrical impulses through the myocardium. Heart has synchronized contraction stimulated by the transmission of electrical impulses to the myocardial cells. Sinoatrial (SA) node: main pacemaker of heart. Normal rhythmic, self-excitatory impulse is generated. Inherent firing rate of per minute, but changes based on body’s needs. Atrioventricular (AV) node: impulses conducted from SA node through AV node, after a slight delay which allows the atria to contract and fill the ventricles with blood, the AV node sends the electrical impulse to the ventricles through the bundle of His (located in septum). If the SA node doesn’t fire, the AV node will take over the fire at rate of per minute.

Conduction system Photo Source: St. Francis Hospitals & Health Centers,

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

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. Contraction – shortening or increase in muscle tension. Utilizes chemical energy to do the work of contraction 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.

Autonomic Nervous System Control
Cardiac Muscle Sympathetic (Adrenergic) Parasympathetic (Cholinergic) Systemic blood Vessels Sympathetic – vasoconstriction Parasympathetic – vasodilation Cardiac Cycle: with systole, pressure in the ventricles rises causing the atrioventricular valves to close, preventing backflow into the atria. The rapidly rising pressure inside both ventricles forces the pulmonic and aortic valves to open and blood is ejected into the lungs and aorta. When the blood from each beat has been ejected from the heart, the pressure quickly decreases causing the pulmonary and aortic valves to close again. This begins diastole. In diastole ventricles are relaxed and AV valves are open, blood returning from the body flows into right atrium. Toward the end of diastole, the atria contracts when it receives impulse from SA node and blood is pushed into ventricles. Systemic blood Vessels Sympathetic response causes vasoconstriction Parasympathetic response causes vasodilation

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

Other Chemical Controls of Blood Pressure
Kidney Adrenal cortex - aldosterone Renin-angiotensin system Antidiuretic hormone (vasopressin) Other Chemical Controls of Blood Pressure Kidney releases renin, an enzyme that is required for angiotensin I to convert to angiotensin II, a potent vasoconstrictor. This renin-angiotensin stimulation also causes aldosterone to be released from adrenal cortex. Aldosterone is a hormone that makes kidney retain sodium and water, and excrete potassium Antidiuretic hormone (ADH, vasopressin) is released by pituitary when body senses fluid volume too low. ADH prevents water loss in the kidney, so kidney retains water and thus, blood fluid volume.

System Assessment Evaluate Patient’s History
Pain Dyspnea Cyanosis Fatigue Palpitations Syncope Hemoptysis Edema Condition of Extremities Evaluate patient’s history-assess for chest pain (when it occurs, precipitating factors if there are any, accompany symptoms such as dyspnea, nausea, sweating, fatigue, palpitations, dizziness). Assess Risk factors for cardiac diseases or disorders:

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

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

Auscultate heart sounds
Heart sounds – frequency, pitch, intensity, duration Murmurs Systolic Diastolic Pericardial friction rubs Heart sounds (S-1, S-2): frequency, pitch, intensity, duration. Also, if murmurs radiate or are louder on certain positions Gallops (S-3, S-4): diastolic filling sounds when blood enters a chamber that can’t stretch. S-3: early sign of heart failure S-4: Left ventricle may have decreased compliance Murmurs: turbulent blood flow causes murmurs. Heard when blood flow through a malfunctioning valve is either stenotic or incompetent (blood leaks backwards) Systolic: heard during first heart sound (S-1) Diastolic: heard during second heart sound (S-2) Holosystolic murmurs: heard throughout systole; sometimes sounds like one sound, a “whoosh” instead of S-1 Pericardial friction rubs-seen in pericarditis. Harsh, grating sound throughout systole and diastole.

Other parameters to assess
Arterial pressure Carotid blood vessels for bruit Palpate and percuss thorax Evaluate chest x-rays Assess lung sounds Other Parameters to assess Arterial pressure Carotid blood vessels for bruit (partial blockage possible if bruit ausculated) Palpate and percuss thorax, heart for palpable thrill Evaluate chest x-rays-observe for enlarged heart, fluid in lungs Assess lung sounds-crackles. In CHF, bibasilar crackles more frequent as the extra fluid goes to the lung bases due to gravity Assess Risk factors for cardiac diseases or disorders: Smoking, high-fat diet, exercise (or lack of), hypertension, stress, diabetes, obesity, family history/genetics.

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 Diagnostic Tests & Procedures Laboratory Studies CK-MB isoenzyme: specific cardiac enzyme, peaks 24 hours after myocardial inury or myocardial infarction (MI) Troponin: any elevation indicates myocardial injury or infarction Myoglobin: rule out MI 2-7 hours after onset Brain Natriuretic Peptide (BNP): helps diagnose heart failure and grades its severity. Also evaluates risk in people who have chest pain. A high BNP predicts an increased risk of MI -measures the effectiveness of treatment for CHF, diagnoses CHF, grades severity of CHF Homocysteine: elevations indicate risk for cardiovascular disease Platelet elevation: may increase risk of thrombus formation Hemoglobin: hemoglobin carries oxygen to cells. If moderately or severely anemic, may precipitate a myocardial infarction in some patients Coagulation factors: patient may be on aspirin; TPA may be needed Lipids - assessfor cardiac risk factors K, Magnesium - evaluate for potential arrhythmias (if levels are low). vital to cellular depolarization and repolarization2 Calcium- needed for cellular depolarization and repolarization Blood glucose- rule out diabetes, a risk factor for cardiac disease

Diagnostic Procedures
Electrocardiogram Central Venous Monitoring Cardiac Catheterization Echocardiography Angiography Chest x-rays Diagnostic Procedures Electrocardiogram (EKG): evaluates left ventricular hypertrophy (LVH) a significant risk factor for MI. Twelve to fourteen leads look at heart from many angles, can diagnose myocardial infarction and its location. Cardiac Catheterization: observe coronary vessels for blockages or strictures. Also can evaluate ejection fraction of heart, valvular function. Echocardiography: ultrasound of heart; can measure cardiac output (ejection fraction, valves, amount of regurgitation or stenosis of valves). Used to evaluate heart murmurs Transesophageal Echocardiography (TEE): performs role of echocardiogram through esophagus looking at back of heart not usually accessible (left atrium, mitral valve, aortic arch)

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),

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

Myocardial Ischemia / Angina Pectoris
Decreased oxygen to heart Exercise-induced chest pain Unstable angina Other risk factors Episodes of chest pain or pressure from coronary blood flow not adequate Decreased oxygen supply to heart (via coronary vessels) Physical exertion can cause angina because of the increased need for oxygen to the heart (stable angina). Stable angina relieved by rest Unstable angina-chest pain occurs without a certain pattern, or without exertion Exposure to cold, eating a heavy meal, stress can increase myocardial workload=angina

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) Clinical Manifestations: May be asymptomatic unless ischemia episode is occurring (can have disease and not know it until there is an ischemic episode) Chest pains or pressure, may radiate to jaw, back, shoulder Palpitations, weakness Dyspnea Syncope Nausea Excessive fatigue EKG changes (T wave inversion if ischemia)

Coronary Ischemia/Angina
Silent angina - no symptoms, but EKG changes. Often occurs in diabetic patients with CAD. Coronary Ischemia/Angina Silent angina: no symptoms, but EKG changes. Often occurs in diabetic patients with CAD. Diabetics can have a myocardial infarction and not know it as they sometimes do not experience chest pain. Discovered on EKG with new Q-waves or changes noted.

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 Patient Teaching CAD/angina Stop activity and rest at onset of angina. If patient knows he gets angina with particular activity, take nitroglycerin prior to prevent the chest pain from occurring. If angina occurs, stop, rest, take nitroglycerin. If unrelieved by 3rd nitroglycerin, call 911. Nitroglycerin: onset 30 seconds to one minute, peaks in 2-5 minutes. Effects last for 30 minutes. If chest pain not relieved by first nitroglycerin, then can take a second 5 minutes after the first (first has already reached peak effectiveness by then). The second nitroglycerin increases what the first one did by vasodilating even further. Important to teach patients to sit down as they may get dizzy and faint with nitroglycerin which vasodilates ALL vessels in the body, not just coronary vessels.

Unstable Angina Oxygen: 2-4L nasal cannula Nitroglycerin Morphine
Aspirin Baseline vital signs 12 lead EKG Monitor for dysrhythmias, heart failure Nursing Management of Patient with Unstable Angina Goal: 1) Eliminate the chest pain (decrease the myocardial oxygen demand and increase the oxygen supply to the myocardium) 2) Reduce the cardiac workload 3) Stabilize the rhythm. The acronym given in Advanced Cardiac Life Support (ACLS) is MONA, although the order is actually ONMA O = Oxygen 2-4 liters per nasal cannula N = Nitroglycerin (if not already tried outside hospital); relieves pain (spray every 5 minutes x 3) M = Morphine relieves pain, decreases anxiety, increases venous pooling A = Aspirin prevents platelet aggregation at the site of obstruction Baseline vital signs 12-lead electrocardiogram (EKG) Monitor for dysrhythmias (can happen anytime, but risk in first 1-2 hours of unrelieved angina or if it develops to an MI). Monitor for respiratory distress (heart failure)

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

MI: Signs and Symptoms Pain Nausea Impending doom Diaphoresis Dyspnea
Dysrhythmias Acute Myocardial Infarction Acute ischemia of one or more coronary arteries caused by a clot or vasospasm. Unless circulation restored within six hours, will lead to infarction (necrosis) of heart muscle beyond the blockage. Diagnosis: Combination of signs and symptoms, 12-lead EKG, and laboratory tests. Signs and Symptoms A typical presentation will include severe (10 of 10) substernal chest pain radiating down the left arm and up into the jaw, nausea, and a profound sense of impending doom. This will last 30 minutes or more and responds only to opiates (morphine). Also may have diaphoresis, dyspnea, dysrhythmias. NOTE: Females may not present with typical symptoms when having an MI. Women may have different heart attack symptoms than men. Women may have symptoms such as: A burning sensation in the upper abdomen Lightheadedness An upset stomach Sudden weakness or unexplained tiredness. NOTE: Elderly may not notice severe chest pain but will complain of other associated symptoms, especially gastric distress

12-lead EKG Normal Ischemia Injury Acute infarct Old infarct
In general: ST depression, T-wave inversion: strongly suspicious for ischemia ST elevation: suspicious for myocardial injury Baseline - normal Ischemia—tall or inverted T wave (infarct), ST segment may be depressed (angina) Injury—elevated ST segment, T wave may invertInfarction (Acute)—abnormal Q wave ST segment may be elevated and T wave may be inverted Infarction (Age Unknown)—abnormal Q wave, ST segment and T wave returned to normal Reference: American Heart Association 2006 Specific areas of injury: LAD (called the “sudden death” coronary artery): obstruction leads to anterior or septal MI (25% of all MIs). Most likely to have heart failure and ventricular dysrhythmias; V2-4 looks at anterior area of heart Circumflex: posterior or lateral wall MI with sinus dysrhythmias; leads I, AVL and V 5 & 6 look at lateral area of heart Right coronary: Inferior wall MI with bradycardia, severe nausea and vomiting; leads II, III, AVF look at inferior area of heart

LABS Myoglobin – non specific Troponin CK-MB BNP = CHF
Laboratory tests Myoglobin: protein that helps transport oxygen, found in cardiac and skeletal muscle. Increases within 1-3 hours, peaks in 12 hours. Not specific in identifying acute cardiac event. Can repeat it in 3 hours if first test negative Troponin: protein in heart; myocardial contractility. Monitor for unstable angina or acute MI. Level increases within few hours, peaks in 24, lasts for 3 weeks CK with isoenzymes CK-MB (heart): increases within few hours, peaks in 24 hours BNP: diagnose or grade severity of heart failure, also assess treatment effectiveness (the higher the level of BNP, the worse the CHF)

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? Collaborative Management: follow Advanced Cardiac Life Support (ACLS) protocol: Immediate assessment (<10 minutes) Measure vital signs (automatic/standard BP cuff) Measure oxygen saturation Obtain 12-lead ECG (physician reviews) Perform brief, targeted history and physical exam; focus on eligibility for fibrinolytic therapy Obtain initial serum cardiac marker levels Evaluate initial electrolyte and coagulation studies Request, review portable chest x-ray (<30 minutes) Immediate general treatment (MONA) Establish IV access Oxygen at 4 L/min Aspirin 160 to 325 mg Nitroglycerin SL or spray Morphine IV (if pain not relieved with nitroglycerin) Beta Blockers A beta blocker is another possible medication to use if heart rate or blood pressure are elevated with continued chest pain, not relieved by above measures. Beta blockers depress the pumping action so you want to see if the person has a HIGH HR and HIGH BP.

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

Reperfusion Strategies
Thrombolytics Percutaneous Transluminal Coronary Angioplasty (PTCA) Stent Procedure Reperfusion strategies to open the impaired coronary arteries will prevent an infarction. Thrombolytics: break up the fibrin network that binds clots together Indications: ST elevation >1 mm in 2 or more contiguous leads or new left bundle branch block (LBBB) or new BBB that obscures ST Time of symptom onset must be <12 hours Caution: fibrinolytics can cause death from brain hemorrhage Agents differ in their mechanism of action, ease of preparation and administration, cost, need for heparin 5 agents currently available: alteplase (tPA, Activase), anistreplase (Eminase), reteplase (Retavase), streptokinase (Streptase), tenecteplase (TNKase) Followed by heparin infusion to prevent formation of new clots Percutaneous transluminal coronary angioplasty (PTCA): balloon inserted in area of blockage, held open for approximately 15 min and pushes plaque, etc to sides of vessel so that the coronary artery becomes more open. Approximately 20% re-occlude in 6 months. Stent-procedure similar to PTCA or cardiac catheterization as stylus inserted in right groin and wire advanced to area of blockage. Stent is placed inside the blockage, opened up, and it forces the vessel to open and stay open. It takes about 3 weeks for epithelial tissue to be laid down on the stent and it becomes permanent part of the vessel, keeping the vessel open. Requires aspirin and sometimes anti-platelet agent Such as clopridogel (Plavix) to prevent clots from forming over the stent until epithelial tissue is laid down. Photo Source: National Heart, Lung and Blood Institute (NHLBI),

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 Post Procedural Care: Monitor V/S frequently Assess distal pulses, groin site for bleeding, swelling, hematoma Bed rest with limb straight for 6 – 8 hours, sometimes a sandbag gives additional pressure over groin area Antiplatelet agents – prevent thrombus formation. Examples: abciximab (ReoPro), eptifibitide (Integrilin), tirofiban (Aggrastat) Monitor IV nitroglycerin – prevent coronary artery spasms ASA once a day permanently Assist planning lifestyle modification

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 Nursing Management Nursing assessment includes physical and extensive client history Pain - symptom management/pain control Assess for new murmurs, rhythm changes Monitor vital signs, potassium and magnesium (if either are low, can precipitate arrhythmia, especially in a cardiac patient). Close observation and monitoring for signs of heart failure Provide emotional support, information, clarify test results Following acute episode, bed rest for 24 hours with gradual increased activity

Rehabilitation Diet Progressive exercise
Change modifiable risk factors Weight loss Stress reduction Lipid-lowering drugs Anti-hypertensives Aspirin Cardiac Rehabilitation Teach diet, progressive exercise, encourage change of modifiable risk factors such as weight loss, stress reduction, lipid-lowering drugs, anti-hypertensive medications, aspirin (start post-op day 2-3, will remain on aspirin)

Coronary Artery Bypass Graft (CABG)
Bypass grafts sewn from aorta to below area of blockage Fluid overload Pacemaker? Bleeding Atrial fibrillation Cardiovascular Surgery (CABG): bypass grafts sewn from aorta to below area of blockage. Site of donor graft usually saphenous vein in leg or left internal mammary artery Collaborative Management fluid overload: patient gains 5-10 pounds of fluid while on heart-lung machine. Diuretics given post-op, so potassium monitored to avoid hypokalemia, since furosemide (Lasix) is usually the diuretic of choice. Also, monitor magnesium level as low levels can cause dysrhythmias Temporary pacemaker wires (epicardial) often placed after surgery to use prn Assess for bleeding (more than 100ml/hr from chest tubes is too much) Approximately 15-20% patients will experience atrial fibrillation post-operatively - manage with IV diltiazem (Cardizem) or amiodarone (Cordarone)

Nursing Management Control pain Early ambulation Incentive spirometer
Change dressings: watch for infection Monitor: VS, lungs, heart, weight, I&O, labs, EKG Nursing management Pain control Encourage early ambulation, incentive spirometer Change dressings on chest and leg (graft site) Monitor vital signs, lung sounds, heart sounds (observe carefully for new heart sound changes) Monitor weight (know pre-op weight), I & O, labs, EKG for changes Assess for stroke, cardiac tamponade, bleeding, cardiac arrhythmias, postcardiotomy syndrome

Complications Stroke Tamponade: pulsus paradoxus Bleeding Dysrhythmias
Post-cardiotomy syndrome Monitor for complications: stroke, cardiac tamponade, bleeding, cardiac arrhythmias, postcardiotomy syndrome Cardiac Tamponade: fluid between the heart and its pericardial layer (pericardial effusion) starts to compress on the heart and prevents the heart from filling normally (less room to fill because it is compressed by this surrounding fluid. Reduced venous return to the heart and this causes decreased cardiac output. Symptoms: narrowing pulse pressure, shortness of breath, fatigue, distant heart sounds, chest pain or fullness, decrease in systolic blood pressure (but may fluctuate), and pulsus paradoxus Echocardiogram may confirm diagnosis. RX: pericardiocentesis. Postcardiotomy syndrome: Pericarditis associated with pericardial surgery that often follows extensive pericardiotomy. NOTE: Pulsus Paradoxus-systolic blood pressure that can be heard only on exhalation, not on inhalation. The difference between the blood pressure measurement that can be heard during exhalation and the point where it can be heard during inhalation is measured. Pulsus Paradoxus greater than 10 mmHg is significant and is abnormal.

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. Normal ECG tracing. P waves are present P wave configuration is constant Each P wave is followed by a QRS complex QRS complexes are of normal width The intervals between QRS complexes are equal The heart rate is between 60 and 100 beats per minute Sinus bradycardia is present if the heart rate is lower than 60 beats per minute Sinus tachycardia is present if the heart rate is higher than 100 beats per minute NOTE: low rates may be normal for some patients, especially since so many are on beta blockers

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. P waves are present and appear in regular rhythm. There is a progressive lengthening of the PR interval until a blocked P wave occurs. QRS complexes do not appear in a regular rhythm. Treatment none; usually does not progress to more lethal blocks.

A-V block: 2nd Degree Mobitz I
P waves are present and appear in a regular rhythm. There is a progressive lengthening of the PR interval until a blocked P wave occurs. QRS complexes do not appear in a regular rhythm. Treatment none; usually does not progress to more lethal blocks.

AV Block: 2nd Degree Mobitz II
P waves are present and appear in a regular rhythm P waves precede each QRS complex in a regular interval, until one or several QRS complexes are blocked QRS complexes do not appear in a regular rhythm The interval between two QRS complexes is a multiple of a P-P interval Treatment: likely to progress to third degree block – prepare pacemaker

A-V Block: 3rd Degree P waves, if present, appear in a regular rhythm
QRS complexes appear in an independent regular rhythm different from the rhythm of the P waves (atrioventricular dissociation) the rate of the QRS complexes is below 60 beats per minute Treatment: requires pacemaker if symptomatic, may need permanent pacing

Supraventricular Tachycardia
Rhythm originates from the SA node Atrial and ventricular rhythms are regular Rate: above 100 bpm, enough to cause symptoms (dizziness, syncope, hypotension) Treatment: vagal/valsalva maneuvers to attempt to slow heart down (bear down, cough, hold breath, etc); adenosine (Adenocard), diltiazem (Cardizem); carotid sinus massage (MD only); cardioversion if symptomatic

Atrial Fibrillation There are no P waves present.
Instead of P waves, fibrillarory "F" waves with a rate higher than 350 per minute are present. The interval between QRS complexes is variable and there is no apparent rule in the rhythm of the QRS complexes (absolute arrhythmia.) Depending on the frequency of the QRS complexes may need treatment for tachycardia-induced decreased cardiac output. Cardioversion, Coumadin to prevent thrombi leading to stroke

Premature Ventricular Contractions (PVCs)
Premature ventricular contractions result from irritable areas in the ventricles. Multifocal PVCs indicate more than one area is irritable. Wide, bizarre QRS complexes followed by a pause No P wave precedes a PVC Treatment: depending on frequency, may decrease cardiac output & cause symptoms such as dizziness, weakness. If symptomatic give amiodarone (Cordarone) to decrease irritability NOTE: If PVCs occur as “escape beats” in a bradycardia, no suppression is needed

Ventricular Tachycardia
Rhythm originates from the ventricle No visible atrial rhythm; ventricular rhythm regular – abnormal, wider than 0.12 seconds Rate: above 100 bpm usually less than 200 bpm NOTE: Can cause cardiac arrest if going so fast that blood can’t fill cardiac chambers Treatment (with pulse): amiodarone, synchronized cardioversion Treatment (no pulse): CPR, defibrillation, epinephrine; consider amiodarone, lidocaine, magnesium

Ventricular Fibrillation
Rhythm: None: ventricles quivering (fibrillating) and no blood is being ejected or even entering the atria. Cardiac Arrest. Treatment: CPR, defibrillate immediately, up to three times consecutively at 200, 300, and 360 joules (new guidelines 2006: defibrillate 360J monophasic, J biphasic – no change for multiple shocks); epinephrine, amniodarone, lidocaine as prescribed or per ACLS/emergency protocol guidelines.

Defibrillation Options
Paddles AED ICD Defibrillation options: Paddle electrodes with gel pads or conduction gel. Automatic external defibrillators (AED)-can be used by lay people. Found in health clubs, airports, government buildings, etc. Implantable cardioverter defibrillator (ICD). Placed surgically. It is pre-set to identify a fast rhythm and will defibrillate the patient at a low voltage (since electrodes are on the heart itself). Even if patient has a known ICD, treat as if patient doesn’t have an ICD and defibrillate and do CPR. Shock potential for CPR providers, but small shock. Some sources say shock is minimized by wearing gloves. Photo Source: Wikimedia Commons (Creative Commons),

CPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below:
Asystole/PEA CPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypoglycemia, Hypothermia Toxins, Tamponade (cardiac); Tension pneumothorax; Thrombosis (coronary or pulmonary); Trauma Rhythm: None. Cardiac arrest with no rhythm Management: CPR, epinephrine, vasopressin, atropine; consider 6 H’s, 5 T’s below: Hypovolemia Hypoxia Hydrogen ion (acidosis) Hypo-/hyperkalemia Hypoglycemia Hypothermia Toxins Tamponade, cardiac Tension pneumothoax Thrombosis (coronary or pulmonary) Trauma

Cardiac Pacemaker Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the patient’s intrinsic pacemaker fails to provide a perfusing rhythm. Cardiac Pacemaker: Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the client’s intrinsic pacemaker fails to provide a perfusing rhythm. Settings: Synchronous or demand-pacemaker will fire only if needed. Set at a certain rate, can see patient’s own rate, then if a pause, pacemaker will fire Asynchronous or fixed rate-used for clients who do not have ability for heart to beat steadily on its own, so the heart requires every beat to be started by pacemaker. Overdrive pacing-if patient has problem with tachyarrhythmia, pacemaker can sense it, speed up and go faster than the tachyarrythmia, take over the rhythm, and then slow down the rate (takes control of the heart rate and brings it back down to normal)

Pacemakers Types of Pacemakers Temporary
Transvenous invasive temporary pacing Epicardial invasive temporary Permanent Types of Pacemakers Transcutaneous cardiac pacemakers generate electrical stimuli that pace the heart through external electrodes that adhere to the chest wall Temporary transvenous: placed as wires, sometimes after cardiac surgery (epicardial). Wires pulled out, pacer disconnected when no longer needed (few days) Permanent: placed surgically. After placed, patient needs to keep left arm in a sling or at least close to the body for approximately 3 days so the wires that are inserted will have time to create scar tissue and become stable on the heart. If patient has recurrent hiccups after pacer surgery, this is a sign that the electrodes may have been displaced and patient will have to go back to surgery to put them back on the correct area so can fire properly.

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 Pacemaker: Patient Education Programmed rate (client should know rate-medical alert bracelet) Signs of battery failure and 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. Wear pacemaker identification and medic alert Take pulse rate daily, maintain diary of pulse rate Instruct patient that if any unusual feelings occur when near any electrical devices, to move t to 10 feet away and check pulse

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. Wear loose-fitting clothing Avoid contact sports Inform all health care providers that a pacemaker has been inserted Inform patient that most electrical appliances can be used without any interference with the functioning of the pacemaker

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 Inability of the heart to maintain adequate circulation to meet the metabolic needs of the body, because of impaired pumping actions. (weak, enlarged pump). Cardiac output diminished and peripheral tissue not adequately perfused. Most CHF includes at least to some degree both right and left heart failure. 75% caused by hypertension

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. Left-Sided Heart Failure: Decreased cardiac output: General fatigue and weakness, Daytime oliguria, Confusion, restlessness, dizziness Tachycardia Weak peripheral pulses, cool extremities Pulmonary congestion: Dyspnea, tachypnea, crackles bibasilar, cough, worse at night, 2 or more pillow orthopnea, S3 or S4 gallop Right-Sided Heart Failure: Systemic congestion: Jugular distention, Enlarged liver and spleen, anorexia, nausea, dependent edema polyuria at night, weight gain

CHF: Collaborative Mgmt
Vasodilators: Nitrates Positive inotropes: increase contraction Digoxin (Lanoxin) Beta blockers (though some  contractility & are contraindicated) ACE inhibitors Diuretics Collaborative Management Vasodilators Nitrates such as isosorbide (Imdur) Positive inotropes to increase contractility Digoxin (Lanoxin) Beta blockers such as carvedilol (Coreg) or metoprolol (Lopressor) Angiotensin converting enzyme (ACE) inhibitors to decrease hypertension captopril (Capoten), benazepril (Lotensin), enalapril (Vasotec), lisinopril (Prinivil, Zestril) Diuretics Furosemide (Lasix) Torsemide (Demadex) Bumetanide (Bumex) Hydrocholorthiazide (HydroDiuril) Metolazone (Zaroxolyn) Spironolactone (Aldactone) is potassium sparing

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. Nursing Management Elevate head Supplemental oxygen Arrange activities to decrease oxygen demand If exacerbation: identify precipitating factors TEACH: low salt diet, medications and their rationale, weigh every day, encourage exercise but pace activities. Wait 90 min after meals before exercise to minimize stress on heart. Avoid extremes in weather when exercising Teach foods high in sodium (to avoid) and potassium (to include due to diuretics that lose potassium from kidney)

Cardiac Valve Disorders
Mitral stenosis Mitral prolapse Aortic stenosis Aortic regurgitation Mitral stenosis: usually results from rheumatic fever infection, leads to CHF from blood backing up into lungs from left atrium; later cardiac output falls. Mitral valve prolapse; part of mitral valve leaflet falls backward into atrium during systole causing blood to reguritate from left ventricle into left atrium (also Mitral Regurgitation); also caused by rheumatic fever; leads to increased left heart volume and hypertrophy, CHF and decreased cardiac output. Aortic stenosis: narrowing of opening between left ventricle and aorta; progressive with age. Obstruction increases pressure on the let ventricle causing hypertrophy of left ventricle, decreased cardiac output - dyspnea, angina, syncope on exertion. Aortic regurgitation: blood flows back into left ventricle from aorta during diastole (can be caused by inflammatory lesions on leaflets of aortic valve); left ventricle dilates, eventually failing – exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND) Photo Source: National Heart, Lung and Blood Institute (NHLBI),

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

Photo Source: Lippincott, Williams, & Wilkins Connection Image Bank,

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

CHF Management (continued)
Treat heart failure if present Atrial fibrillation? Antibiotic prophylaxis Weigh daily Collaborative Management Treat for heart failure as above If atrial fibrillation develops, must be treated to restore atrial contractions If unsuccessful, amiodarone (Cordarone) or flecanide (Tambocor) given to slow ventricular rate response if atrial fibrillation continues anticoagulation with warfarin (Coumadin) needed to prevent clot formation Nursing Management Teach: Antibiotic prophylaxis for dental work, colonoscopy, etc. These procedures can cause bacteria to be released into blood stream and may reach abnormal heart valve & start growing “vegetation” on this valve causing damage. Teach to weigh every day and report increase in weight 2 lbs overnight, or 5 lbs in a week

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 Pericarditis: inflammation of pericardial sac. Can be caused by malignant neoplasms, infection after cardiac surgery, or after myocardial infarction (Dressler’s syndrome)

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

Pericarditis Collaborative Management NSAIDs or corticosteroids
Pericardiocentesis or surgical pericardial window Collaborative Management Nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids to decrease inflammation of pericardial sac, treat pain Monitor for cardiac tamponade: distant heart sounds, jugular distension, paradoxical pulse, signs of decreased cardiac output fluid between heart and pericardial sac causes heart to be compressed inside the sac=decreased blood pressure and shock treated with emergency pericardiocentesis recurrence of tamponade requires surgical pericardectomy

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 Nursing Management Position for comfort: usually upright, leaning slightly forward 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 or anticoagulants – may increase risk of tamponade

Infective Endocarditis
Valves infected, spreads to endothelium Leaflets deform, leak High risk: elderly, prosthetic valves, IV drug abusers, immunosuppressed Infective Endocarditis: Valves and endothelial surface of the heart become infected. More common in elderly, possibly due to less effective immune system, those with prosthetic heart valves, and also IV drug abusers. Cardiac valve disorders are usually predisposed to endocarditis, but hospitalized patients with IV catheters or immuno-suppressed patients are at risk as well. Organism infects endocardium, can cause deformity of the leaflets of the valve it affects.

Manifestations Slow onset Major complication: embolus
Flu-like symptoms, anorexia, weight loss, joint & back pain, fever, splinter hemorrhages undernails, petechiae, murmur, headache? Major complication: embolus Diagnosis: blood culture, echocardiogram Clinical Manifestations Slow onset. Symptoms are from the toxic effect of the infection, the valvular changes from the organism, and occasionally the vegetation of the organism becomes an embolus and causes a problem (possible stroke). Flu-like symptoms, anorexia, weight loss, joint and back pain are common. Fever may be absent or intermittent. Splinter hemorrhages (red-brown streaks under nails), petechiae in mucus membranes or conjunctiva. Heart murmur or change in heart murmur as condition progresses. Patient may have headache. Major Complication: arterial embolus caused by fragments breaking loose and travel to distant organs. Diagnosis: positive blood culture, echocardiogram, especially transesophageal (TEE)

Management IV antimicrobials based on cultures Teach prevention
Monitor: sepsis, new murmur, stroke, meningitis, CHF Collaborative Management: Intravenous antimicrobials, based on culture results, for 4-6 weeks Anticoagulants not beneficial Nursing Management Teach prevention: antibiotic prophylaxis prior to dental procedures, surgery, or vaginal delivery (any risk of organism entering blood stream can cause this condition) Monitor for sepsis, heart sounds, monitor for new murmur or change in murmur (significant for worsening of valvular damage). Monitor for stroke, meningitis, congestive heart failure. Monitor IV sites, especially central line sites carefully for infection.

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. Systolic blood pressure ≥ 135 mmHg and/or diastolic blood pressure ≥ 85 mmHg. Normal in adults = less than 120 mmHg systolic and less than 80 mmHg diastolic. The higher the blood pressure, increasing coronary, cerebral, renal and peripheral vascular disease % unknown cause-idiopathic

Hypertension Clinical manifestations Risk factors
Usually asymptomatic “silent killer” Some report headache, especially early morning Risk factors Family history Age Diabetes Obesity Heavy alcohol High sodium intake Clinical manifestations Usually asymptomatic “silent killer” Some report headache, especially early morning. Obtain BP on both arms, after sitting 5 minutes, at least 30 minutes after smoking or drinking caffeine to get most accurate reading. Family history, weight, dietary patterns, salt intake. Identify medication therapy, make sure patient takes medications as prescribed. Assess cardiac, neuro, renal, diagnostic and lab studies. The risk factors of hypertension include family history, age, diabetes, obesity, heavy ETOH consumption, and high dietary sodium intake and low dietary intake of potassium, Ca++, and magnesium.

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.

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 Collaborative management Medications: diuretics, beta blockers, ace inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockers Trend is to combine some of the above medications in low dosages as they have additional benefits other than treating hypertension Monitor and routine follow-up with EKG, lipid lowering agents if needed JNC VI and JNC VII (the Sixth and Seventh Report of the Joint National Committee) are the guidelines for prevention, detection, evaluation, and treatment of High Blood Pressure (see Web Resources at end of this outline). Recommendations (see chart below). Two or more medications usually needed: thiazide diuretic + Calcium channel blocker (CCB): amlodipine (Norvasc), diltiazem (Cardizem ACE inhibitor: captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil) Angiotensin receptor blockers (ARBs): candesartan (Atacand), losartan (Cozaar) Aldosterone receptor blockers: eplerenone (Inspra) Once a day dosage best When new medication is added, continue previous anti-hypertensives

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. Nursing Management The goal of hypertension management is to control the disease and reduce morbidity and mortality by the least intrusive means possible. Nurses play an important role in educating patients with hypertension. Lifestyle Modifications Adoption of healthy lifestyles by all persons is critical for the prevention of high BP and is an indispensable part of the management of those with hypertension. Major lifestyle modifications shown to lower BP include: Weight reduction in those individuals who are overweight or obese - adoption of the Dietary Approaches to Stop Hypertension (DASH) eating plan which is rich in potassium and calcium, dietary sodium reduction Physical activity Moderation of alcohol consumption. Lifestyle modifications reduce BP, enhance antihypertensive drug efficacy, and decrease cardiovascular risk. For example, a 1,600 mg sodium DASH eating plan has effects similar to single drug therapy. Combinations of two (or more) lifestyle modifications can achieve even better results. Monitor for target-organ problems. Teach potential problems if hypertension untreated. Promote screening for early detection. Encourage patients to take blood pressures at home, record on calendar, report to MD. Follow-up is usually every 6-12 months if blood pressure is stable. Teach potential side effects of medications, give rationales for hypertensive medications to increase compliance and patient understanding

Classification Category Systolic Diastolic Normal <120 mmHg
Pre-HTN or 80-89 Stage 1 or 90-99 Stage 2 ≥ 160 or ≥ 100 Collaborative Management: Medications

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

Hypertensive Crisis: Mgmt
Lower BP slowly IV nitrates (nitroglycerin) Nitroprusside (Nipride) Enalapril (Vasotec) Beta blockers Diuretics Monitor rhythm, vital signs Treatment: lower blood pressure, usually slowly (or could cause a stroke). Needs to be monitored carefully, cardiac rhythm and frequent vitals. RX: IV nitrates, nitroprusside (Nipride), intravenous enalapril (Vasotec), beta blockers, diuretics

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

Peripheral Arterial Disease
Stage I: Asymptomatic Stage II: Claudication Stage III: Rest pain Stage IV: Necrosis Peripheral Arterial Disease A chronic deprivation of oxygen and nutrients to the lower extremities, usually caused by atherosclerosis. Sometimes called lower extremity arterial disease (LEAD). Clinical Manifestations Stage I: Asymptomatic Bruit or aneurysm may be present Pedal pulses decreased or absent Stage II: Claudication Pain or burning in calves when walking Pain relieved with rest Stage III: Rest Pain Leg pain while resting, awakens patient at night Numbness, burning in the distal extremities (toes, arch, heel) Pain relieved by lowering extremities to dependent position Stage IV: Necrosis Ulcers, blackened tissue on toes, plantar area and heel Gangrenous odor may be present

PVD: Management Medications Control hypertension Angioplasty, bypasses
Exercises Position Vasodilation Avoid vasoconstriction Collaborative Management Medications: Pentoxifylline (Trental) increases blood cell flexibility Aspirin and clopidogrel (Plavix) prevent platelet clumping Control hypertension to maintain perfusion without vasoconstriction Angioplasty: artery dilated with a balloon catheter, stent placed to maintain patency. Nursing recovery same as in PTCA (see Coronary Syndromes outline). Arterial revascularization: bypasses to improve arterial flow Nursing Management Teach exercises to build collateral circulation Position: avoid raising legs above heart level Promote vasodilation: warm environment, socks, insulated shoes. NOTE: Never apply direct heat as sensitivity is decreased; drink enough fluids to maintain blood flow Avoid vasoconstriction: avoid cold, emotional stress, caffeine, nicotine Avoid crossing legs Teach to observe skin of lower extremities to identify skin problems early

Arterial Bypass Monitor for graft occlusion Promote graft patency
Monitor for compartment syndrome Postoperative bypass nursing care: Monitor for graft occlusion: Color, Sensation and Warmth (CSM) checks every 15 minute at first. Use Doppler to assess pulses where marked in surgery. Ischemic pain (like that before surgery) may indicate occlusion; throbbing pain is expected due to increased blood flow Promote graft patency: keep normotensive, limit range of motion of affected limb, avoid bending hip and knee , bedrest for 24 hours Monitor for compartment syndrome: when tissue pressure increases, blood flow decreases evidenced by worsening pain, sense of fullness, swelling, tenseness of tissues – report immediately

Peripheral Venous Insufficiency
Stasis dermatitis lower legs Edema Ulcers over malleoli Anterior leg ulcers if arterial flow impaired Venous Insufficiency Prolonged venous hypertension stretches veins, damages valves. Blood backs up creating edema. Stasis results leading to stasis ulcers, swelling, cellulitis Clinical Manifestations Stasis dermatitis along ankles, extending up calves Edema Stasis ulcers over malleoli

Peripheral Vascular Disease
Compression stockings Sequential compression pump Manage ulcers Elevate legs Avoid prolonged sitting or standing No compression of legs Collaborative Management Compression stockings for edema Sequential compression pump Manage ulcers Nursing Management Elevate legs at least 20 minutes 4-5 times per day Avoid prolonged sitting or standing Do not cross legs, ankles are okay for short periods No tight pants or underwear

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) Damaged media layer of 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 can occur causing great loss of blood, shock, death)

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

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 Clinical Manifestations Palpate enlarged aorta over abdomen, possible bruit auscultated If rupture, sudden pain in back or abdomen with shock symptoms (tachycardia, hypotension, anxiety, feeling of impending doom, etc); hemorrhage, shock, death unless emergent surgical intervention If tearing, pain can occur in abdominal area or back; can be slowly progressive over hours, weeks, months Abdominal Aortic Aneurysm Pulsating mass at abdomen, or above umbilicus Systolic bruit over aorta Tenderness on deep palpation Abdominal or lower back pain

Manage Abdominal Aneurysm
Non-surgical: Modify risk factors Monitor BP Regular exams for size, pulsation Report: chest/back pain, SOB, Difficulty swallowing, hoarseness Abdominal Aortic Aneurysm: Non-surgical Modify risk factors Monitor BP Regular visits to MD Report occurrence of chest/back pain, shortness of breath, difficulty swallowing, hoarseness.

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

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 Thoracic Aortic Aneurysms: 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 Nursing Management Teach importance of hypertensive medications Nursing assessment directed to anticipating a rupture Monitor for dissection or rupture Collaborative Management Follow-up by CT scan, ultrasound, MRI at intervals depending on severity Most require surgery to repair

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

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