12 Lead ECG Basics PDF

12 Lead ECG Basics The Normal 12 Lead ECG By Dr. Hala Sanad  Objectives By the end of this lecture you will be able to: Define ECG Identify the conductive system of the heart Discuss the characteristics of the cardiac muscles...

12 Lead ECG Basics The Normal 12 Lead ECG By Dr. Hala Sanad  Objectives By the end of this lecture you will be able to: Define ECG Identify the conductive system of the heart Discuss the characteristics of the cardiac muscles List the “12” Leads of the 12 Lead ECG Discuss the clinical uses of ECG  Objectives List the different leads of ECG and their significance Discuss the components of the ECG tracing paper Recognize the “normal” appearance of each lead Analyze ECG strip Discuss the characteristics and significance of ECG waveforms, segments and intervals Calculate the heart rate in a given ECG strip  Definition It is a graphic recording of the electrical activity of the heart  Clinical Uses of the ECG To diagnose: - Dysrhythmias - Conduction abnormalities - Enlarged heart chambers - Myocardial ischemia or infarction - Electrolyte imbalance To evaluate the effectiveness of medications  Characteristics of the Cardiac Muscles Excitability: the ability to respond to an electrical stimulus Automaticity: the ability of the cardiac cells to initiate an electrical impulse Conductivity: the ability of the cardiac muscle to move an impulse from cell to cell Contractility: the ability of the cardiac muscle to shorten in response to an electrical impulse  Conduction System ECG waveform represents the function of the heart’s conduction system which normally initiates &conducts the electrical activity  Conduction System (cont.) SA node: Sino Atrial node AV node: Aterioventricular node. Bundle of His Right bundle branch & Left bundle branch. Purkinjie fibers  Normal electrical conduction Impulse originates in SA node in Rt. atrium Impulse travels from SA node through the atria to the AV node causing atria to contract Impulse travels very quickly along the Rt. & Lt. bundle brunches & Purkinje fibers ( located in ventricular muscle) causing ventricles to contract  Conduction System S A Node Bachmann’s Bundle A V Node LBB Anterior Division Bundle of His Posterior Division RBB CHS AHA ITO  12 Lead ECG Basics The leads of the 12 lead ECG are divided into 6 Limb Leads and 6 Precordial or Chest Leads.  12 Lead ECG Basics Limb Leads: Vertical Plane Lead I aVR Lead II aVL Lead III aVF  12 Lead ECG Basics Limb Leads Lead P wave QRS T wave I upright upright upright II upright upright upright III upright upright upright  12 Lead ECG Basics Augmented Limb Leads Lead P wave QRS T wave negative/upr aVR negative negative ight aVL upright upright upright aVF upright upright upright  12 Lead ECG Basics Precordial Leads: horizontal plane V1 V4 V2 V5 V3 V6  12 Lead ECG Basics Chest Leads Lead P wave QRS T wave upright/ small R V1 wave / QS upright biphasic upright/ small R V2 wave / QS upright biphasic equipahsic V3 upright QRS - upright upright 12 Lead ECG Basics Chest Leads Lead P wave QRS T wave V4 upright upright upright V5 upright upright upright V6 upright upright upright Precordial Leads  Chest Lead Placement Midclavicular Line – MCL Anterior Axillary Line – AAL Angle of Louis Midaxillary Line - MAL V1 = Placed 4th IC space Right Sternal Border V2 = Placed 4th IC space Left Sternal Border V3 = Halfway between V2 and V4 V4 = 5th IC Space, MCL V5 = Same horizontal plane as V4, AAL V6 = Same horizontal plane as V4, MAL Lead Placement is Important!  The ECG Paper - Horizontally One small box - 0.04 s One large box - 0.20 s - Vertically One large box - 0.5 mV  The ECG Paper (cont) 3 sec 3 sec Every 3 seconds (15 large boxes) is marked by a vertical line. This helps when calculating the heart rate. NOTE: the following strips are not marked but all are 6 seconds long. Heart Rate Determination  The P wave The P wave: represents atrial depolarization Location: Precedes QRS complex Duration: 0.06 to 0.11 seconds,( shorter than 0.11 seconds) The P-R interval: represents the time it takes an impulse to travel from the atria through the AV node, bundle of His, and bundle branches to the Purkinje's fibers Location: Extends from the beginning of the P wave to the beginning of the QRS complex Duration: 0.12 to 0.20 seconds  The QRS complex The QRS complex: represents ventricular depolarization. Location: Follows the P-R interval Duration: less than or equal to 0.12 seconds The Q-T Interval: This interval represents the time necessary for ventricular depolarization and repolarization.  The T wave The T wave: represents the repolarization of the ventricles. On rare occasions, a U wave can be seen following the T wave. The U wave reflects the repolarization of the His-Purkinje's fibers. Location: Follows the S wave and the S-T segment Duration: Not usually measured The S-T segment: represents the end of the ventricular depolarization and the beginning of ventricular repolarization. Location: Extends from the end of the S wave to the beginning of the T wave Duration: Not usually measured  Method I - Times Ten Simplest, quickest, most commonly used technique that is particularly useful if the rhythm is irregular. 1. Obtain a 6-inch or 6-second rhythm strip 2. Calculate the number of R waves within 6 sec. 3. Multiply this number by 10,  Method II – 1500 OR 300 Method Use only if cardiac rhythm is regular. 1) Identify two consecutive R waves. 2) Count the number of small blocks between two R-R. 3) Divide 1500 by the number of small blocks counted OR Divide 300 by the number of big blocks counted between two R-R ECG Rhythm Interpretation How to Analyze a Rhythm  Rhythm Analysis Step 1: Calculate rate. Step 2: Determine regularity. Step 3: Assess the P waves. Step 4: Determine PR interval. Step 5: Determine QRS duration. Calculate rate  Step 2: Determine regularity R R Look at the R-R distances (using a caliper or markings on a pen or paper). Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular? Interpretation? Regular  Step 3: Assess the P waves Are there P waves? Do the P waves all look alike? Do the P waves occur at a regular rate? Is there one P wave before each QRS? Interpretation? Normal P waves with 1 P wave for every QRS  Step 4: Determine PR interval Normal: 0.12 - 0.20 seconds. (3 - 5 boxes) Interpretation? 0.12 seconds  Step 5: QRS duration Normal: 0.04 - 0.12 seconds. (1 - 3 boxes) Interpretation? 0.08 seconds  Rhythm Summary Rate 90-95 bpm Regularity regular P waves normal PR interval 0.12 s QRS duration 0.08 s Interpretation? Normal Sinus Rhythm THANK YOU MYOCARDIAL INFARCTION Dr. Hala Sanad  Objectives By the end of the presentation you will be able to: Analyze the prevalence of MI incidence in Bahrain & the world. Discuss the etiology and predisposing factors of M.I. Inference the clinical manifestations of MI related to pathophysiology. Justify the diagnostic tests done to diagnose M.I.  Objectives explain the collaborative management of patients with M.I. in Health Center and Government Hospital. predict the complications of M.I. Apply the nursing process in caring for MI patient in acute stage. Design a comprehensive Health education plan for a discharged MI patient after an attack of acute MI.  Acute Coronary Syndrome Refers to any group of clinical symptoms compatible with acute myocardial ischemia and includes: unstable angina (UA) non—ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).  Myocardial Infraction Is a life-threatening condition characterized by the formation of localized necrotic areas within the myocardium. the myocardial cells in the heart are permanently destroyed. Occlusion of Coronary Artery Intermittent Completely Occlusion Unstable occlusion angina AMI  Incidence Age: Increasing age Sex: Men > women Menopausal women  Race: African American > Caucasians Major Coronary Arterial System and Structure they Perfuse  Pathophysiology -Coronary Atherosclerosis The inflammatory response involved with the development of atherosclerosis begins with injury to the vascular endothelium and progresses over many years. The injury may be initiated by smoking or tobacco use, hypertension, hyperlipidemia, and other factors. The endothelium undergoes changes and stops producing the normal antithrombotic and vasodilating agents. The presence of inflammation attracts inflammatory cells, such as macrophages. The macrophages ingest lipids, becoming “foam cells” that transport the lipids into the arterial wall. Some of the lipid is deposited on the arterial wall, forming fatty streaks. Activated macrophages also release biochemical substances that can further damage the endothelium by contributing to the oxidation of low-density lipoprotein (LDL). The oxidized LDL is toxic to the endothelial cells and fuels progression of the atherosclerotic process.  Pathophysiology -Coronary Atherosclerosis Following the transport of lipid into the arterial wall, smooth muscle cells proliferate and form a fibrous cap over a core filled with lipid and inflammatory infiltrate. These deposits, called atheromas, or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow. Plaque may be stable or unstable, depending on the degree of inflammation and thickness of the fibrous cap. If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can resist the stress of blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable plaque. At this point, the lipid core may grow, causing the fibrous plaque to rupture. A ruptured plaque attracts platelets and causes thrombus formation. A thrombus may then obstruct blood flow, leading to acute coronary syndrome , which may result in an acute myocardial infarction. When an MI occurs, a portion of the heart muscle no longer receives blood flow and becomes necrotic.  Pathophysiology - unstable angina There is reduced blood flow in a coronary artery, often due to rupture of an atherosclerotic plaque. A clot begins to form on top of the coronary lesion, but the artery is not completely occluded. This is an acute situation that can result in chest pain and other symptoms that may be referred to as preinfarction angina because the patient will likely have an MI if prompt interventions do not occur.  Pathophysiology- MI plaque rupture and subsequent thrombus formation result in complete occlusion of the artery, leading to ischemia and necrosis of the myocardium supplied by that artery. Vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (e.g., from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (e.g., from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine) are other causes of MI. In each case, a profound imbalance exists between myocardial oxygen supply and demand.  Pathophysiology- MI The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction, or the death of cells. The expression “time is muscle” reflects the urgency of appropriate treatment to improve patient outcomes. Approximately every 40 seconds, an American will have an MI (Benjamin et al., 2019), and many of these people will die as a result. Early recognition and treatment of patients presenting with an MI will improve their chances of survival.  Q wave AMI Non Q wave Depends on the degree and duration of the occlusion.  Non Q Wave MI When abnormal level cardia serum markes is released only ST segment eleviation or T wave abnormalities. ST Segment deviation should be identified for reperfusion therapy. A door – to – needle time < 30 mts.  Clinical Manifestations 1) Pain Persistent severe immobilizing chest pain not relieved by rest or nitroglycerin. It’s crushing, heaviness, tightness, constriction, vise like more severe than angina. It occurs suddenly.  Clinical Manifestations: Location of chest pain: Substernal, retrosternal, radiating to neck, jaw, arms or back. It may occur suddenly onset may be few minutes > 20 or 30 minutes. It may occur while the client is active or at rest, asleep or awake.  Clinical Manifestations Pain may be precipitated by emotion or exertion. Associated symptoms may include nausea, indigestion, dyspnea, dizziness, weakness and sense of impending doom. Sympathetic stimulation diaphoresis, clammy & cool skin (cool sweat). Fever: Inflammatory process.  Cardiovascular Manifestations B.P: Initially , later  Cardiac output  urine output  pulmonary edema  Rales (crackles) over lungs Jugular veins distended. Cardiac examination  murmurs  Diagnostic Studies  History :( Present symptom , previous illness, Family Hx, Risk factor)  Laboratory Tests (cardiac enzymes & biomarkers, coagulation profile, lipid profile) 12 lead ECG findings : ischemia, injury, infarction. Chest x-ray.  Echocardiogram. Cardiac stress test Cardiac Catheterization  Creatine Kinase and Its Isoenzymes There are three CK isoenzymes: CK-MM (skeletal muscle) CK-MB (heart muscle) CK-BB (brain tissue). CK-MB is the cardiac-specific isoenzyme; it is found mainly in cardiac cells and therefore increases when there has been damage to these cells. Elevated CK-MB is an indicator of acute MI; the level begins to increase within a few hours and peaks within 24 hours of an infarct.  Myoglobin Is a heme protein that helps in transporting O2. Found in cardiac and muscular muscle.  Myoglobin not specific indication of cardiac event. Negative result is excellent parameter of ruling out MI Begins to rise 1 - 3 hrs Peaks within 1hrs of onset of symptoms Return to Normal 12 hrs  Troponin Is a protein found in myocardial cells, regulates the myocardial contractile process. There are three isomers of troponin: C, I, and T. Troponins I and T are specific for cardiac muscle, and these biomarkers are currently recognized as reliable and critical markers of myocardial injury. An increase in the level of troponin in the serum can be detected within a few hours during acute MI. It remains elevated for a long period, often as long as 2 weeks, and it therefore can be used to detect recent myocardial damage. It should be noted that cardiac troponin levels may rise during inflammation and other forms of mechanical stress on the myocardium. These include sepsis, heart failure, and respiratory failure.  Chest X-ray To determine the size, contour, position of heart. Does not aid in diagnosis of MI but can confirm complications.  Echocardiogram Noninvasive ultrasound test to examine the size, shape, motion of cardiac structure. Purposes: Indicated in diagnosis of MI if ECG is non diagnostic. To determine ejection friction.  Echocardiogram con’t Evaluate valves and chambers of the heart Evaluate heart murmurs. Check the pumping function of the heart Evaluate patients who have had heart attacks. Screening test for heart disease in certain groups of patients  12 Leads ECG Should be obtained within 10 minutes from arrival to A/E. Serial ECG should be taken. Classic ECG changes: T wave inversion ST segment elevation Development of abnormal Q wave  Electrocardiogram The 12-lead ECG provides information that assists in ruling out or diagnosing an acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the ED. By monitoring serial ECG changes over time, the location, evolution, and resolution of an MI can be identified and monitored. The ECG changes that occur with an MI are seen in the leads that view the involved surface of the heart. The expected ECG changes are T-wave inversion, ST-segment elevation, and the development of an abnormal Q wave. Because infarction evolves over time, the ECG also changes over time.  Electrocardiogram The first ECG signs of an acute MI are usually seen in the T wave and ST segment. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert. Myocardial injury also causes ST-segment changes. The ST segment is normally flat on the ECG tracing. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line (the area between the T wave and the next P wave is used as the reference for the isoelectric line). This change is measured 0.06 to 0.08 seconds after the end of the QRS—a point called the J point. An elevation in the ST segment in two contiguous leads is a key diagnostic indicator for MI (i.e., STEMI). Relation between leads with ST-segment elevations and ischemic area  Cardiac stress test Noninvasive means of assessing certain aspects of cardiac function. Evaluate cardiac function during physical stress and heart response to  O2 demand. During an exercise stress test, the patient walks or runs on a treadmill or pedals a stationary bicycle. A protocol guides exercise intensity based on the patient’s age and heart rate goal. During the test, the following are monitored: two or more ECG leads for heart rate, rhythm, and ischemic changes; BP; skin temperature; physical appearance; perceived exertion; and symptoms, including chest pain, dyspnea, dizziness, leg cramping, and fatigue. The test is stopped when the target heart rate is achieved or if the patient experiences signs of myocardial ischemia. Abnormal findings include chest pain, ventricular arrhythmia, ST-segment depression, and lack of heart rate or BP elevation with exercise.  Purposes of Treadmill Assist in the diagnosis of Cardiac pain. To screen for ischemic heart disease. To determine the functional capacity of the heart after MI. To assess the effectiveness of medication. To identify dysrhythmias that occur during physical activity. Aid in the development of physical fitness program.  Cardiac Catheterization Invasive diagnostic procedure in which one or more catheters are introduced into the heart and selected blood vessels. Purposes: To measure pressure in the heart chamber. To detect O2 saturation of blood. To assess the patency of coronary arteries. To determine appropriate treatment.  Medical Management Medical Management Goal Minimize myocardial infarction Preserve myocardial function Prevent complications HOW?  1. By reperfusion the area with thrombolytic medication & PCI 2.  Myocardial O2 demand  O2 Supply(medication, oxygen, & bed rest)  Management Initial Assessment:  Targeted HX  Vital signs and physical examination  12 lead ECG  Chest x-ray  ECG monitoring arrhythmias  I.V. lifeline with normal saline  Initial Management (MONA) The patient with suspected MI should immediately receive supplemental oxygen, aspirin, nitroglycerin, and morphine. Morphine is the drug of choice to reduce pain and anxiety. It also reduces preload and afterload, decreasing the work of the heart. The response to morphine is monitored carefully to assess for hypotension or decreased respiratory rate. A beta-blocker may also be used if arrhythmias occur. If a beta-blocker is not needed in the initial management period, it should be introduced within 24 hours of admission, once hemodynamics have stabilized and it is confirmed that the patient has no contraindications. Unfractionated heparin or LMWH may also be prescribed along with platelet-inhibiting agents to prevent further clot formation.  Emergent Percutaneous Coronary Intervention The patient with STEMI is taken directly to the cardiac catheterization laboratory for an immediate PCI. The procedure is used to open the occluded coronary artery and promote reperfusion to the area that has been deprived of oxygen. Superior outcomes have been reported with the use of PCI when compared to thrombolytic agents. Thus, PCI is preferred as the initial treatment method for acute MI in all age groups. The procedure treats the underlying atherosclerotic lesion. Because the duration of oxygen deprivation determines the number of myocardial cells that die, the time from the patient’s arrival in the ED to the time PCI is performed should be less than 60 minutes. This is frequently referred to as door-to-balloon time.  Thrombolytics is initiated when primary PCI is not available or the transport time to a PCI-capable hospital is too long. These agents are administered IV according to a specific protocol. The thrombolytic agents used most often are alteplase, reteplase, and tenecteplase. The purpose of thrombolytics is to dissolve the thrombus in a coronary artery (thrombolysis), allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the infarction and preserving ventricular function. although thrombolytics may dissolve the thrombus, they do not affect the underlying atherosclerotic lesion. The patient may be referred for a cardiac catheterization and other invasive procedures following the use of thrombolytic therapy. Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder. They should be given within 30 minutes of symptom onset for best results. This is frequently referred to as door-to-needle time.  Pharmacological Therapy Aspirin Morphine (Analgesic) Nitroglycerin Beta- Blockers Angiotensin-Converting Enzyme Inhibitor (ACE) Inhibitors  Aspirin Why? (Actions) Blocks formation of thromboxane A2 (thromboxane A2 causes platelets to aggregate and arteries to constrict) These actions will reduce Overall mortality from AMI Nonfatal reinfarction Nonfatal stroke  Aspirin Cont’d When? (Indications) As soon as possible! Standard therapy for all patients with new pain-suggestive of AMI Give within minutes of arrival How? (Dose) 150- to 300-mg tablet taken as soon as possible (chewing) Watch Out! (Precautions) Relatively contraindicated in patients with active peptic ulcer disease or asthma Contraindicated in patients with known aspirin hypersensitivity Bleeding disorders Severe hepatic disease  Analgesics Morphine Sulfate I/V Why? (Actions) To reduce pain of ischemia To reduce anxiety To reduce extension of ischemia by reducing oxygen demands When? (Indications) Continuing pain Evidence of vascular congestion (acute pulmonary edema) Systolic blood pressure >90 mm Hg No hypovolemia  Analgesics How? (Dose) 2 to 4 mg titrated to effect Goal: Eliminate pain Watch out for (Precautions) Drop in blood pressure, especially in patients with Volume depletion Increased systemic resistance RV infarction Depression of ventilation Nausea and vomiting (common) Bradycardia  Nitroglycerin Why? (Actions) Decreases pain of ischemia Increases venous dilation Decreases venous blood return to heart Decreases preload and cardiac oxygen consumption Dilates coronary arteries Increases cardiac collateral flow  Nitroglycerin Con’t When? (Indications) Class I: First 24 to 48 hours in patients with ST-segment elevation or depression including Large anterior infarction Persistent ischemia Suspected ischemic chest pain Unstable angina (change in angina pattern) Acute pulmonary edema (if BP >90 mm Hg systolic)  Nitroglycerin Con’t How? (Dose) Sublingual: 0.3 to 0.4 mg; repeat every 5 minutes Spray inhaler: 2 metered doses at 5-minute intervals IV infusion: 12.5 to 25 g bolus, 10 to 20 g/min infusion, titrated  Nitroglycerin Con’t Watch out for (Precautions) Use extreme caution if systolic BP 7.45 - PaCo2 : normal - Hco3 > 26 mmol/L Cont…. PFT is a test used to (refer page 486,15th ed) Confirm COPD diagnosis Determine disease severity Monitor disease progression Spirometry is a test used to: Evaluate airflow obstruction by the ratio of air volume the patient can Forcibly Exhale in one second (FEV) to Forced Vital Capacity (FVC)  Medical Management Risk Reduction (Smoking Cessation, Influenza vaccination etc…) Pharmacologic therapy Oxygen Therapy Incentive spirometry Chest physiotherapy Managing exacerbations Pulmonary Rehabilitation  Pharmacologic Therapy Bronchodilator: Relieve bronchospasm & reduce airway obstruction by allowing increased O2 distribution throughout the lung & improving alveolar ventilation. (page 615-617, 15th ed) Eg: Beta-adrenergic Agonist (Ventolin) Anticholinergic Agents (Atrovent) Methyzanthines (Aminophylline)  Cont’ Other medications : Diuretics agents Antibiotic agents Mucolytic agents Analgesic / Antipyretic agents Corticosteroids Alpha 1-antitrypsin augmentation therapy Pneumococcal vaccine Influenza vaccine  Other management Oxygen therapy: via Venturi Mask to provide low level of supplemental oxygen. Incentive Spirometry: Devices used to encourage deep breathing in patients at risk for collapse of lung. Pulmonary rehabilitation: Deep breathing & coughing exercise, breathing exercises, positioning (Fowlers or Semi fowlers), pursed-lip breathing.  Cont’ Chest physiotherapy; includes postural drainage, percussion, & vibration, helps to move secretions from deep inside the lung. Influenza Vaccinations to reduce the incidence of Pneumonia.  Management of Exacerbation Exacerbation of COPD is defined as an event in the natural course of the disease characterized by acute changes (worsening) in the patient’s respiratory symptoms beyond the normal day to day variations(Gold,19) Causes of exacerbation: Viral Infection (rhinovirus) Bacterial infections and Environmental factors Management of Exacerbation cont… S/S of exacerbation: Increase dyspnea Increase sputum production Respiratory failure Change in mental status Worsening of blood gas abnormalities Management of Exacerbation (A/E) Identify the primary cause and treat the Exacerbation. Roflumilast is a selective phosphodiesterase-4(PDE4) used to reduce the risk of Exacerbation (pt who had a h/o Exacerbation) Assess respiratory rate, effort & breath sound Q 2-4 hrs in order to detect the degree of hypoxemia. Administer O2 as Dr. ordered. Administer bronchodilator. Administer medications such as steroids, diuretics, cough suppressant & antibiotics as order. Place the patient in fowlers or semi fowlers position. Perform chest physiotherapy (positioning, percussion, vibration). Teach the client deep breathing & coughing exercise.  Pulmonary Rehabilitation Goals Reduce symptoms Improve the quality of life Increase physical and emotional participation in ADLs  Pulmonary Rehabilitation Multidisciplinary approach Include the following: Assessment Education Smoking cessation Physical conditioning Nutritional counseling Skill training Psychological support.  Possible Nursing Diagnoses Impaired Gas exchange R/T chronic inhalation of toxin Impaired Gas exchange R/T ventilation –perfusion inequality Impaired airway clearance R/T bronchoconstriction ,increased mucous production and ineffective cough Ineffective breathing pattern R/T shortness of breath. Activity intolerance R/T fatigue. Ineffective coping R/T reduced socialization.  Nursing Management Assessing the patient Achieving airway clearance Improving breathing patterns Improving activity tolerance Monitoring and managing the complication  Complications of COPD Respiratory insufficiency or failure Pneumonia Pulmonary infection Chronic Atelectasis Pneumothorax Cor pulmonale (pulmonary arterial hypertension)  Health education Encourage smoking cessation Encourage breathing and coughing exercise Encourage patient to avoid bronchial irritants Preventing Bronchopulmonary infections Avoiding extremes temperature Modifying Lifestyle Revised 2023  Objectives: By the end of the presentation, the student will be able to: Define Peripheral vascular disease (PVD). Classify peripheral vascular disease. Analyze the prevalence of peripheral arterial disease in kingdom of Bahrain and worldwide. Identify the predisposing factors/etiology of peripheral arterial disease. Inference the clinical manifestations of PAD in relation to its pathophysiology.  Cont’d Predict the common complications of peripheral arterial disease. Justify the investigations done in a patient with peripheral arterial disease. Explain the pharmacological, surgical and nursing management of a client with peripheral arterial disease. Design a nursing care plan on the problem of peripheral altered tissue perfusion in a client with PAD. Formulate a health education plan for a client with PAD.  Peripheral Vascular Disease Definition Disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation. PVD affects lower extremities more than upper extremities. Classification of Peripheral Vascular Disease Peripheral Vascular Disease Peripheral Arterial Peripheral Venous Disease (PAD) Disease (PVD)  Peripheral Venous Disease (PVD) Peripheral venous disease is the blockage of a vein by a blood clot.  CLASSIFICATION Venous: Venous thromboembolism Chronic venous insufficiency/postthrombotic syndrome Leg ulcers Varicose veins  Peripheral Arterial Disease (PAD) Arterial insufficiency of the extremities occurs most often in men and is a common cause of disability. PAD is a hardening and narrowing of the lumen of peripheral arteries (partial or total arterial occlusion).  Peripheral Arterial Disease (PAD) In PAD, obstructive lesions are predominantly confined to segments of the arterial system extending from the aorta below the renal arteries to the popliteal artery. Distal occlusive disease is frequently seen in patients with diabetes and in older patients  CLASSIFICATION Arterial disorders Arteriosclerosis Atherosclerosis Peripheral Arterial disorders Upper extremity arterial disease Aneurysm Aortic dissection Arterial embolism and arterial thrombosis Thromboangitis obliterans Raynaud’s phenomenon  Incidence of PAD Refer to international statistics and Health statistics in Bahrain  Risk factors Nonmodifiable Increasing age Family predisposition Modifiable Nicotine use(tobacco products, smoking, chewing tobacco) Diabetes (speeds the atherosclerotic process by thickening the basement membranes of both large and small vessels) Hypertension Hyperlipidemia Diet (contributing to hyperlipidemia) Sedentary lifestyle Stress Elevated C- reactive protein Hyperhomocysteinemia  Arterial and Venous Insufficiency Venous Arterial Aching, throbbing, cramping Intermittent claudication to sharp, Pain unrelenting, constant Present may be difficult to palpate Diminished or absent Pulses through edema Pigmentation in gaiter area (area of Dependent rubor-with elevation pallor of foot, Skin Characteristics medial & lateral malleolus), skin dry shiny skin, cool to cold temp, loss of hair thickened &tough, may be reddish over toes & dorsum of foot, nails thickened & blue ridged With associated dermatitis  Arterial and Venous Insufficiency Venous Arterial Medial malleolu, lateral malleolus, or Tip of toes, toe webs, heel or other pressure areas Ulcer Characteristics & anterior tibial area if patient is immobile Location Minimal pain to very painful Very painful Pain Superficial Deep often involving joint spaces Depth of ulcer Irregular borders Circular Shape Granulation tissue—beefy red to Pale to black and wet to dry gangrene Ulcer base yellow fibrinous in chronic long- term ulcer Moderate to sever Minimal unless extremities kept in Leg Edema dependent position to relieve pain  Arteriosclerosis and Atherosclerosis Arteriosclerosis (hardening of the arteries) is the most common disease of the arteries. It is a diffuse process whereby the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened. Atherosclerosis involves a different process, affecting the intima of large and medium-sized arteries. These changes consist of the accumulation of lipids, calcium, blood components, carbohydrates, and fibrous tissue on the intimal layer of the artery. These accumulations are referred to as atheromas or plaques.  Location Atherosclerosis can develop in any part of the vascular system regions where arteries bifurcate or branch into smaller vessels are more vulnerable In the proximal lower extremity, these include the distal abdominal aorta, the common iliac arteries, the orifice of the superficial femoral and profunda femoris arteries, and the superficial femoral artery in the adductor canal, which is particularly narrow. Distal to the knee, atherosclerosis can occur anywhere along the course of the artery. Common sites of atherosclerotic obstruction in the major arteries  Pathogenesis: Reaction-to-injury theory Vascular endothelial cell injury results from prolonged hemodynamic forces such as: Shearing stresses and turbulent flow Irradiation, Chemical exposure Chronic hyperlipidemia.  Pathogenesis: Reaction-to-injury theory Injury to the endothelium increases the aggregation of platelets and monocytes at the site of the injury. Smooth muscle cells migrate and proliferate, allowing a matrix of collagen and elastic fibers to form. Gradual narrowing of the arterial lumen stimulates the development of collateral circulation which arises from preexisting vessels that enlarge to reroute blood flow around a hemodynamically significant stenosis or occlusion. Collateral flow allows continued perfusion to the tissues, but it is often inadequate to meet increased metabolic demands, and ischemia results. Development of collateral blood flow in response to occlusion of Rt. Common iliac artery  Pathophysiology of Atherosclerosis Fatty substance accumulate at the site of vessels wall injury ↓ Formation of plaque ↓ Thrombus formation ↓ Occlusion ↓ Decrease blood flow ↓ Tissues deprive from Oxygen and nutrients Pathophysiology of Arteriosclerosis and Atherosclerosis Direct results of atherosclerosis in arteries include: stenosis (narrowing) of the lumen obstruction by thrombosis aneurysm ulceration rupture  Pathophysiology of Arteriosclerosis and Atherosclerosis Indirect results are: Malnutrition (reduction in the supply of nutrients and oxygen) subsequent fibrosis of the organs that the sclerotic arteries supply with blood cells undergo ischemic necrosis (death of cells due to deficient blood flow) replaced by fibrous tissues, which require much less blood flow Progression of atherosclerosis  Clinical manifestation Intermittent claudication ( pain may be aching, cramping, inducing fatigue or weakness) occurs distal to the area of stenosis or occlusion that occurs with some degree of activity or exercise, which is relieved with rest. As the disease progresses, the patient may have a decreased ability to walk the same distance as before or may notice increased pain with ambulation. With severe arterial insufficiency, severe pain at rest worse at night unrelieved by opioids.  Clinical manifestation Elevating the extremity or placing it in a horizontal position increases the pain, whereas placing the extremity in a dependent position reduces the pain. In an attempt to prevent or relieve the pain, some patients sleep with the affected leg hanging over the side of the bed or sleep in a reclining chair.  Diagnostic Evaluation History P.E Exercise testing (tread mill) Segmental blood pressure measurement Doppler Ultrasound flow studies Duplex ultra sonography Angiography MRI Diagnostic Evaluation Duplex Ultrasonography  Medical management Weight reduction (diet, exercises) Cessation of tobacco Drugs:- Cilostazol Antiplatelet agents (aspirin or clopidogrel) Trental, Aspirin, Plavix Statins  Medical management Endovascular interventions: Balloon angioplasty Stent Stent graft Atherectomy  Surgical management The choice of the surgical procedure depends on the degree, length, and location of the stenosis or occlusion and whether there are single or multiple lesions. Endarterectomy Angioplasty Arterial bypass surgery Bypass grafts Amputation Surgical Management  Medical Management- Angioplasty Is a medical procedure in which a balloon is used to open a blockage in a coronary (heart) artery narrowed by atherosclerosis Flexible Stent Aortoiliac Endarterectomy  Postoperative care-Maintain circulation maintain adequate circulation through the arterial repair Assess pulse, color, temperature, capillary refill, sensory& motor function are checked and compared with those of the other extremity. Initially every 15 minutes and then at progressively longer intervals if the patient’s status remains stable. Doppler evaluation: ankle-brachial index (ABI) should be evaluated at least once every 8 hours for the first 24 hours Once each day until discharge  Monitoring Complications 1. Fluid imbalance: Urine out put Central venous pressure Mental status Pulse rate, rhythm, volume Bleeding& hematoma Thrombosis-avoid leg crossing & prolonged dependent position Edema-encourage active exercises, elevate limb, Elastic compression stockings Compartment syndrome Infection  Health education Diet Foot care Exercise Skin care Pain management Smoking cessation Drugs S/s of infection, occlusion of the artery or graft, and decreased blood flow  Pulmonary Tuberculosis Revised by Adult Team 2023  Objectives  Define Tuberculosis  Analyze the prevalence of Tuberculosis in worldwide health problem.  Examine the etiology and its pre-disposing factors for Pulmonary Tuberculosis.  Inference the clinical manifestations of Pulmonary tuberculosis in relation to its pathophysiology.  Justify the investigations done to diagnose Pulmonary Tuberculosis  Objectives  Explain the collaborative (medical and nursing) management of patients with Tuberculosis.  Identify the psychological consequences for TB patient, in relation to isolation and discuss ways to deal with it.  Discuss the role of infection control department and public health department in controlling the spread of Tuberculosis.  Predict the common complications of Pulmonary Tuberculosis  Formulate a health education plan to patient, family and community in preventing spread of Tuberculosis. De8nition Tuberculosis (TB) is an infectious disease that primarily affects the lung parenchyma. It also may be transmitted to other parts of the body, including the meninges, kidneys, bones, and lymph nodes. The primary infectious agent, M. tuberculosis, is an acid-fast aerobic rod that grows slowly and is sensitive to heat and ultraviolet light. De8nition Mycobacterium bovis and Mycobacterium avium have rarely been associated with the development of a TB infection. TB is a worldwide public health problem that is closely associated with; o poverty, o malnutrition, o overcrowding, o substandard housing, and o inadequate health care. TB Personal Stories - Nicole – YouTube TB Personal Stories - Khayr - YouTube Incidence Mortality and morbidity rates continue to rise; M. tuberculosis infects an estimated one third of the world’s population and remains the leading cause of death from infectious disease in the world. In 2017, 10 million people were sick with TB throughout the world and there were 1.3 million TB-related deaths (CDC, 2018b). In the United States, 9,105 cases of TB were reported in 2017,which is a 2.3% decrease from 2016. (CDC, 2018b)  Incidence Factors that prevent elimination of TB in the United States include: o The prevalence of TB among foreign-born residents, o Delays in detecting and reporting cases of TB, o The lack of protection of contacts of people with infectious cases of TB, o The presence of a substantial number of people with latent TB, and o Maintaining clinical and public health expertise in this disease. (CDC, 2015d) Transmission and Risk Factors  How TB transmitted? TB spreads from person to person by airborne transmission. An infected person releases droplet nuclei (usually par@cles 1 to 5 mcm in diameter) through talking, coughing, sneezing, laughing, or singing. Larger droplets seIle; smaller droplets remain suspended in the air and are inhaled by a suscep@ble person. Chart 23-7 lists risk factors for TB. Chart 23-8 summarizes the CDC’s recommendations for the prevention of TB transmission in health care settings Risk Factors- Tuberculosis Close contact with someone who has ac@ve TB. Inhala@on of airborne nuclei from an infected person is propor@onal to the amount of @me spent in the same air space, the proximity of the person, and the degree of ven@la@on. Immunocompromised status: (e.g., those with HIV infec@on, cancer, transplanted organs, and prolonged high-dose cor@costeroid therapy). Substance abuse (IV/injec@on drug users and alcoholics). Risk Factors- Tuberculosis Any person without adequate health care: (the homeless; impoverished; minori@es, par@cularly children > Barotrauma  Types of Delivery: Pressure-cycled ven7la7on (PCV): Inspira%on ends when a percent pressure reached A peak inspiratory pressure (PIP) is applied and the pressure diPerence between the ven%lator and the lungs results in inWa%on un%l the peak pressure is ahained. – PCV= Wow (fxed) -------pressure (fxed)--- volume (diPer) – Variable TV >>> Volutrauma – Commonly used for infants and pediatrics below 10 kg. 5% used in adults such as ARDS and pneumoectomy – The dynamic changes in pulmonary mechanics would aPect TV  Volume vs. Pressure Control Ven7la7on Volume Ventilation Pressure Ventilation Volume delivery constant Volume delivery varies Inspiratory pressure varies Inspiratory pressure constant Inspiratory Wow constant Inspiratory Wow varies Inspiratory %me determined by set Wow Inspiratory %me set by clinician and Vt  Ques7on 1 T/F: in Volume-Cycled Ven%la%on, inhala%on proceeds un%l a set pressure is delivered followed by passive exhala%on  Modes ofMODES Ven7la7on: Volume Pressure Spont BiPAP PSV PEEP (AC/SIMV) (AC/SIMV) (PSV/CPAP) IPAP&EPAP  Modes of Ven7la7on: Con7nuous Mandatory Ven7la7on (CMV): – Breath are delivered at present intervals regardless of the pa%ent ePort – U%lized most olen in paralyzed or apenic pa%ent – It can increase WOB if respiratory ePort are present Assist-control ven7la7on (A/C): – The ven%lator delivers preset breaths in coordina%on with the respiratory ePort of the pa%ent – the ven%lator delivers a full assisted %dal volume – Spontaneous breathing independent of the ven%lator between A/C breaths is not allowed  Con7nuous Mandatory Ven7la7on (CMV): Lung Volume PEEP Airway Pressure M M M M Time  Assist-control ven7la7on (A/C): Lung Volume Airway Pressure M M P P Time  Modes of Ven7la7on Synchronous intermiNent mandatory ven7la7on (SIMV): – The ven%lator delivers preset breaths in coordina%on with the respiratory ePort of the pa%ent – Spontaneous breathing is allowed between breaths Con7nuous Posi7ve Airway Pressure (CPAP): A con%nuous level of elevated pressure is provided through the pa%ent circuit to maintain adequate oxygena%on and decrease the work of breathing, and decrease the work of the heart – The pa%ent must ini%ate all breaths – Variable Vt dictated by ePort  Synchronous intermiNent mandatory ven7la7on (SIMV): Lung Volume Airway Pressure M M P P Time  CPAP + PS Lung Volume Airway Pressure P P P P Time  Bilevel Posi7ve Airway Pressure –It is two pressures: –IPAP: –EPAP: –The diPerence is pressure support –BIPAP aPect ven7la7on –FIO2 –IF NECESSARY,BACK UP RESP RATE –Increase PS lungs expansion increasing –the ven7la7on –Where is my oxygena7on? In EPAP EPAP IPAP  BiLevel EPAP prevents airway and alveolar collapse, prevents atelectasis, and maintains func%onal residual capacity at increased levels. – EPAP maintains oxygena%on, IPAP augments %dal volume, increases airway pressure, and decreases fa%gue. Bilevel is similar to pressure support ven%la%on. With BiPAP,supplemental oxygen is diluted by the high Wow of air through the system. In the spontaneous mode, Bilevel response to the pa%ent’s own Wow rate and cycles between high-pressure inspira%on and low- pressure exhala%on.  Ques%on 2 T/F: BiPAP is the ideal mode of ven6la6on for pa6ent with hypercapnea such as COPD.  Ques%on 3 T/F: It is eBec6ve to use CPAP mode with apnic pa6ent or during CPR.  Ini%al Se0ngs Select your mode of ventilation Set sensitivity at Flow trigger mode Set Tidal Volume Set Rate Set Inspiratory Flow (if necessary) Set PEEP Set Pressure Limit Humidification  Adjustments To aBect oxygena6on, adjust: To aBect ven6la6on, adjust: – Respiratory Rate – FiO2 – PEEP MAP – Tidal Volume VE – I 6me – PIP  Post Ini%al Se0ngs Obtain an ABG (arterial blood gas) about 30 minutes after you set your patient up on the ventilator. An ABG will give you information about any changes that may need to be made to keep the patient’s oxygenation and ventilation status within a physiological range.  ABG Goal: Keep patient’s acid/base balance within normal range: pH 7.35 – 7.45 PCO2 35-45 mmHg PO2 80-100 mmHg  Ques%on 4 T/F: Pa6ent who suBers from COPD or pulmonary emphysema prefers longer inspiratory 6me than other pa6ent. Non-Invasive Posi%ve Pressure Ven%la%on (NIPPV)  NIPPV: Poten%al BeneCts Reduce WOB Reduce PaCO2 Improve oxygena6on Decrease mortality Decrease morbidity Less trauma6ze to the pa6ent No need for intuba6on To decrease the number of ven6lators Decrease cost  Contraindica%ons To NIPPV Rapid deteriora6on Decreased mental status Aspira6on risks Facial instability Excess secre6ons  44 Assessment of NIV in Clinical Use Criteria for success Cancella%on criteria X – Improvement in alveolar ven6la6on – Hypercapnia during NIV (PaCO2 falls) – Hypoxemia with SaO2< 85% – Improvement in pulmonary gas – Acidosis (pH < 7,2) exchange (SaO2 rises) – Rise in respiratory rate – Unloading of respiratory pump Dyspnea – Decrease in cardiac rate – Loss of consciousness – Decrease in respiratory rate – Circulatory instability – Reduces agita6on, angst – Increasing agita6on, angst – Reduc6on in dyspnea  HumidiCca%ons Heated Humidifier Heated/moisture exchange (HME) Should provide a 30 mg/L or water with a temp of 30 C or higher  Nurses’ Role In Mechanical Ven%la%on Always assess the pa6ent \rst, Not the ven6lator Check ven6lator se]ngs and mode Synchrony Assess the pa6ent’s comfort Inspec6on: bilateral chest rise, RR, exhaled Vt, Use of accessory muscles Palpa6on, Percussion, and ausculta6on Humidi\ca6on V/S including SPO2  Nurses’ Role In Mechanical Ven%la%on Evidence of hypoxia (restless, anxiety, tachycardia, RR, cyanosis, etc) Pt. spontaneous ven6latory eBort Chest physiotherapy Minimizing disconnec6on of the ven6lator circuits Assess pain and seda6on needs Elevate HOB to 45 degrees  Nurses’ Role In Mechanical Ven%la%on Anxious Pa6ent – Can be due to a malfunc6on of the ven6lator – Pa6ent may need to be suc6oned – Frequently the pa6ent needs medica6on for anxiety or seda6on to help them relax  Monitoring Pa%ent During Mechanical Ven%la%on: The nurse should monitor PIP: a sudden decline in PIP indicate leakage in the tube or the pa6ent ET A sudden increase in the PIP indicate blockage: – Secre6ons in the ET --------------- suc6on the pa6ent – Blockage of the ET----------------- suc6on, if not, replace – Pa6ent is coughing or \gh6ng the against the ven6lator--- \nd the cause – Bronchospasim--------------- auscultate, then tx by nebulizer  Monitoring: Things That Go Wrong! Increase in PIP Decrease in PIP Secreations in the ET Leak in the circuit Blockage of the ET Disconnected circuit Biting the tube Change in the PIP Ventilator Alarm! Patient Coughing ET cuff Pressure Asynchrony Exhalation valve leak Fighting Bronchospasim Change in Compliance Self extubated Increase RAW  Making it Run Smoothly! Endotracheal Tube Issues! Dislodged! Blocked Placed too deep HME \lter issue: Ven6lator Calcula6ng the Oxygen:  Ven%lator-Libera%on Weaning Methods – Rapid Weaning: Post Surgery – Rou6ne Weaning: Rapid Shallow Breathing Index (RSBI) performed daily – Gradual Weaning: CPAP – Ven6lator Dependent pa6ents  Ven%lator-Libera%on Objec%ve: To iden6fy pa6ents readiness for discon6nua6on of mechanical ven6la6on, and possible extuba6on Level of seda%on: Pt should not be on vasopressor agents, benzodiazepines, or seda6ves agents (A6van, Versed, Propofol). Pa6ent might be receiving intermieent dose of seda6ve agents. Dopamine or dobutamine should not exceed 5 mq/kg/mint.  Ven%lator Libera%on Oxygena%on: – The pa6ent's FiO2 must be 20cmH2O indicates an adequately strong diaphragm P/F RaGo – PaO2/FiO2 –