Presentation on theme: "NCLEX RN Preparation Program"— Presentation transcript:
1 NCLEX RN Preparation Program Cardiovascular DisordersModule 5, Part 2 of 3
2 Cardiovascular System IntroductionThe heart and the circulatorysystem comprise oneof the most essentialparts of the body.Failure to functionresults in death ofthe organism.Photo Source: National Heart, Lung and Blood Institute (NHLBI)
3 Gross Structure of the Heart Layers:PericardiumFibrousSerous PericardiumEpicardiumMyocardiumEndocardiumThe heart is composed of 3 layers:Pericardium- fibrous outer layerMyocardium – middle layer of muscle fibers, creates the pumping actionEndocardium - lines the inside of the heart
4 Chambers of the HeartHeart, a muscular organ divided by a septum into two halves. Right or venous chamber and left or arterial chamber.Right ChambersRight AtriumRight VentricleLeft ChambersLeft AtriumLeft VentricleChambers of the heart:Right Chambers distribute venous blood to the lungs through the pulmonary arteryRight Atrium-receives blood returning from the body via the superior vena cava. Contains the SA node, the pacemaker of the heartRight Ventricle-pumps into the lungs through the pulmonic valveLeft Chambers distribute oxygenated blood to the bodyLeft Atrium-receives oxygenated blood through lungsLeft Ventricle-pumps blood throughout body through aortic valve
5 Coronary Blood Supply Right Coronary Artery Left Coronary Artery Left anterior descendingCircumflexCoronary 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 circumflexLAD: most of left ventricle and septumCircumflex: 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%) nodesPhoto Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program
6 Valves of the HeartValves are strong membranous openings that provide one-way flow of blood.Atrioventricular valves – prevent backflow of blood from ventricles to atria during systole.TricuspidMitralSemilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole.PulmonicAorticValves: 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 ventricleMitral-has 2 cusps or leaflets. Between left atrium and left ventricleSemilunar valves – prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole.Pulmonic-between right ventricle and pulmonary arteryAortic-between left ventricle and aorta
7 Valves of the HeartPhoto Source: U.S. National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program
8 Conduction systemSpecialized tissue that allows rapid transmission of electrical impulses through the myocardiumSinoatrial 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.
9 Conduction systemPhoto Source: St. Francis Hospitals & Health Centers,
10 Gross Structure of Vasculature Arteries: transport blood under high pressure to body tissuesPrecapillary sphinctersArteriovenous shuntsCapillaries – exchanging fluid and nutrients between blood and interstitial space.Veins: acts as conduits for transport of the blood from tissues back to heart
11 Physiology of the Heart Contraction – shortening or increase in muscle tension. Utilizes chemical energy to do the work of contractionCardiac 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 contractionFrank 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 Autonomic Nervous System Control Cardiac MuscleSympathetic (Adrenergic)Parasympathetic (Cholinergic)Systemic blood VesselsSympathetic – vasoconstrictionParasympathetic – vasodilationCardiac 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 VesselsSympathetic response causes vasoconstrictionParasympathetic response causes vasodilation
13 Baroreceptor Reflex (Pressoreceptors) Located in the walls of large systemic arteriesRise in pressure results in baroreceptors transmitting signals to CNS (Central Nervous System) to inhibit sympathetic actionOther 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.
14 Other Chemical Controls of Blood Pressure KidneyAdrenal cortex - aldosteroneRenin-angiotensin systemAntidiuretic hormone (vasopressin)Other Chemical Controls of Blood PressureKidney 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 potassiumAntidiuretic 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.
15 System Assessment Evaluate Patient’s History PainDyspneaCyanosisFatiguePalpitationsSyncopeHemoptysisEdemaCondition of ExtremitiesEvaluate 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:
16 Evaluate veins and arterial pulses through inspection/palpation Neck veinsArm and hand veinsLeg and foot veinsArteriesCentralPeripheral pulses
18 Auscultate heart sounds Heart sounds – frequency, pitch, intensity, durationMurmursSystolicDiastolicPericardial friction rubsHeart sounds (S-1, S-2): frequency, pitch, intensity, duration. Also, if murmurs radiate or are louder on certain positionsGallops (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 complianceMurmurs: 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-1Pericardial friction rubs-seen in pericarditis. Harsh, grating sound throughout systole and diastole.
19 Other parameters to assess Arterial pressureCarotid blood vessels for bruitPalpate and percuss thoraxEvaluate chest x-raysAssess lung soundsOther Parameters to assessArterial pressureCarotid blood vessels for bruit (partial blockage possible if bruit ausculated)Palpate and percuss thorax, heart for palpable thrillEvaluate chest x-rays-observe for enlarged heart, fluid in lungsAssess lung sounds-crackles. In CHF, bibasilar crackles more frequent as the extra fluid goes to the lung bases due to gravityAssess Risk factors for cardiac diseases or disorders:Smoking, high-fat diet, exercise (or lack of), hypertension, stress, diabetes, obesity, family history/genetics.
20 Diagnostic Tests & Procedures Laboratory StudiesCardiac EnzymesCK-MBLDHTroponinMyoglobinBNPCBCBlood coagulation factorsSerum lipidsElectrolytesK, NaCalciumPhosphorusMagnesiumBUNBlood glucoseDiagnostic Tests & ProceduresLaboratory StudiesCK-MB isoenzyme: specific cardiac enzyme, peaks 24 hours after myocardial inury or myocardial infarction (MI)Troponin: any elevation indicates myocardial injury or infarctionMyoglobin: rule out MI 2-7 hours after onsetBrain 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 CHFHomocysteine: elevations indicate risk for cardiovascular diseasePlatelet elevation: may increase risk of thrombus formationHemoglobin: hemoglobin carries oxygen to cells. If moderately or severely anemic, may precipitate a myocardial infarction in some patientsCoagulation factors: patient may be on aspirin; TPA may be neededLipids - assessfor cardiac risk factorsK, Magnesium - evaluate for potential arrhythmias (if levels are low). vital to cellular depolarization and repolarization2Calcium- needed for cellular depolarization and repolarizationBlood glucose- rule out diabetes, a risk factor for cardiac disease
21 Diagnostic Procedures ElectrocardiogramCentral Venous MonitoringCardiac CatheterizationEchocardiographyAngiographyChest x-raysDiagnostic ProceduresElectrocardiogram (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 murmursTransesophageal Echocardiography (TEE): performs role of echocardiogram through esophagus looking at back of heart not usually accessible (left atrium, mitral valve, aortic arch)
22 Acute Coronary Syndromes Coronary Artery Disease (CAD)Narrowing or obstructionof one or more coronaryarteries as a result ofatherosclerosis, anaccumulation oflipid-containing plaquein the arteries.Photo Source: National Heart, Lung and Blood Institute (NHLBI),
23 PathophysiologyAtherosclerosis - fat deposited in intima of arterial wallInflammatory response beginsMacrophages inflitrate area to ingest lipids, then dieSmooth 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 Myocardial Ischemia / Angina Pectoris Decreased oxygen to heartExercise-induced chest painUnstable anginaOther risk factorsEpisodes of chest pain or pressure from coronary blood flow not adequateDecreased 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 restUnstable angina-chest pain occurs without a certain pattern, or without exertionExposure to cold, eating a heavy meal, stress can increase myocardial workload=angina
25 Coronary Artery Disease Myocardial ischemia CLINICAL MANIFESTATIONS:May be asymptomatic unless ischemia occursChest pains or pressure, may radiate to jaw, back, shoulderPalpitations, weaknessDyspneaSyncopeNauseaExcessive fatigueEKG 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, shoulderPalpitations, weaknessDyspneaSyncopeNauseaExcessive fatigueEKG changes (T wave inversion if ischemia)
26 Coronary Ischemia/Angina Silent angina - nosymptoms, butEKG changes.Often occurs indiabeticpatients with CAD.Coronary Ischemia/AnginaSilent 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.
27 Teaching for Angina Rest at onset of chest pain Take one nitroglycerin, repeat 2 more prnNo relief by 3rd, call 911Previous angina with particular activity, take nitroglycerin prior to activityPatient Teaching CAD/anginaStop 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.
28 Unstable Angina Oxygen: 2-4L nasal cannula Nitroglycerin Morphine AspirinBaseline vital signs12 lead EKGMonitor for dysrhythmias, heart failureNursing Management of Patient with Unstable AnginaGoal:1) Eliminate the chest pain (decrease the myocardial oxygen demand and increasethe oxygen supply to the myocardium)2) Reduce the cardiac workload3) Stabilize the rhythm.The acronym given in Advanced Cardiac Life Support (ACLS) is MONA, although the order is actually ONMAO = Oxygen 2-4 liters per nasal cannulaN = Nitroglycerin (if not already tried outside hospital); relieves pain (spray every 5minutes x 3)M = Morphine relieves pain, decreases anxiety, increases venous poolingA = Aspirin prevents platelet aggregation at the site of obstructionBaseline vital signs12-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)
29 Myocardial Infarction Photo Source: National Heart, Lung and Blood Institute (NHLBI),
30 MI: Signs and Symptoms Pain Nausea Impending doom Diaphoresis Dyspnea DysrhythmiasAcute Myocardial InfarctionAcute 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 SymptomsA 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 abdomenLightheadednessAn upset stomachSudden weakness or unexplained tiredness.NOTE: Elderly may not notice severe chest pain but will complain of other associated symptoms, especially gastric distress
31 12-lead EKG Normal Ischemia Injury Acute infarct Old infarct In general:ST depression, T-wave inversion: strongly suspicious for ischemiaST elevation: suspicious for myocardial injuryBaseline - normalIschemia—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 invertedInfarction (Age Unknown)—abnormal Q wave, ST segment and T wave returned to normalReference: American Heart Association 2006Specific 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 heartCircumflex: posterior or lateral wall MI with sinus dysrhythmias; leads I, AVL and V 5 & 6 look at lateral area of heartRight coronary: Inferior wall MI with bradycardia, severe nausea and vomiting; leads II, III, AVF look at inferior area of heart
32 LABS Myoglobin – non specific Troponin CK-MB BNP = CHF Laboratory testsMyoglobin: 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 negativeTroponin: protein in heart; myocardial contractility. Monitor for unstable angina or acute MI. Level increases within few hours, peaks in 24, lasts for 3 weeksCK with isoenzymes CK-MB (heart): increases within few hours, peaks in 24 hoursBNP: diagnose or grade severity of heart failure, also assess treatment effectiveness (the higher the level of BNP, the worse the CHF)
33 Collaborative Management Immediate assessmentVital signs with oxygen saturation12-lead EKGCardiac enzymesChest x-rayElectrolytes – 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 saturationObtain 12-lead ECG (physician reviews)Perform brief, targeted history and physical exam; focus on eligibility for fibrinolytic therapyObtain initial serum cardiac marker levelsEvaluate initial electrolyte and coagulation studiesRequest, review portable chest x-ray (<30 minutes)Immediate general treatment (MONA)Establish IV accessOxygen at 4 L/minAspirin 160 to 325 mgNitroglycerin SL or sprayMorphine IV (if pain not relieved with nitroglycerin)Beta BlockersA 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.
34 MONAAcronym from Advanced Cardiac Life Support (ACLS) though order is ONMA.O = Oxygen 2-4 liters per nasal cannulaN = Nitroglycerin (if not already tried outside hospital); relieves painM= Morphine relieves pain, decreases anxiety, increases venous pooling (to reduce cardiac workload)A = Aspirin prevents platelet aggregation at the site of obstruction
35 Reperfusion Strategies ThrombolyticsPercutaneous Transluminal Coronary Angioplasty (PTCA)Stent ProcedureReperfusion strategies to open the impaired coronary arteries will prevent an infarction.Thrombolytics: break up the fibrin network that binds clots togetherIndications: ST elevation >1 mm in 2 or more contiguous leads or new left bundle branch block (LBBB) or new BBB that obscures STTime of symptom onset must be <12 hoursCaution: fibrinolytics can cause death from brain hemorrhageAgents differ in their mechanism of action, ease of preparation and administration, cost, need for heparin5 agents currently available: alteplase (tPA, Activase), anistreplase (Eminase), reteplase (Retavase), streptokinase (Streptase), tenecteplase (TNKase)Followed by heparin infusion to prevent formation of new clotsPercutaneous 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 agentSuch 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),
36 Post-PCTA Care Monitor V/S Assess distal pulses Bed rest with limb straight for 6 – 8 hoursAnticoagulants/antiplatelet agents – prevent thrombus formationMonitor IV nitroglycerin – prevent coronary artery spasmsASA once a day permanentlyAssist planning lifestyle modificationPost Procedural Care:Monitor V/S frequentlyAssess distal pulses, groin site for bleeding, swelling, hematomaBed rest with limb straight for 6 – 8 hours, sometimes a sandbag gives additionalpressure over groin areaAntiplatelet agents – prevent thrombus formation. Examples: abciximab (ReoPro), eptifibitide (Integrilin), tirofiban (Aggrastat)Monitor IV nitroglycerin – prevent coronary artery spasmsASA once a day permanentlyAssist planning lifestyle modification
37 Acute Myocardial Infarction Bed rest for 24 to 36 hrsPain controlMonitor rhythmAssess for new murmursMonitor potassium, magnesiumMonitor for heart failureGradual increase of activitiesNursing ManagementNursing assessment includes physical and extensive client historyPain - symptom management/pain controlAssess for new murmurs, rhythm changesMonitor 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 failureProvide emotional support, information, clarify test resultsFollowing acute episode, bed rest for 24 hours with gradual increased activity
38 Rehabilitation Diet Progressive exercise Change modifiable risk factorsWeight lossStress reductionLipid-lowering drugsAnti-hypertensivesAspirinCardiac RehabilitationTeach 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)
39 Coronary Artery Bypass Graft (CABG) Bypass grafts sewn from aorta to below area of blockageFluid overloadPacemaker?BleedingAtrial fibrillationCardiovascular 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 arteryCollaborative Managementfluid 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 dysrhythmiasTemporary pacemaker wires (epicardial) often placed after surgery to use prnAssess 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)
40 Nursing Management Control pain Early ambulation Incentive spirometer Change dressings: watch for infectionMonitor: VS, lungs, heart, weight, I&O, labs, EKGNursing managementPain controlEncourage early ambulation, incentive spirometerChange 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 changesAssess for stroke, cardiac tamponade, bleeding, cardiac arrhythmias, postcardiotomy syndrome
41 Complications Stroke Tamponade: pulsus paradoxus Bleeding Dysrhythmias Post-cardiotomy syndromeMonitor for complications: stroke, cardiac tamponade, bleeding, cardiac arrhythmias, postcardiotomy syndromeCardiac 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.
42 Cardiac Dysrhythmias Normal Sinus Rhythm/Regular Sinus Rhythm Rhythm originates from the SA nodeAtrial and ventricular rhythms are regularRates are : beats per minute.Normal ECG tracing.P waves are presentP wave configuration is constantEach P wave is followed by a QRS complexQRS complexes are of normal widthThe intervals between QRS complexes are equalThe heart rate is between 60 and 100 beats per minuteSinus bradycardia is present if the heart rate is lower than 60 beats per minuteSinus tachycardia is present if the heart rate is higher than 100 beats per minuteNOTE: low rates may be normal for some patients, especially since so many are on beta blockers
43 Cardiac Dysrhythmias Sinus bradycardia Atrial and ventricular rates below 60 beats per minuteTreatment may be necessary if symptomaticNote: 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.
44 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.
45 AV Block: 2nd Degree Mobitz II P waves are present and appear in a regular rhythmP waves precede each QRS complex in a regular interval, until one or several QRS complexes are blockedQRS complexes do not appear in a regular rhythmThe interval between two QRS complexes is a multiple of a P-P intervalTreatment: likely to progress to third degree block – prepare pacemaker
46 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 minuteTreatment: requires pacemaker if symptomatic, may need permanent pacing
47 Supraventricular Tachycardia Rhythm originates from the SA nodeAtrial and ventricular rhythms are regularRate: 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
48 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
49 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 pauseNo P wave precedes a PVCTreatment: depending on frequency, may decrease cardiac output & cause symptoms such as dizziness, weakness. If symptomatic give amiodarone (Cordarone) to decrease irritabilityNOTE: If PVCs occur as “escape beats” in a bradycardia, no suppression is needed
50 Ventricular Tachycardia Rhythm originates from the ventricleNo visible atrial rhythm; ventricular rhythm regular – abnormal, wider than 0.12 secondsRate: above 100 bpm usually less than 200 bpmNOTE: Can cause cardiac arrest if going so fast that blood can’t fill cardiac chambersTreatment (with pulse): amiodarone, synchronized cardioversionTreatment (no pulse): CPR, defibrillation, epinephrine; consider amiodarone, lidocaine, magnesium
51 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.
52 Defibrillation Options PaddlesAEDICDDefibrillation 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),
53 CPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below: Asystole/PEACPR, epinephrine, vasopressin, atropine Consider 6 H’s, 5 T’s below:Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalemia, Hypoglycemia, HypothermiaToxins, Tamponade (cardiac); Tension pneumothorax; Thrombosis (coronary or pulmonary); TraumaRhythm: None. Cardiac arrest with no rhythmManagement: CPR, epinephrine, vasopressin, atropine; consider 6 H’s, 5 T’s below:HypovolemiaHypoxiaHydrogen ion (acidosis)Hypo-/hyperkalemiaHypoglycemiaHypothermiaToxinsTamponade, cardiacTension pneumothoaxThrombosis (coronary or pulmonary)Trauma
54 Cardiac PacemakerTemporary 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 fireAsynchronous 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)
55 Pacemakers Types of Pacemakers Temporary Transvenous invasive temporary pacingEpicardial invasive temporaryPermanentTypes of PacemakersTranscutaneous cardiac pacemakers generate electrical stimuli that pace the heart through external electrodes that adhere to the chest wallTemporary 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.
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/legsPacemaker identification, medic alertMeasure pulse daily, keep recordPacemaker: Patient EducationProgrammed 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 alertTake pulse rate daily, maintain diary of pulse rateInstruct patient that if any unusual feelings occur when near any electrical devices, to move t to 10 feet away and check pulse
57 Patient Education (continued) Wear loose-fitting clothingAvoid contact sportsInform all health care providers of pacemakerMost 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 clothingAvoid contact sportsInform all health care providers that a pacemaker has been insertedInform patient that most electrical appliances can be used without any interference with the functioning of the pacemaker
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 perfusedCongestion of the lungs and periphery may occur.Classification: Acute and ChronicTypes: Right-sided/left-sided heart failuresInability 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
59 Congestive Heart Failure Clinical manifestationsWeight gain, I & 0, edema, if severe: ascitesCrackles 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 beatBNP lab test - the higher the number, the worse the CHF is. Can monitor severity of CHF, improvement due to treatment regimen, timely diagnosing of CHFJugular vein distension, LOC, pulse oximetry.Left-Sided Heart Failure:Decreased cardiac output: General fatigue and weakness, Daytime oliguria, Confusion, restlessness, dizzinessTachycardiaWeak peripheral pulses, cool extremitiesPulmonary congestion: Dyspnea, tachypnea, crackles bibasilar, cough, worse at night, 2 or more pillow orthopnea, S3 or S4 gallopRight-Sided Heart Failure:Systemic congestion: Jugular distention, Enlarged liver and spleen, anorexia, nausea, dependent edemapolyuria at night, weight gain
60 CHF: Collaborative Mgmt Vasodilators: NitratesPositive inotropes: increase contractionDigoxin (Lanoxin)Beta blockers (though some contractility & are contraindicated)ACE inhibitorsDiureticsCollaborative ManagementVasodilatorsNitrates such as isosorbide (Imdur)Positive inotropes to increase contractilityDigoxin (Lanoxin)Beta blockers such as carvedilol (Coreg) or metoprolol (Lopressor)Angiotensin converting enzyme (ACE) inhibitors to decrease hypertensioncaptopril (Capoten), benazepril (Lotensin), enalapril (Vasotec), lisinopril (Prinivil, Zestril)DiureticsFurosemide (Lasix)Torsemide (Demadex)Bumetanide (Bumex)Hydrocholorthiazide (HydroDiuril)Metolazone (Zaroxolyn)Spironolactone (Aldactone) is potassium sparing
61 CHF: Nursing Management Elevate head of bedGive oxygenDecrease oxygen demandExacerbation? Identify precipitating factorsTeach: 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 ManagementElevate headSupplemental oxygenArrange activities to decrease oxygen demandIf exacerbation: identify precipitating factorsTEACH: 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 exercisingTeach foods high in sodium (to avoid) and potassium (to include due to diuretics that lose potassium from kidney)
62 Cardiac Valve Disorders Mitral stenosisMitral prolapseAortic stenosisAortic regurgitationMitral 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),
63 Cardiac Valve Disorders Clinical Manifestations:Heart murmurLeft ventricular hypertrophy seen on EKG
65 Congestive Heart Failure Collaborative ManagementDigoxin (inotropic)Diuretics (lasix, aldactone)Coreg - beta blocker shown to improve cardiac function in CHF patientAce inhibitor - shown to improve cardiac function in CHF patientOxygen, cardiac rehab
66 CHF Management (continued) Treat heart failure if presentAtrial fibrillation?Antibiotic prophylaxisWeigh dailyCollaborative ManagementTreat for heart failure as aboveIf atrial fibrillation develops, must be treated to restore atrial contractionsIf unsuccessful, amiodarone (Cordarone) or flecanide (Tambocor) given to slow ventricular rate responseif atrial fibrillation continues anticoagulation with warfarin (Coumadin) needed to prevent clot formationNursing ManagementTeach: 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
67 PericarditisInflammation of pericardial sac. Can be caused by viral infection, complicaton after cardiac surgery 10 days to 2 months, or after MIIdiopathic cause, or disorder of connective tissue (lupus), cancer, radiation therapy, etcPericarditis: inflammation of pericardial sac. Can be caused by malignant neoplasms, infection after cardiac surgery, or after myocardial infarction (Dressler’s syndrome)
68 Pericarditis: Manifestations Chest pain on inspiration, worse when patient leans forward, lying down or turningPericardial friction rubSymptoms of right-sided heart failureMild fever, elevated WBC, ESRAtrial fibrillation common12 lead EKG may have elevation in ALL leadsCan worsen to cardiac tamponade
69 Pericarditis Collaborative Management NSAIDs or corticosteroids Pericardiocentesis or surgical pericardial windowCollaborative ManagementNonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids to decrease inflammation of pericardial sac, treat painMonitor for cardiac tamponade: distant heart sounds, jugular distension, paradoxical pulse, signs of decreased cardiac outputfluid between heart and pericardial sac causes heart to be compressed inside the sac=decreased blood pressure and shocktreated with emergency pericardiocentesisrecurrence of tamponade requires surgical pericardectomy
70 Pericarditis: Nursing Mgmt Position for comfortMonitor 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 soundsTeach: gradual increases of activityTeach: avoid aspirin, anticoagulantsNursing ManagementPosition for comfort: usually upright, leaning slightly forwardMonitor 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 soundsTeach gradual increases of activity.Teach: avoid aspirin or anticoagulants – may increase risk of tamponade
71 Infective Endocarditis Valves infected, spreads to endotheliumLeaflets deform, leakHigh risk: elderly, prosthetic valves, IV drug abusers, immunosuppressedInfective 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.
72 Manifestations Slow onset Major complication: embolus Flu-like symptoms, anorexia, weight loss, joint & back pain, fever, splinter hemorrhages undernails, petechiae, murmur, headache?Major complication: embolusDiagnosis: blood culture, echocardiogramClinical ManifestationsSlow 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)
73 Management IV antimicrobials based on cultures Teach prevention Monitor: sepsis, new murmur, stroke, meningitis, CHFCollaborative Management:Intravenous antimicrobials, based on culture results, for 4-6 weeksAnticoagulants not beneficialNursing ManagementTeach 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.
74 Hypertension Pathophysiology 90-95% unknown cause 5-10% secondary causesSome genetic tendency, obesity, stress, excess sodium intakeProlonged 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
75 Hypertension Clinical manifestations Risk factors Usually asymptomatic “silent killer”Some report headache, especially early morningRisk factorsFamily historyAgeDiabetesObesityHeavy alcoholHigh sodium intakeClinical manifestationsUsually 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.
76 Hypertension Goals: reduce BP. Goal: 120/80 Ask for S/S indicative of HTNObtain BP on both armsFamily history, weight, dietary patternsIdentify medication therapyAssess cardiac, neuro, renal, diagnostic and lab studies.
77 Hypertension Collaborative Management Medications: diuretics, beta blockers, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockersMonitor and routine follow-up with EKG, lipid lower agents if neededCollaborative managementMedications: diuretics, beta blockers, ace inhibitors, angiotensin receptor blockers, calcium channel blockers, alpha blockersTrend is to combine some of the above medications in low dosages as they have additional benefits other than treating hypertensionMonitor and routine follow-up with EKG, lipid lowering agents if neededJNC 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 (CardizemACE inhibitor: captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil)Angiotensin receptor blockers (ARBs): candesartan (Atacand), losartan (Cozaar)Aldosterone receptor blockers: eplerenone (Inspra)Once a day dosage bestWhen new medication is added, continue previous anti-hypertensives
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.Nursing ManagementThe 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 ModificationsAdoption of healthy lifestyles by all persons is critical for the prevention ofhigh 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 reductionPhysical activityModeration 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
80 Hypertensive Crisis… Assessment Diastolic pressure > 120 mm Hg.HeadacheDrowsinessConfusionChanges in LOCTachycardia and tachypneaDyspnea/cyanosis/seizureHypertensive Crisis Diastolic pressure > 120 mm Hg.HeadacheDrowsinessConfusionChanges in LOCTachycardia and tachypnea
81 Hypertensive Crisis: Mgmt Lower BP slowlyIV nitrates (nitroglycerin)Nitroprusside (Nipride)Enalapril (Vasotec)Beta blockersDiureticsMonitor rhythm, vital signsTreatment: 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
82 Peripheral Vascular Disease (PVD) PathophysiologyGeneralized atherosclerosis (plaque development) or arteriosclerosis (hardening of the arteries)Narrowing of lumen, obstruction by thrombosisBifurcation or branch areas higher risk of blockage.If have PVD, at risk of having CAD as well
83 Peripheral Arterial Disease Stage I: AsymptomaticStage II: ClaudicationStage III: Rest painStage IV: NecrosisPeripheral Arterial DiseaseA chronic deprivation of oxygen and nutrients to the lower extremities, usually caused by atherosclerosis. Sometimes called lower extremity arterial disease (LEAD).Clinical ManifestationsStage I: AsymptomaticBruit or aneurysm may be presentPedal pulses decreased or absentStage II: ClaudicationPain or burning in calves when walkingPain relieved with restStage III: Rest PainLeg pain while resting, awakens patient at nightNumbness, burning in the distal extremities (toes, arch, heel)Pain relieved by lowering extremities to dependent positionStage IV: NecrosisUlcers, blackened tissue on toes, plantar area and heelGangrenous odor may be present
84 PVD: Management Medications Control hypertension Angioplasty, bypasses ExercisesPositionVasodilationAvoid vasoconstrictionCollaborative ManagementMedications:Pentoxifylline (Trental) increases blood cell flexibilityAspirin and clopidogrel (Plavix) prevent platelet clumpingControl hypertension to maintain perfusion without vasoconstrictionAngioplasty: 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 flowNursing ManagementTeach exercises to build collateral circulationPosition: avoid raising legs above heart levelPromote vasodilation: warm environment, socks, insulated shoes. NOTE: Never apply direct heat as sensitivity is decreased; drink enough fluids to maintain blood flowAvoid vasoconstriction: avoid cold, emotional stress, caffeine, nicotineAvoid crossing legsTeach to observe skin of lower extremities to identify skin problems early
85 Arterial Bypass Monitor for graft occlusion Promote graft patency Monitor for compartment syndromePostoperative 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 flowPromote graft patency: keep normotensive, limit range of motion of affected limb, avoid bending hip and knee , bedrest for 24 hoursMonitor for compartment syndrome: when tissue pressure increases, blood flow decreases evidenced by worsening pain, sense of fullness, swelling, tenseness of tissues – report immediately
86 Peripheral Venous Insufficiency Stasis dermatitis lower legsEdemaUlcers over malleoliAnterior leg ulcers if arterial flow impairedVenous InsufficiencyProlonged venous hypertension stretches veins, damages valves. Blood backs up creating edema. Stasis results leading to stasis ulcers, swelling, cellulitisClinical ManifestationsStasis dermatitis along ankles, extending up calvesEdemaStasis ulcers over malleoli
87 Peripheral Vascular Disease Compression stockingsSequential compression pumpManage ulcersElevate legsAvoid prolonged sitting or standingNo compression of legsCollaborative ManagementCompression stockings for edemaSequential compression pumpManage ulcersNursing ManagementElevate legs at least 20 minutes 4-5 times per dayAvoid prolonged sitting or standingDo not cross legs, ankles are okay for short periodsNo tight pants or underwear
88 Abdominal Aortic Aneurysm Localized dilatation of the wall of the abdominal aorta caused by congenital weakness, trauma, disease, atherosclerosisRisk factors: smoking, hypertensionProgressive weakening and enlarging of areaof vesselIf 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)
89 Aortic AneurysmsGoal of treatment: limit progression of the condition by modifying risk factors, controlling BP, recognizing symptoms early, and preventing ruptureGoal 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),
90 Abdominal Aortic Aneurysm Clinical Manifestations:Can palpate enlarged aorta, possible bruit ausculatedIf rupture, sudden pain in back or abdomenIf tearing, pain in abdominal area or back; can be slowly progressiveIf rupture-hemorrhage, shock, death unless emergent surgical interventionClinical ManifestationsPalpate enlarged aorta over abdomen, possible bruit auscultatedIf rupture, sudden pain in back or abdomen with shock symptoms (tachycardia, hypotension, anxiety, feeling of impending doom, etc); hemorrhage, shock, death unless emergent surgical interventionIf tearing, pain can occur in abdominal area or back; can be slowly progressive over hours, weeks, monthsAbdominal Aortic AneurysmPulsating mass at abdomen, or above umbilicusSystolic bruit over aortaTenderness on deep palpationAbdominal or lower back pain
91 Manage Abdominal Aneurysm Non-surgical:Modify risk factorsMonitor BPRegular exams for size, pulsationReport: chest/back pain, SOB, Difficulty swallowing, hoarsenessAbdominal Aortic Aneurysm:Non-surgicalModify risk factorsMonitor BPRegular visits to MDReport occurrence of chest/back pain, shortness of breath, difficulty swallowing, hoarseness.
92 Thoracic Aortic Aneurysm Pain: neck, shoulders, lower back or abdomenSyncopeDyspneaTachycardiaCyanosisWeaknessThoracic AneurysmPain on neck, shoulders, lower back or abdomenSyncopeDyspneaTachycardiaCyanosisWeakness
93 Manage Thoracic Aneurysm Monitor V/SAssess for pain – abdominal or back pains.Check peripheral pulses, including temperature and colorObserve for signs of ruptureNote tenderness/distention of abdomenThoracic Aortic Aneurysms:Monitor V/SAssess for pain – abdominal or back pains.Check peripheral pulses, including temperature and colorObserve for signs of ruptureNote tenderness/distention of abdomenNursing ManagementTeach importance of hypertensive medicationsNursing assessment directed to anticipating a ruptureMonitor for dissection or ruptureCollaborative ManagementFollow-up by CT scan, ultrasound, MRI at intervals depending on severityMost require surgery to repair
94 Photo Acknowledgement: All unmarked photos and clip art contained in this module were obtained from the Microsoft Office Clip Art Gallery.