Exam 1 Study Guide PDF - Nursing Management & Interventions

Exam 1 Study Guide Exam one will consist of 50 multiple choice questions, including select all that apply, fill in the blank as well as two case study questions that are 6 points each for a total of 60 points. *know nursing diagnoses for each condition. Risk factors PE ​ Obesity...

Exam 1 Study Guide Exam one will consist of 50 multiple choice questions, including select all that apply, fill in the blank as well as two case study questions that are 6 points each for a total of 60 points. *know nursing diagnoses for each condition. Risk factors PE ​ Obesity ​ Smoking ​ Chronic heart disease ​ A-fib ​ Fracture ​ Hip or knee replacement ​ Major surgery ​ Major trauma ​ Spinal cord injury ​ History of previous VTE ​ Estrogen use (birth control) ​ Age > 50 ​ Pregnancy Major DVT risk factor: Virchow’s Triad -​ Venous stasis -​ Vessel wall damage (HTN, cholesterol) -​ Hypercoagulability -​ These conditions can cause immobility ·​ Causes/Patho ​ Blood clot lodge in pulmonary artery - PE -​ It can also be air, tumor amniotic fluid, fat -​ V/Q mismatch (ventilation/ perfusion mismatch) ·​ Clinical Manifestations -​ Dyspnea -​ Pleuritic chest pain (stabbing pain) -​ Tachypnea -​ Tachycardia -​ Hemoptysis -​ Cough -​ Accessory muscle use -​ Anxiety/ restlessness feeling of doom  ·​ Diagnostics ​ ECG to r/o MI ​ CXR to r/o other causes of respiratory distress ​ CT scan with contrast to identify PE ​ VQ scan to visualize PE if CT is not available ( VQ must be > 0.8) ​ Pulmonary angiography is the most definitive test Laboratory Studies: ​ D- Dimer (Is there any fibrin left over) ​ ABG’s ​ Beginning phases respiratory alkalosis – progresses to metabolic acidosis ·​ Treatment-pharmacological and nonpharmacological (ex. IVC filter). Pharmacological: ​ Anticoagulants (heparin and warfarin) s/e: n/v, easy bruising, uncontrolled bleeding, sob, weakness ​ Thrombolytics (tPA, Alteplase, Streptokinase) s/e: allergic reaction, hypotension and bleeding Nonpharmacological: ​ Oxygen (non-rebreather) Surgical management: ​ Embolectomy ​ Catheter ​ Surgical - most common if thrombolytics are contraindicated ​ Inferior vena cava filter (can be permanent or temporary) o Know side effects and teaching for pharmacological treatment ·​ Nursing management/interventions Nursing Mgmt: ​ Assessment and analysis sxs are nonspecific (cardiac failure or respiratory failure) – PE is a medical Emergency – Sudden onset (pleuritic chest pain, dyspnea, tachypnea, others: hypotension, anxiety, impending doom, change in mental status – in some cases (cardiac. Pulmonic arrest or code blue) Nursing intervention: ​ Airway (priority) ​ Oxygenation ​ Frequent VS ​ Chest pain ​ Laboratory values: ABGs, lactic acid, aPTT, PT/INR ​ Urine output: -​ < 0.5 mL/Kg/hr sign of shock  -​ < 30 mL/hr is never a good sign Nursing Action: ​ Elevate the head of the bed ​ Administer IV fluids ​ Administer medication (thrombolytics or anticoagulants) ​ Institute bleeding precautions (assess GI stools, INR, PT) ​ Be prepared to intubation and resuscitation How to prevent complications ​ Disease process/ lifestyle modifications ​ Medications ​ Bleeding precautions ​ Diet ​ Signs/ symptoms of recurrent PE/ DVT ·​ Be familiar with a therapeutic range of PTT if on a heparin drip and goal INR for Warfarin ​ When on a heparin drip PTT (40-90) ​ Goal INR (2.0- 3.0) Nursing Dx: ​ Impaired gas exchange Chest Trauma ·​ What is the purpose of a chest tube? Review nursing care for chest tubes. ​ The main purpose of a chest tube is to drain fluid or air to re-expand a collapsed lung and the main purpose is to restore a normal negative pressure within pleural space ​ One-way drainage system, below the chest Care Chest Tube: 1)​ Suction control chamber (gentle steady or continuous bubbling – good amount of suctioning applied) (a child sucking a milkshake, not vigorous) 2)​ Water seal chamber & air leak monitor (one-way valve to help drain fluid or air, tidaling (rise & fall) = good “continuous bubbling” = bad air leak monitor 3)​ Collection chamber (helps to drain fluid) (notify HCP “bright red blood” over 100 ml/hr + (after 1st hour of placement) -​ Dark bloody drainage = normal -​ Document & you monitor (old blood) -​ Never clamp a chest tube, makes the bleeding worse Stopped or decreased drainage? 1.​ Assess the patient first then the machine by listening/ osculating 2.​ Diminished breath sounds = priority 3.​ Turn cough & deep breath 4.​ Reposition the patient Signs and symptoms of tension pneumothorax and cardiac tamponade, treatment for each condition. Tension pneumothorax: ​ Air or blood collection in pleural space ​ Tracheal deviation - cardinal sign ​ Can lead to pressure on heart and PEA arrest Cardiac Tamponade: (pericardial sac filled with fluid or blood, causing increased intrapericardial pressure, that compresses the heart so it can no longer fill) ​ The heart cannot adequately fill or contract because of the compression of the ventricles ​ Hypotension, muffled heart sounds, and distended neck veins (Beck’s triad) ​ Causes of PEA arrest ​ Pericardiocentesis (essential draining of the extra fluid in the pericardium) Signs and symptoms of chest wall contusion: damage to chest wall and lungs leading to problems with ventilation and oxygenation ​ Tachypnea (increase O2 to tissues) ​ Tachycardia ​ SOB ​ Decreased oxygenation ​ Decreased LOC ​ Decreased or absent lung sounds ​ Asymmetrical chest excursion (in the case of a flail chest) ​ subcutaneous emphysema ​ Restlessness ​ Confusion Nursing Dx: ​ Impaired gas exchange ​ Acute pain ​ Decreased cardiac output Respiratory Failure/ARDS ·​ The signs/symptoms of respiratory failure 2 Types: ​ Hypoxemic failure (Low O2) ( PaO2 60 or less) ​ HyperCapnic failure (High CO2) (PaCO2 Over 50) Can be group into three categories: -​ Impaired ventilation (airway obstruction, myasthenia gravis, chest wall injury, anesthesia, opioids) -​ Ventilation-Perfusion Mismatch (COPD, restrictive lung disease, atelectasis, PE, pneumothorax, ARDS)  -​ Impaired Diffusion (PE, Pneumonia, ARDS) Pathophysiology: Hypoxemic respiratory failure, impaired oxygenation r/t VQ mismatch ​ Gas exchange can not occur in alveolar capillary bed ​ Decreased circulating oxygen > hypoxia Hypercapnic respiratory failure ​ Impaired ventilation ​ CO2 trapping in lungs ​ alveoli become hardened due to capillaries being inflamed and fluid-filled leaky barrier fluid in alveoli ​ Exudative phase- occurs 24-48 hours after injury, inflammatory mediators release, proteins in the alveoli, hydrostatic pressures disrupted ​ Proliferative phase – neutrophils/inflammatory mediators cross the ACM, V/Q mismatch, increasing pulm. HTN and R HF ​ Fibrotic phase – fibrosis and scarring ​ Stiff lungs Signs/symptoms of ARDS -​ Sudden SOB (within 12-24 hours of lung injury) -​ Labored & fast breathing (tachypnea) -​ Agitation -​ Restlessness -​ Confusion -​ Tachycardia -​ Coughing -​ Tiredness -​ Dizziness -​ Headache -​ Cyanosis -​ Refractory hypoxemia (low O2 despite oxygen delivery) (low PaO2 despite oxygen delivery, resistant to oxygen) Management/Treatment/Complications of ARDS ​ Mechanical ventilation (low tidal volume and High (positive end-expiratory pressure) ​ High-flow nasal cannula ​ ECMO  ​ Prone position (16 hours prone, 8 hours supine) ​ Recruit alveoli Medications: ​ Antibiotics (after culture is done) ​ Neuromuscular blockade (train of 4 paralyzing medications: analgesia, anesthesia) ​ Promote vent synchronization ​ Hydration (thin secretions) ​ Nutrition (tube feeding) Complications ​ Barotrauma (alveoli trauma d/t high peep) ​ Atelectasis, pneumothorax ​ Renal failure (2/2 hypotension, medication) ​ MODS ​ VAP (nursing sensitive indicator) Nursing Dx: ​ Impaired gas exchange (priority) ​ Anxiety ​ Imbalanced nutrition, less than body requirements Ventilator Setting: 1.​ Suction OUT - never in “Never apply suction when inserting a catheter into the airway” 2.​ 10 seconds or less 3.​ 100% oxygen 30 seconds before 4.​ Avoid suctioning before an ABG 5.​ Avoid suctioning “routinely” - Acute Lung Injury Only when needed Ventilator Therapy ·​ Have a general understanding of: o FiO2 - a fraction of inspired O2 delivered to the patient (21 - 100%) Goal: spO2 > 92%, PaO2 > 60 - 80 mm Hg -​ Higher = more severe -​ FiO2 (Fi-eed me O2) o Peep - positive pressure applied at end of expiration of ventilator breaths (usual setting 5 cm H20) -​ Keeps the alveoli open at the end of respiration -​ caution : barotrauma -​ PEEP improves has gas exchange o Tidal Volume - volume of air exchanged with each breath (normally 500 mL) Tidal wave of air  o Pressure Support - positive pressure used to augment patient’s inspiratory pressure (usual settings 5-10 cm H20) ·​ The goal of medications for patient on ventilator therapy ​ Sedation Vacation: ​ Drips: propofol, precedex, versed ​ IVP: fentanyl, versed, Dilaudid ​ You need to have orders for these to titrate based on RASS score ⛹️🏀 ​ Paralytic: Nimbex Sepsis/MODS (Drei Baling-it ) ·​ Pathophysiology: Invasion of a pathogen initiates the body’s inflammatory response mechanism. Excessive release of proinflammatory cytokines causing 1.​ Vasodilation *drop in BP damages vital organs cause not enough perfusion* 2.​ Decreased vasomotor tone *decreased mean arterial pressure must maintain >65 3.​ Increased capillary permeability ·​ Clinical manifestations Early​(Warm Sepsis/ Hyperdynamic)​ Late (Hypodynamic/ Cold Sepsis) Tachycardia *to compensate for low Cool, pale skin BP but BP could be normal* Bounding pulses,warm, flushed skin. Weak, thready pulses Fever Tachycardia Confusion and decreased urine output Hypotension *signs of decreased organ perfusion* ·​ Labs to monitor 1.​ ABGs (asian baby girls): a.​ Initial Stage: Hyperventilation = Resp alkalosis related to Hypercapnia and hypoxia b.​ Later stage: Metabolic acidosis related to organs not getting enough O2 therefore anaerobic methods 2.​ Lactate i.​ Poor perfusion to cells Normal level is 65; resort to Vasopressors such as norepinephrine ​ Antibiotics (within 1 hour upon arrival * Cultures should be done before*) ​ Corticosteroid therapy ○​ Adrenal insufficiency keep in mind hyperglycemia, hypernatremia and neuromuscular weakness ·​ Complications of septic shock ​ Stress ulcers ○​ Impaired mucosal protection from increased bile salts and toxins ○​ Mechanical ventilation and coagulopathy ○​ Pt is immobile ○​ PPI (pantoprazole) and h2 (famotidine, pepcid) can help ​ Disseminated Intravascular coagulopathy ​ Enhanced coagulation results from the release of procoagulant factors such as part of the inflammatory response ​ abnormal activation of the clotting cascade, leading to the formation of small blood clots throughout the bloodstream. ​ Too much consumption of our clotting factors can lead to uncontrollable bleeding ​ Multiple Organ Dysfunction Syndrome (MODS) ○​ MODS usually occurs as a result of systemic inflammation triggered by a severe infection (e.g., sepsis), injury, or a critical illness. ○​ The body's inflammatory response leads to the release of cytokines and other mediators that can damage tissues, impair blood flow, and disrupt normal organ function.  ○​ Organs commonly affected include the lungs, kidneys, liver, heart, and gastrointestinal system. ○​ S/Sxs ​ Respiratory system: SOB, Tachypnea, Hypoxemia, Cyanosis ​ CV: Low BP, Tachycardia, Weak/absent pulse, cold/clammy skin, edema, heart arrhythmia ​ Renal: Oliguria (decreased urine output), swelling(edema), elevated Cr and BUN, Electrolyte imbalance ​ CNS: confusion, lethargy ​ lactic acidosis ·​ Nursing management/intervention ​ ABGs, Lactate, CBC, BMP, VO2, APTT ​ Oxygenation ​ Blood cultures ​ Fluids ​ Vaso Support ​ Mouth care (important cause most likely on vent) Shock ​ Shock - circulatory system is unable to supply adequate oxygen to tissues to meet the body’s basic metabolic needs. (i.e., inadequate perfusion). Can lead to systemic inflammatory response syndrome (SIRS) or multi-organ dysfunction syndrome (MODS). ​ Review stages of shock and symptoms ○​ 4 Stages of Shock and their S/S ​ Initial - hypoxia d/t decreased O2 delivery to cells. Clinical manifestations are minimal but cellular damage is occurring. ​ Subtle HR changes (slight increase) ​ Decreased cardiac output ​ Compensatory ​ Neural compensation ​ Endocrine compensation ​ Chemical compensation ​ Manifestations ○​ Tachycardia, tachypnea, low but normal BP with a narrow pulse pressure, decreased urine output ​ Progressive - failure of the compensatory mechanisms to maintain adequate blood pressure and fluid volume → extensive shunting of blood to vital organs (away from the periphery) ​ Manifestations: ○​ Profound hypoperfusion and hypotension ○​ Worsening metabolic acidosis  ○​ Respiratory acidosis ○​ electrolyte imbalance ​ Refractory - prolonged lack of perfusion → cell death → multisystem organ failure → irreversible ○​ Assessment: ​ CNS - restlessness, confusion, irritability, lethargy, and coma due to lack of O2 to the brain ​ Cardiovascular - hypotension, narrow pulse pressure (SBP and DBP are getting closer), tachycardia then bradycardia when no longer able to compensate, poor skin color, weak peripheral pulses, cap refill > 3 secs ​ Respiratory - tachypnea, ABGs (acidotic), low Spo2 ​ Renal - oliguria (< 20 ml/ hr or < 400 ml/day) then anuria, increased CR and BUN ​ GI - hypoactive bowel sounds, N/V ​ Labs ​ Acidotic ABG results ​ Low SVO2 ​ High lactate ​ H/H could be low depending on cause of shock (hypovolemic) ​ Elevated glucose due to elevated cortisol ​ Elevated CR/ BUN d/t poor kidney perfusion and resulting low urine output ​ AST/ ALT could be elevated bc low liver perfusion ​ Lactic dehydrogenase ​ Review the different types of shock, know the differences (such as patho, symptoms) between them, causes and treatment/ nursing management of each type of shock ○​ Hypovolemic Shock - caused by a loss of intravascular volume (dehydration, burns, or severe blood loss) that leads to hypoperfusion of organs and tissues. ​ Acute volume loss (due to either blood or fluids) results in reduced venous return, decreased stroke volume/ cardiac output, and thus decreased tissue perfusion. ​ S/S: restlessness, confusion, decreased urine output, pale cool clammy skin, weak pulses, hypotension, tachycardia, delayed cap refill, tachypnea, hyperventilation > respiratory alkalosis, hypoactive  bowel sounds d/t shunting of blood, and hyperglycemia d/t elevated cortisol caused by stress. ​ Medical Management: administer O2, fluid resuscitation with LR (unless they have a liver condition then NS), identification and treatment of underlying cause. ​ Labs: ABGs, SVO2, H/H, metabolic profile (CMP), CBC, and lactate ○​ Cardiogenic - Heart or “pump” failure. Decreased cardiac output results in hypotension and increased filling volumes → compensatory mechanisms increases vasoconstriction which increases SVR thus increasing myocardial workload. An ever-worsening cycle. ​ Risk factors: end stage heart failure, cardiomyopathy, HTN, DM, multi-vessel disease, acute vascular disease, MI ​ S/S: chest pain, diaphoresis, N/V, decreased cardiac output, hypotension, tachypnea, tachycardia, decreased LOC, decreased urine output, weak pulses, cool skin, hypoactive bowel sounds, metabolic acidosis ​ Medical Management/ Assessment: ​ ECG, cardiac enzymes (troponin, creatine kinase (CK), CK-MB), chest x-ray ​ airway/ oxygenation ​ Emergency revascularization (CABG), mechanical circulatory support (ECMO) ​ Vasopressors, inotropes (levophed, dobutamine, etc.) ​ Labs: ABGs, SVO2, CMP, lactate ○​ Obstructive - extracardiac disorders that impair ventricular filling/ emptying including cardiac tamponade, tension pneumothorax, or PE. ​ S/S: ALOC, decreased urine output, weak pulses, pale/ cool skin, decreased bowel sounds, chest pain, N/V, shortness of breath, hypotension, tachypnea, tachycardia ○​ Distributive ​ Neurogenic & Anaphylactic ○​ Patho for Neurogenic: SNS disruption ​ Decreased vascular tone, increased peripheral vascular volume, decreased venous return, decreased cardiac output d/t relative hypovolemia, unopposed PNS activity that has PROFOUND BRADYCARDIA, systemic hypoperfusion (hypotension)  ​ s/s: warm dry skin, flushed appearance, decreased cardiac output. ​ Tx: vasoactive meds, fluid resuscitation, atropine, transcutaneous/transvenous pacing, dobutamine, raise head of bed slowly d/t orthostatic hypotension ​ Nursing Dx: altered tissue perfusion ○​ Anaphylaxis ​ Patho: hypersensitivity reaction, histamine release, widespread vasodilation, increased cap permeability, smooth muscle contraction ​ Manifestations: SOB, tachypnea, wheezing, stridor, cyanosis, confusion, urticaria ​ Med mgmt: removal of trigger, epi, maintain airway, circulatory support. Give steroids and histamine in hospital ​ Nursing Dx: impaired gas exchange, impaired tissue perfusion ​ Labs to monitor ​ Review hemodynamic findings for each type of shock Hemodynamics (pg. 274) ​ Understand what information can be gathered from the various central lines ○​ Pulmonary artery catheter - a catheter placed in the pulmonary artery after passing through the RA and RV. ​ Measures right atrial pressure (RAP), pulmonary artery pressure (PAP), pulmonary arterial occlusion pressure (PAOP)/ pulmonary artery wedge pressure (PAWP), and cardiac output. It can also be used to draw SVO2 samples. ​ PAOP reflects left heart preload or the amount of blood in the left ventricle at the end of diastole, also referred to as left ventricular end-diastolic pressure. ​ RAP (right atrial pressure) is a reflection of right heart preload and right ventricular end-diastolic volume. ○​ Central Line/ Central Venous Catheter - a line placed in a vein that ends up at the superior vena cava immediately above the right atrium. ​ Central venous pressure (CVP) is measured using a central line. CVP, similar to right atrial pressure (RAP), is used as an estimate of volume returning to the right heart or right heart preload, or the right  ventricular end-diastolic volume. The CVP and RAP are typically the same or very similar. ○​ Arterial Line - a line typically placed in the radial artery used to continuously measure/ monitor blood pressure and have easily accessible arterial blood samples for ABGs. ​ General causes for when CVP, PA, PAOP are abnormally high/low (look at the chart). Hypovolemic Cardiogenic Obstructive Anaphylactic Neurogeni Early Septic Late septic Shock c ​ ↑ SVR ​ ↑ SVR ​ ↑ ​ ↓ SVR ​ ↓ ​ ↓ ​ Variable ​ ↓ CVP ​ ↑ CVP SVR ​ ↓ CVP SV SVR SVR & PAOP & ​ Varia & R ​ ↓ ​ Variable PAOP ble PAOP ​ ↓ CVP CVP & CVP CV & PAOP & P& PAOP PAO PA P OP ​ SVR is typically increased in hypovolemic, cardiogenic, and obstructive shock to help maintain blood pressure when there is a loss of blood ​ Decrease in CVP in hypovolemic shock means a significant amount of blood returning to the heart through the vena cava is reduced, leading to a lower pressure within the vena cava, which directly lowers CVP reading. ​ Decrease in PAOP in hypovolemic shock because of reduce venous return to the heart, leading to decrease in left ventricular filling pressure and essentially losing circulating blood volume due to blood loss or fluid depletion, resulting in a lower pressure within the pulmonary circulation CVP (Preload) Normal: 2-6 mmHg Abnormal low Abnormal High ​ Hypovolemia or peripheral ​ right heart failure, tension vasodilation pneumothorax, HTN, or pericardial tamponade Swan/ PA Cath PA: PAS 15-30 mmHg, PAD 4-12 mmHg Abnormal low Abnormal High ​ May be normal or signs ​ Pulmonary HTN, right heart failure Hypovolemia or peripheral vasodilation PCWP: (8-12 mm HG) Elevated: -​ Fluid overload -​ AS/AR -​ MS -​ LV Failure -​ Tamponade Decreased: -​ Hypovolemia -​ Vasodilation ​ Nurse management/considerations of the central lines ○​ Pulmonary catheter and how much do we fill the syringe to? ​ The tip of the balloon for PAOP is filled with 1.5 ml of air only, anymore risks rupturing the pulmonary artery. ○​ Arterial line Myocardial infarction ·​ Pathophysiology 1)​ Destruction of Heart Muscle from lack of oxygenated blood supply 2)​ Most common cause is atherosclerosis  ·​ Diagnostic tests: imaging, labs -​ Medical Management: 1)​ Troponin 2)​ CK 3)​ CK-MB 4)​ EKG (Diagnostics) 5)​ Stress Test (DIagnostics) 6)​ ECHO (DIagnostics) 7)​ Coronary Angiography (DIagnostics) ·​ Treatment options: pharmacological, reperfusion therapy, CABG o Know the differences between each treatment and the nursing management for each treatment -​ Complications:  1)​ If troponin is positive, Heart Attack (MI) PRIORITY = Remove the clot 2)​ Increase blood flow to cardiac tissue or reperfusion therapy -​ Maximize Oxygenation -​ Control Pain -​ Dilate Coronary Arteries -​ Prevent Clots -​ Decrease Myocardial Workload ​ Dysrhythmias prone first 48 hours -​ Nursing Management/Interventions: 1)​ Medications: (Stop using MONA to manage MI) -​ Oxygen -​ Nitroglycerin -​ Aspirin -​ Pain Medication -​ Antiplatelets and Antithrombotics are the main focus (ASA, Heparin, LMWH, Plavix) THROMBINS (Theophyllines, Heparin, RAAS drugs, Oxygen, Morphine, Beta blockers, intervention, Nitro, statins) -​ Surgical Management: 1)​ Coronary artery bypass graft: revascularization intervention that bypasses blockages in the coronary arteries causing myocardial muscle damage -​ Complications: 1)​ Heart Failure 2)​ Arrhythmias (Due to SA node dysfunction) Asystole, symptomatic bradycardia, heart block, and ventricular arrhythmias. -​ Nursing Interventions and Management: 1)​ LOC (Pupils, and responsiveness) 2)​ I and O 3)​ Skin color and temperature, pulses, edema, and capillary refill 4)​ Chest tube output, color, and volume 5)​ Labs, 6)​ BP 7)​ Fluids 8)​ Medication administration 9)​ Wound care  ·​ Teaching post MI -​ Signs of infection -​ Sternal precaution -​ Cardiac Rehabilitation Cardiomyopathy ·​ Review the various types of cardiomyopathy and clinical manifestations ·​ Be familiar with medications and their indications for cardiomyopathy Three different types: Dilated: Distended heart muscle Restrictive: Rock-hard heart muscle Hypertrophic: Huge trophy-like heart muscle Sxs: ​ Low oxygen ​ Restlessness, agitation, altered level of consciousness ​ Syncope, dizziness/ fatigue Heart failure signs: -​ Left side = lung fluid -​ Right sided = rocks the body with fluid (edema, ascites, JVD) Dilated cardiomyopathy -​ S3 murmur -​ Cardiomegaly (dilated heart) Restrictive Cardiomyopathy -​ Same general low oxygen & HF Hypertrophic cardiomyopathy -​ Typically asymptomatic (no s/s) until heavy exercises then the child DIES! Medication Goal -​ Treat the clinical manifestation -​ Prevent worsening of function -​ Reduce complication -​ ACE -​ ARB -​ Beta-blocker -​ CCB -​ SGLT2 -​ Mineralocorticoid receptor antagonist -​ Diuretics -​ Digoxin Surgical management: -​ Septal myectomy -​ Surgical ventricular remodeling -​ Transmyocardial revascularization -​ Left ventricular assist device -​ Heart transplant -​ Heart valve replacement may be done with these procedures (prosthetic vs mechanical) – lifetime warfarin Pacemaker intervention -​ Pacemaker and AICD can be combined into one device, referred to as a biventricular implantable cardioverter defibrillator Nursing DX: -​ Decreased cardiac output EKGs ·​ Be able to interpret rhythm strips ·​ Be familiar with interval ranges ECGs and ACLs Prep: -​ SA Node: 60 - 100 BPM -​ AV node in Right Atrium: 40 - 60 BPM -​ Purkinje Fibers: 15 - 40 BPM -​ P Wave: Contraction of the atria -​ QRS: Contraction of the ventricles -​ T Wave: Repolarization of the ventricles -​ U wave: repolarization of the Purkinje fibers (usually seen with electrolyte abnormalities -​ One small box = 0.04 seconds -​ One large box = 0.2 seconds -​ PR interval is usually 0.12 - 0.20 seconds (3 small boxes - 5 small boxes) -​ QRS interval is usually 0.06 - 0.10 seconds (1.5 - 3 small boxes) -​ QT Interval is usually equal to or less than 0.44 seconds (9 - 11 boxes) -​ Along the vertical axis, one small box = 0.1mV and one large box = 0.5mV Premature Atrial Contraction (PAC): -​ Rhythm is regular with premature beats -​ Rate is usually regular -​ P Waves are premature, differ in shape from sinus P waves, can be lost in T waves -​ PR interval is usually normal or prolonged -​ QRS usually normal Supraventricular Tachycardia (SVT): -​ Rhythm: regular -​ Rate: 150 - 200 BPM -​ P waves differ from sinus P waves and may be hidden in T waves -​ PR interval is difficult to measure; can be shorter or longer than usual -​ QRS us 0.12 seconds or less Atrial Flutter (A Flutter): -​ Atrial rate: 250 - 350 BPM -​ P waves: no identifiable P waves -​ PR interval: unable to measure -​ QRS Complex: usually normal -​ Seesaw tooth pattern Atrial Fibrillation (A fib): -​ Rhythm: Ventricular rhythm is usually irregularly irregular -​ Atrial rate 400 - 600 BPM -​ P waves: no identifiable P waves -​ PR interval is not measurable -​ QRS duration: usually normal Junctional Rhythm: -​ The AV node is now pacing the heart and the impulse must travel backward to activate the atria -​ Rate is normal or irregular depending on the underlying rhythm -​ P waves are absent, inverted before the QRS, or inverted after the QRS -​ If p waves are present, the PR interval is usually normal -​ QRS complexes are usually normal Premature ventricular complexes: -​ Rhythm is regular with premature beats -​ Rate is usually within range1 -​ P waves are usually absent or appear after the QRS complex -​ PR interval: none -​ QRS duration: 0.12 seconds or greater, wide Ventricular Tachycardia: -​ Ventricular rhythm is essentially regular -​ Rate: 101 - 250 bpm -​ P waves: absent -​ PR interval: None -​ QRS: 0.12 sec or greater Ventricular Fibrillation (V fib) -​ Rhythm: rapid, chaotic, no pattern -​ Rate: cannot be determined -​ P waves: absent -​ PR interval: none -​ QRS complex duration: unable to determine Asystole: -​ Absence of ventricular electrical activity -​ No pulse, start cpr Cardioversion: -​ Synchronized shock delivered only during the R-wave of the QRS complex -​ Lower amount of energy needed -​ Patient’s are stable (ex: A-fib) Defibrillation: -​ Asynchronous shocks done with an automated external defibrillator -​ Higher amount of energy required -​ Unstable patients. (ex: V tach or V fib) Heart Blocks: -​ Electrical activity in the heart slows through the AV node, making the area vulnerable to blocks in conduction -​ AV blocks occur when a delay or interruption in impulse conduction occurs from the atria to ventricles -​ There are 1st Degree, 2nd Degree, and 3rd Degree type blocks 1st Degree Blocks: -​ Due to a conduction delay in the AV node -​ All components of the cardiac cycle are WNL but the PR interval is longer than usual (> 0.20 sec) -​ “Husband is constantly late” 2nd Degree Mobitz (Type) 1 Block: -​ One or more but not all sinus impulses are blocked from reaching the ventricles -​ P Waves occur at regular intervals across the rhythm but not every P wave will be followed a QRS Complex -​ So you have more P waves than QRS complexes -​ “Husband comes later and later until one day he doesn't come” -​ Longer longer than you have a wenckebach 2nd Degree Mobitz (Type) II: -​ One or more but not all sinus impulses are blocked from reaching the ventricles -​ P waves occur at regular intervals across the rhythm but not every P wave will be followed by a QRS complex -​ Conduction delay occurs below the AV node -​ “Randomly dropped QRS”  3rd Degree Heart Block: -​ There is a complete block in conduction of impulses between the atria and ventricles -​ A junctional or ventricular pacemaker takes over QRS and may be normal or wide -​ Not compatible with life, This is an emergency -​ “Divorce, Atria does its own thing and ventricle does its own things” COPD possible case study?