Nursing 4N15/313 Final_Exam_STUDY GUIDE,100% CORRECT

F&E  10 IV fluid and electrolyte replacement - Type of Solution According to Concentration o Hypotonic Solution  solution of lower osmotic pressure that regularly gives up fluid and water o Hypertonic Solution  solution with higher osmotic pressure  Osmotic pressure  the amount of pressure required to stop the osmotic flow of water; drawing power of a solution - Isotonic Solution  solution of the same osmotic pressure; does not cause any molecule movement or shift of fluid o Hypotonic  provides more water than electrolytes, diluting the ECF.  Osmosis produces a movement of water from the ECF to the ICF  Although 5% dextrose in water is considered isotonic, the dextrose is quickly metabolized, and the net result is the administration of free water (hypotonic)  Do not give to pts with increased ICP – head trauma, CVA, or neuro surgery  Do not give to pts with third spacing  burn pts (swells more), ascites (low albumin  no oncotic pressure to hold fluids in) - Isotonic  expands only ECF o Ideal fluid replacement for a pt with an ECF volume deficit o Ex: LR  contains sodium, potassium, chloride, calcium, and lactate (the precursor of bicarbonate) in about the same concentrations as those of the ECF  Contraindicated in the presence of lactic acidosis because of the body’s decreased ability to convert lactate to bicarbonate o Monitor for signs of fluid overload  #1 is pulmonary edema o Be careful giving to CHF or HTN pts o Don’t give to pts with pH greater than 7.5 o Don’t give LR to pts with liver disease  they can’t metabolize lactate o D5W  don’t give to pts with increased ICP – water causes swelling - Hypertonic  initially raises the osmolality of ECF and expands it o Useful in treatment of hypovolemia and hyponatremia o The higher osmotic pressure draws water out of the cells into the ECF o Increased risk of intravascular fluid volume excess  monitor BP, lung sounds, and serum sodium levels frequently o Do not give in any condition that may cause cellular dehydration  diabetes How does F&E replacement therapy relate to various dx?  i.e. diabetes, SIADH - Diabetes  F&E can be approached from different ways o Elevated Glucose causes osmotic diuresis  increased blood osmolality  decreased Potassium, Sodium, and Phosphorus o This F&E imbalance is dangerous because it can lead to Anuria, Shock, and Death due to severe dehydration (Fluid Volume Deficit) o For Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Non-Ketotic Syndrome  If blood sugar is over 250 mg/dl  start IV 0.45%-0.9% Normal Saline • 0.45% NS can be used to help re-hydrate the cells if severely dehydrated, as well as help uptake Insulin upon IV administration. • 0.9% NS can also be used to ensure equal flow between ICF, and ECF  IV Regular Insulin can be administered • Early potassium replacement is essential because hypokalemia is significant cause of unnecessary and avoidable death during treatment of DKA. o Potassium is initially high, but decreases rapidly once therapy starts as insulin drives potassium into the cells, leading to life-threatening hypokalemia • Potassium replacement is also indicated for HHNS, but not as dire as DKA (according to the book)  If blood sugar does return below 250 mg/dl • D5 0.45% NS or D5 0.9% NS can be given to prevent further cellular uptake of serum glucose (hypoglycemia) - Syndrome of Inappropriate Anti-Diuretic Hormone  ADH is increased  Fluid Retention (Dilutional Na factor) o Treatment  IV hypertonic solution (3-5% Normal Saline), administer very slowly via pump, if serum sodium is less than 120 mEq/L with neurologic symptoms  Hypertonic decreases tonicity of cells by DRAWING FLUID OUT  A diuretic then can help excrete the fluid drawn out from these cells o DO NOT GIVE IV FLUIDS WITH WATER  Can cause Water Intoxication - Diabetes Insipidus  Hyposecretion of ADH  Kidneys fail to reabsorb water o Treatment  Give IV hypotonic solution (0.45% NS or D5W)  0.45% Normal Saline draws fluid into the cell, preventing cellular dehydration  Dextrose 5% in Water—Needed primarily as a source of WATER replacement • Remember, once the body utilizes the Dextrose (Glucose), the solution goes from ISOTONIC to HYPOTONIC!  Drawing fluid into cells - Addison’s Disease  Low Aldosterone  Low Sodium  High Potassium o Fluid replacement (large volume of 0.9% saline solution)—because of dehydration/shock-like state  5% dextrose can also be given if blood sugar is really low Assessment findings overhydration or dehydration - Fluid Volume Deficit  can occur with abnormal loss of body fluids (i.e. diarrhea, fistula, drainage, hemorrhage, polyuria), inadequate intake, or a plasma-to-interstitial fluid shift o NOT dehydration (dehydration refers to loss of pure water alone without corresponding loss of sodium) o Decrease in circulating blood volume  decrease in BP o Treatment goal  correct underlying cause and replace both water and any needed electrolytes  Balanced IV solutions  Lactated Ringers  NS is used when rapid volume replacement is needed  Blood is indicated when deficit is due to blood loss o Causes:  Increased insensible water loss or perspiration, DI, osmotic diuresis, hemorrhage, vomiting, NG suction, diarrhea, fistula drainage, overuse of diuretics, inadequate fluid intake, third-space fluid shifts (burns, intestinal obstruction)  Manifestations: • Restlessness, drowsiness, lethargy, confusion, thirst, dry mouth, decreased skin turgor, decreased cap refill, postural hypotension, increased pulse/CVP, decreased urine output, concentrated urine, increased RR, weakness, dizziness, weight loss, seizures, coma - Fluid Volume Excess  may result from excessive intake of fluids, abnormal retention of fluids (i.e. heart failure, renal failure), or interstitial-to-plasma fluid shift o Treatment goal  removal of fluid without producing abnormal changes in the electrolyte composition or osmolality of ECF  Diuretics and fluid restriction  Restriction of sodium intake o Causes:  Excessive isotonic or hypotonic fluids, heart or renal failure, primary polydipsia, SIADH, cushing syndrome, long-term use of corticosteroids o Manifestations:  Headache, confusion, lethargy, peripheral edema, distended neck veins, bounding pulse, increased BP, increased CVP, polyuria (normal renal fxn), dyspnea, crackles, pulmonary edema, muscle spasms, weight gain, seizures, coma Review how effects of protein on F&E balance or imbalance - Oncotic Pressure  osmotic pressure from colloids in a solution o The major colloid in the vascular system contributing to the total osmotic pressure is protein  Protein molecules attract water, pulling fluid from the tissue space to the vascular space o The large molecular size prevents proteins from leaving the vascular space through pores in the capillary walls o Under normal conditions, plasma oncotic pressure is approximately 25 mmHg o Some proteins are found in the interstitial space, they exert oncotic pressure of approximately 1 mmHg - Common Scenario o If there is low Albumin  There is Low Protein  Low oncotic pressure in the vascular space  Fluid seeps out into the interstitial spaces  EDEMA Relate pulmonary congestion in HF to F&E status of a patient - Left-Sided Heart Failure  low ejection fraction allows buildup of fluids in the pulmonary circuit (Excess of ECF) o Excess ECF results in pulmonary congestion and pulmonary edema as increased hydrostatic pressure in the pulmonary vessels forces fluid into the alveoli o Patient will experience shortness of breath, irritative cough, and moist crackles on auscultation o The patient will also demonstrate increased respiratory rate due to decreased issue perfusion and resultant hypoxia o Fluids needs to be replaced to due insensible water loss from tachypnea - Suggested interventions o FLUID RESTRICTION, unless patient has signs of dehydration from insensible water loss o Reduce Sodium intake Nursing care R/T congestion or edema formation - Nursing Therapeutics/Plan of Care o Daily weight taking  early morning, same type of clothing, same weighing scale o Strict I&O (i.e. CHF) – weight after urination and before defecation  Why?  Whatever is in the bladder is not part of your fluids  the bladder is a reservoir. However, the fluid in your stool is reabsorbed. o Enteral replacement of F&E loss  GI, oral fluids, g-tube o Fluid Restriction vs. increase fluid intake  if restriction, divide fluid throughout the day (more should be given throughout day rather than at night when pt is sleeping).  Increase in fluids  monitor for signs of retention • Ex: hx of MI – monitor pulmonary edema  backs up system and causes less cardiac output. Assess for crackles! o Parenteral replacement of F&E  IV fluids o Medication  lasix  Lasix - increase potassium rich foods  Spironolactone – watch potassium rich foods  Potassium sparing  HR, ECG  increase HR, irregularities (arrhythmia could be indicator)  Potassium wasting  slow HR o I&O Monitoring Review concept of isotonic vs hypotonic imbalances – nursing care and assessment - Fluid Volume Deficit o Isotonic Dehydration  Water and dissolved electrolytes are lost in equal proportions  Known as hypovolemia, isotonic dehydration is the most common type of dehydration  Isotonic dehydration results in decreased circulating blood volume and inadequate tissue perfusion  Causes • Inadequate intake of fluids and solutes • Fluid shifts between compartments • Excessive losses of isotonic body fluids o Hypotonic Dehydration  Electrolyte loss exceeds water loss  Clinical problems that occur result form fluid shifts between compartments, causing a decrease in plasma volume  Fluid moves from the plasma and interstitial fluid spaces into the cells, causing a plasma volume deficit and causing the cells to swell  Causes • Chronic illness • Excess fluid replacement • Renal failure • Chronic malnutrition o Assessment  Cardio—Thready, increased pulse rate, decreased blood pressure, orthostatic hypotension, flat neck and hand veins in dependent positions, diminished peripheral pulses  Respiratory—Increased rate and depth of respirations  Neuromuscular—Decreased central nervous system activity from lethargy to coma, fever  Renal—Decreased urinary output, increased urinary specific gravity  Integumentary—Dry skin, Poor turgor, tenting present, dry mouth  Gastrointestinal—Decreased motility and diminished bowel sounds, constipation, thirst, decreased body rate  HYPOTONIC DEHYRATION—Skeletal Muscle Weakness  Laboratory Findings—Increased serum osmolality, increased hematocrit, increased blood urea nitrogen level, increased serum sodium level o Interventions  Monitor cardiovascular, respiratory, neuromuscular, renal, Integumentary, and gastrointestinal status  Prevent further fluid losses and increase fluid compartment volumes to normal ranges  Provide oral rehydration therapy if possible and IV fluid replacement if the dehydration is severe; monitory intake and output  Generally, isotonic dehydration is treated with isotonic fluid solutions, hypertonic dehydration with hypotonic fluid solutions, and hypotonic dehydration with hypertonic fluid solutions  Administer medications as prescribed such as antidiarrheal, antimicrobial, antiemetic, and anitpyretic medications, to correct the cause and treat any symptoms  Monitor electrolyte values and prepare to administer medication to treat an imbalance, if present - Fluid Volume Excess o Isotonic Overhydration  Known as hypervolemia, isotonic overhydration results form excessive fluid in the extracellular fluid compartment  Only the extracellular fluid compartment is expanded, and fluid does not shift between extracellular and intracellular compartments  Isotonic overhydration causes circulatory overload and interstitial edema; when sever or when it occurs in a client with poor cardiac function, congestive heart failure and pulmonary edema can result  Causes • Inadequately controlled IV therapy • Renal Failure • Long-term corticosteroid therapy o Hypotonic Overhydration  Hypotonic overhydration is known as water intoxication  The excessive fluid moves into the intracellular space, and all body fluid compartments expand  Electrolyte imbalances occur as a result of dilution  Causes • Early renal failure • Congestive heart failure • Syndrome of inappropriate antidiuretic hormone secretion • Inadequately controlled IV therapy • Replacement of isotonic fluid loss with hypotonic fluids • Irrigation of wounds and body cavities with hypotonic fluids o Assessment  Cardio—Bounding, increased pulse rate, elevated BP, Distended neck and hand veins, elevated central venous pressure  Respiratory—Increased respiratory rate, dyspnea, moist crackles on auscultation  Neuromuscular—Altered LOC, headache, visual disturbances, skeletal muscle weakness, paresthesias  Integumentary—pitting edema in dependent areas, skin pale and cool to touch  Increased motility in GI tract  Isotonic overhydration results in liver enlargement and ascites  Hypotonic overhydration results in the following • Polyuria • Diarrhea • Nonpitting edema • Dysrhythmias • Projectile Vomiting  Laboratory findings • Decreased serum osmolality, decreased hematocrit, decreased BUN level, Decreased serum sodium level, Decreased urine specific gravity o Interventions  Monitor CV, resp, neuromuscular, renal, Integumentary, and GI status  Prevent further fluid overload, and restore normal fluid balance  Administer diuretics; osmotic diuretics typically are prescribed first to prevent sever electrolyte imbalances  Restrict fluid and sodium intake  Monitor intake, output, and weight  Monitor electrolyte values, and prepare to administer medication to treat imbalances Hypo and hyper focusing on potassium and sodium  understand assessment related to nursing care - Sodium  90% contained in ECF; main concern is water regulation o Function  main cation of the ECF and plays a major role in maintaining the concentration and volume; primary determinant of ECF osmolality o Also important in the generation and transmission of nerve impulses and the regulation of acid-base balance o Normal value  135-145 meq/L o Changes in the serum sodium level may reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two. - Hypernatremia  causes hyperosmolality resulting in a shift of water out of the cells leading to cellular dehydration o Caused by excessive sodium intake o IV Fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarb o Hypertonic tube feedings without water supplements o Near-drowning in salt water o Inadequate water intake  unconscious or cognitively impaired individuals o Excessive water loss  increased insensible water loss (high fever, heatstroke, prolonged hyperventilation), osmotic diuretic therapy, diarrhea o Disease states  diabetes isipidus, primary hyperaldosteronism, Cushing syndrome, uncontrolled DM o Manifestations: dehydration of cells (especially seen in brain cells)  Decreased ECF Volume  restlessness, agitation, twitching, seizures, coma, intense thirst; dry, swollen tongue, sticky mucous membranes, postural hypotension, decreased CVP, weight loss, weakness, lethargy  Normal or Increased ECF Volume  restlessness, agitation, twitching, seizures, coma, intense thirst, flushed skin, weight gain, peripheral and pulmonary edema, increased BP, increased CVP - Hyponatremia  hyponatremia causes hypoosmolality with a shift of water into the cells o Caused by excessive sodium loss o GI losses: diarrhea, vomiting, fistulas, NG suction o Renal losses: diuretics, adrenal insufficiency, sodium wasting renal disease o Skin losses: burns, wound drainage o Inadequate sodium intake: fasting diets o Excessive water gain: excessive hypotonic IV fluids, primary polydipsia o Disease states: SIADH, heart failure, primary hypoalsodteronism o Manifestations: cellular swelling and first manifested in CNS  Decreased ECF volume  irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma, dry mucous membranes, postural hypotension, decreased CVP, decreased JV filling, tachycardia, thready pulse, cold and clammy skin  Normal or Increased ECF volume  headache, apathy, confusion, muscle spasms, seizures, coma, nausea, vomiting, diarrhea, abdominal cramps, weight gain, increased BP, increased CVP - Potassium  main electrolyte intracellularly – 98% o Function  critical for many cellular metabolic functions; neuromuscular and cardiac function, also regulates intracellular osmolality and promotes cellular growth o Normal Value  3.5-5.0 meq/L o 90% of potassium intake is eliminated by the kidneys  if kidney function is significantly impaired, toxic levels of potassium maybe retained o Potassium moves into cells during the formation of new tissues and leaves the cell during tissue breakdown - Hyperkalemia  increased cellular excitability o Caused by:  Excessive potassium intake  excessive or rapid parenteral administration, potassium-containing drugs, potassium-containing salt substitute  Shift of potassium out of cells  acidosis, tissue catabolism (fever, sepsis, burns), crush injury, tumor lysis syndrome  Failure to eliminate potassium  renal disease, potassium-sparing diuretics, adrenal insufficiency, ACE inhibitors (these drugs reduce the kidney’s ability to excrete potassium)  Can also be caused by giving expired blood (hemolysis) o Manifestations: Initially pt may experience cramping leg pain followed by weakness or paralysis of skeletal muscles  Irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyperkalemia sudden or severe  ECG changes  tall, peaked T wave, prolonged PR interval, ST segment depression, loss of P wave, widening QRS, V fib, ventricular standstill - Hypokalemia  decreased cellular excitability o Caused by:  Potassium loss  GI losses (diarrhea, vomiting, fistulas, NG suction), renal losses (diuretics, hyperaldosteronism, magnesium depletion), skin losses (diaphoresis), dialysis  Shift of potassium into cells  increased insulin, alkalosis, tissue repair, increased epinephrine  Lack of potassium intake  starvation, diet low in potassium, failure to include potassium in parenteral fluids if NPO o Manifestations:  Fatigue, muscle weakness, leg cramps, N/V, paralytic ileus, soft, flabby muscles, paresthesias, decreased reflexes, weak, irregular pulse, polyuria, hyperglycemia  ECG changes  ST segment depression, flattened T wave, presence of U wave, ventricular dysrhythmias, bradycardia, enhanced digitalis effect Perioperative Nursing  7 or less Review nursing responsibility r/t preoperative meds (sedatives, narcotics, etc)  nursing care as well as legal implication - Informed Consent  an active, shared decision-making process between the provider and the recipient of care o Voluntary and written for non-emergency surgery o Needed when:  Invasive procedure  Requiring sedation  Have more than a slight risk  injections  Involving radiation  may damage healthy tissue  Emancipated minor  Surgeon may operate for life saving reasons or measures - Three conditions must be met for consent to be valid: o There must be adequate disclosure of the diagnosis; the nature and purpose of the proposed treatment; the risks and consequences of the proposed treatment; the probability of a successful outcome; the availability, benefits, and risk of alternative treatments; and the prognosis if treatment is not instituted o The patient must demonstrate clear understanding and comprehension of the information being provided before receiving sedating preoperative medications o The recipient of care must give consent voluntarily  they must not be persuaded or coerced in anyway - If the pt is unclear about operative plans, the nurse should contact the surgeon about the pts need for additional information - Consent, even when signed, can be withdrawn at any time if the desire to give permission for the procedure changes - If pt is a minor, unconscious, or is mentally incompetent to sign the permit, the written permission may be given by a legally appointed representative or responsible family member - Immediate medical treatment needed and pt unable to give consent  next of kin may give consent o Next of kin impossible to reach?  the physician may institute treatment without consent, but an incident report must be written up because it is an occurrence that is inconsistent with routine facility operations - Preoperative Teaching o Deep breathing/incentive spirometry  oxygenation promotes wound healing o Mobility and active body movement  early ambulation o Pain management  pain scale o Cognitive coping  distraction to guided imagery - Maintaining Safety - Managing Nutrition and Fluids  IV access, patent - Preparing the bowel - Preparing the skin  decrease bacteria during surgery; hair is not removed unless around incision site o We don’t shave or prepare the whole region, only the surgical site  knicks from shaving can cause infection o **Check allergies to iodine and betadine - Done a few hours before surgery - Preop checklist procedure  change pt to hospital gown, obtain baseline VS, remove any metals, cover pts hair with surgical cap, no jewelry, all pts should void - Administering preanesthetic agent  45-75 minutes before induction of anesthetic –promotes effects of anesthesia and decreases anxiety - Maintaining preop record  checklist, consent, and labs should be sent with patient to OR - Transport to presurgical area  keep pt warm - Attend to family needs - Focus on  proper ID of pt (name, allergies, site) - If pt doesn’t want to take wedding band off, put tape around the ring to reduce infection - Preanesthetic agent  decreases secretions - Consent is signed before pre-anesthetic agent is given - Pre-op on call  wait for surgeon to tell you when to give it Review surgical aseptic technique  be able to apply it to a situation - All materials that enter the sterile field must be sterile. - If a sterile item comes in contact with an unsterile item, it is contaminated. - Contaminated items should be removed immediately from the sterile field. - Sterile team members must wear only sterile gowns and gloves; once dressed for the procedure, they should recognize that the only parts of the gown considered sterile are the front from chest to table level and the sleeves to 2 inches above the elbow. - A wide margin of safety must be maintained between the sterile and unsterile fields. - Tables are considered sterile only at tabletop level; items extending beneath this level are considered contaminated. - The edges of a sterile package are considered contaminated once the package has been opened. - Bacteria travel on airborne particles and will enter the sterile field with excessive air movements and currents. - Bacteria travel by capillary action through moist fabrics and contamination occurs. - Bacteria harbor on the patient's and the team members’ hair, skin, and respiratory tracts and must be confined by appropriate attire. - Gowns are considered sterile in front from chest to level of the sterile field - Sterile drapes are used to create a sterile field - Moisture makes the sterile field unsterile Review perioperative nursing roles The Surgical Team - The Patient - Circulating Nurse  monitors pt safety, infection control, verifies consent, supplies and equipment, proper documentation o Reviews anatomy, physiology, and the surgical process o Assists with preparing the room. o Practices aseptic technique in all required activities. o Monitors practices of aseptic technique in self and others. o Ensures that needed items are available and sterile (if required). o Checks mechanical and electrical equipment and environmental factors. o Identifies and admits the patient to the OR suite. o Assesses the patient's physical and emotional status. o Plans and coordinates the intraoperative nursing care. o Checks the chart and relates pertinent data. o Admits the patient to the operating room suite. o Assists with transferring the patient to the operating room bed. o Ensures patient safety in transferring and positioning the patient. o Participates in insertion and application of monitoring devices. o Assists with the induction of anesthesia. o Monitors the draping procedure. o Documents intraoperative care. o Records, labels, and sends to proper locations tissue specimens and cultures. o Measures blood and fluid loss. o Records amount of drugs used during local anesthesia. o Coordinates all activities in the room with team members and other health-related personnel and departments. o Counts sponges, needles, and instruments. o Accompanies the patient to the postanesthesia recovery area. o Reports information relevant to the care of the patient to the recovery area nurses. - Scrub Nurse  sterile nurse, responsible for maintaining sterile field, sets up sterile table, counts for instruments and gauze before surgery, during, and before closure o Reviews anatomy, physiology, and the surgical procedure. o Assists with preparation of the room. o Scrubs, gowns, and gloves self and other members of the surgical team. o Prepares the instrument table and organizes sterile equipment for functional use. o Assists with the draping procedure. o Passes instruments to the surgeon and assistants by anticipating their needs. o Counts sponges, needles, and instruments. o Monitors practices of aseptic technique in self and others. o Keeps track of irrigation solutions used for calculation of blood loss. o Reports amounts of local anesthesia and epinephrine solutions used by ACP and/or surgeon. - Surgeon  responsible for entire surgery and site o Primarily responsible for:  Preoperative medical history and physical assessment, including need for surgical intervention, choice of surgical procedure, management of preoperative workup, and discussion of the risks and alternatives to surgical intervention  Patient safety and management in the OR  Postoperative management of the patient - RNFA (RN First Assistant)  assists surgeon in handling tissue, responsible for providing good visualization of surgical site, can do suturing - Anesthesiologist  captain of surgery o Medical management of patients who are rendered unconscious and/or insensible to pain and emotional stress during surgical, obstetric, and certain other medical procedures o Protection of life functions and vital organs under the stress of anesthetic, surgical, or other medical procedures o Management of problems in pain relief o Management of cardiopulmonary resuscitation o Management of problems in pulmonary care o Management of critically ill patients in special care units - CRNA o Performing and documenting a preanesthetic assessment and evaluation o Developing and implementing an anesthetic plan o Selecting and initiating the planned anesthetic technique o Selecting, obtaining, and administering the anesthesia, adjuvant drugs, accessory drugs, and fluids o Selecting, applying, and inserting appropriate noninvasive and invasive monitoring devices o Managing a patient's airway and pulmonary status o Managing emergence and recovery from anesthesia o Releasing or discharging patients from a postanesthesia care area o Ordering, initiating, or modifying pain relief therapy o Responding to emergency situations by providing airway management, administering emergency fluids, and/or emergency drugs o Additional responsibilities within the expertise of the individual Priority nursing action related to assessment findings PACU - Pt may remain in PACU for 4-6 hours - VS q15 min - Nurse should anticipate type of surgery, anesthesia, and pt needs - Soft colored lighting - Nurse should be good w/ physical exam – know s/s - Nurse should also be ready for any emergency including intubation - Goals: o Recovery from effects of anesthesia o Resumption of motor/sensory function o Stabilize VS o Prevention of Hemorrhage/ other complications Postoperative Interventions - Assess the patients general condition  VS, O2 sat, LOC, response to command, surgical site, monitoring for bleeding, IV fluids, and medication administration - Maintain Patent Airway  prevent hypoxemia, tongue can be cause of obstruction, proper head positioning, check gag reflex - Maintain Cardiovascular Stability  check VS, assess mental status, pts temp of skin and color, urine output - Know pts history  chronic illness, hx of seizures Complications: - Shock/Hypotension  d/t blood loss - Hemorrhage - HTN  sympathetic stimulation secondary to pain – increases BP. A distended bladder can also cause sympathetic stimulation - Dysrhythmias  can be due to electrolyte imbalance - Relieve pain/anxiety  give analgesics - Controlling N/V  administer meds such as zofran, reglan, phenergan - Four W’s: o Wind  prevent respiratory complications o Wound  infection o Water  dehydration o Walk  thrombophlebitis - Four P’s: o Pain o Pallor o Paresthesia o Pulse Cardiac  10 or more Review on nitroglycerin administration nursing care and prioritizing of nursing action - Nitrates  can give max of 3 times in 5 minute intervals o Sublingual  relieve pain in 3 minutes and last 30-60 minutes (20-45 minutes stated in class) o Nitroglycerin Ointment  3-6 hour prophylaxis o Transdermal controlled  maintains steady plasma levels within the therapeutic range during 24 hours o Long-Acting Nitrates o IV nitroglycerin o Take prophylactic nitrate 5-10 minutes before activity  r/t supply and demand o Nitrates dilate peripheral blood vessels and dilate coronary arteries and collateral vessels ECG for arrhythmia  be familiar with tracings and characteristics ECG Review - P  begins with the firing of the SA node and represents depolarization of the fibers of the atria (atrial contraction) o Duration </= 0.12 seconds o Amplitude < 2.5 mm (1 box height wise = 1 mm) - QRS  represents depolarization from the AV node throughout the ventricles (ventricular contraction) o A deep Q wave that can be measured, can be indicative of an MI o Duration 0.06-0.10 seconds (some books say 0.12) - There is a delay of impulse transmission through the AV node that accounts for the time interval between the end of the P wave and the beginning of the QRS wave - T  represents repolarization of the ventricles (relaxation) o Tall peaked T wave can be a sign of hyperkalemia - Big Box  used in measurment = 5 mm = 0.20 seconds - Little Box  single square = 1 mm = 0.04 sec - PR Interval  beginning of P wave to beginning of Q drop atrial contraction o Duration 0.12-0.20 seconds Steps for ECG Interpretation - Determine the rate o Take 6 second method and multiply by 10  6 big boxes in 6 seconds o 300, 150, 100, 75, 60, 50 method  need regular rate (count big box lines between QRS from peak to peak) - Determine the rhythm o Regularity or irregularity of impulses o Are the P and ORS waves spaced equally? o QRS should be narrow o Irregularly irregular rhythm = atrial fibrillation o Ventricular fib never produces a pulse o Anatomical source (SA or ectopic origin)  Are P waves present?  Are QRS complexes present?  Are the P waves related to the QRS complexes? • The P waves before the QRS • The P waves in the same direction as QRS o Generally the QRS is narrow Determining Source - Normal Sinus Rhythm has… o Rate of 60-100 BPM o Rhythm is regular (for P & QRS waves) o P wave before every QRS complex o P waves are all upright and equal in shape o P waves are same direction as QRS o P equal distance between QRS o QRS is narrow - Sinus Bradycardia has… o Rate of < 60 BPM o Rhythm is regular (for P & QRS waves) o P wave before every QRS complex o P waves are all upright and equal in shape o P waves are same direction as QRS o P equal distance between QRS o QRS is narrow - Sinus Tachycardia has… o Rate of > 100 BPM o Rhythm is regular (for P & QRS waves) o P wave before every QRS complex o P waves are all upright and equal in shape o P waves are same direction as QRS o P equal distance between QRS o QRS is narrow Junctional Rhythm - Refers to dysrhythmias that originate in the area of the AV node, primarily because the SA node has failed to fire or the signal has been blocked - Produces an abnormal P wave occurring just before or after the QRS complex or that is hidden in the QRS complex Atrial Flutter - An atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter (F) waves that orginate from a single ectopic focus in the RA - Rhythm is regular with a rate around 110 BPM - Irregularly regular  fires in sequence Atrial Fibrillation - Characterized by total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction - Irregularly Irregular rhythm  P waves are constantly irregular/chaotic Ventricular Tachycardia - Results from abnormal tissues in the ventricles generating a rapid and irregular heart rhythm. - Occurs when an ectopic focus or foci fire repetitively and the ventricle takes control as the pacemaker - Poor cardiac output is usually associated with this rhythm thus causing the pt to go into cardiac arrest. - Shock this rhythm if the patient is unconscious and without a pulse Ventricular Fibrillation - Disorganized electrical signals causes the ventricles to quiver instead of contract in a rhythmic fashion. - No effective contraction or CO occurs - A patient will be unconscious, as blood is not pumped to the brain. Immediate treatment by defibrillation is indicated. - This condition may occur during or after a myocardial infarct. Asystole - Represents the total absence of ventricular electrical activity - No ventricular contraction occurs because depolarization doesn’t occur - Pts are pulseless, unresponsive, and apneic Premature Ventricular Contractions - A contraction originating in an ectopic focus in the ventricles - Premature occurrence of a QRS complex  wide, distorted in shape - Mutifocal PVC  initiated from different foci and appear different in shape - Unifocal PVC  have the same shape - Ventricular Bigeminy  every other beat is a PVC - Ventricular Trigeminy  every third beat is a PVC - Couplet  two consecutive PVCs - V Tach  three or more PVCs First Degree Heart Block - Caused by a conduction delay through the AV node but all electrical signals reach the ventricles. - Every impulse is conducted to the ventricles but the duration of AV conduction is prolonged - The PR interval is prolonged to more than 0.20 second Second Degree Type II Heart Block - A P wave is nonconducted without progressive antecedent PR lengthening - A certain number of impulses from the SA node are not conducted to the ventricles - The QRS complex is almost always more than 0.12 second because of bundle branch block Third Degree AV Block - 3rd degree block or complete heart block occurs when atrial contractions are 'normal' but no electrical conduction is conveyed to the ventricles. - The ventricles then generate their own signal through an 'escape mechanism' from a focus somewhere within the ventricle. The ventricular escape beats are usually 'slow' Atrial fibrillation  assessment, nursing care, and complications - Assessment o EKG  Multiple rapid impulses from many foci depolarize in the atria at a totally disorganized manner at 350-600 beats per minute (atrial pulse)  The atria quiver, which can lead to the formation of THROMBI  No definitive P wave can be observed, only fibrillatory waves before each QRS o Occurs in patients with underlying heart disease such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis o Caused by thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery - Nursing Care o Administer Oxygen o Administer Anticoagulants as prescribed because the risk of emboli  An example is WARFARIN o Administer cardiac medications as prescribed to control the ventricular rhythm and assist in the maintenance of cardiac output  An example is AMIODARONE o Prepare the client for cardioversion as prescribed  If patient has had A-fib for more than 48 hours, anti-coagulation therapy is recommended for at least 3-4 weeks or 4-6 weeks after last successful cardioversion - Complications o Atrial fibrillation can cause decreased Cardiac Output  blood stasis o Blood Stasis  Thrombi formation o An embolized clot can developed and get lodged into the brain  STROKE Understand development of CHF Risk Factors of CHF - CAD - Advancing Age - HTN (major contributing factor) - DM - Obesity - High serum cholesterol - May be caused by any interference with the normal mechanisms regulating CO - CO depends on preload, afterload, myocardial contractility, HR, and metabolic state of the individual  any alteration in these factors can lead to decreased ventricular function and the resultant manifestations of HF Pathophysiology - Pathology of Ventricular Failure o Systolic Failure  most common cause of HF; results from the inability of the heart to pump blood  A defect in the ability of the ventricles to contract (pump)  LV loses its ability to generate enough pressure to eject blood forward through the aorta  over time, the LV becomes thin walled, dilated, and hypertrophied  Hallmark  decreased in LV ejection fraction (the percentage of total ventricular filling volume that is ejected during each ventricular contraction)  Caused by  impaired contractile function (MI), increased afterload (HTN), cardiomyopathy, and mechanical abnormalities (valvular heart disease). o Diastolic Failure  impaired ability of the ventricles to relax and fill during diastole  20-40% of pts have diastolic failure with a normal EF and systolic function  Decreased filling of the ventricles will result in decreased SV and CO  Diastolic failure is characterized by high filing pressures due to stiff or noncompliant ventricles and results in venous engorgement in both the pulmonary and systemic vascular systems  Dx of DF is made on the basis of the presence of pulmonary congestion, pulmonary HTN, ventricular hypertrophy, and normal EF  Usually the result of LV hypertrophy from chronic systemic HTN, aortic stenosis, or hypertrophic cardiomyopathy o Mixed Systolic and Diastolic Failure  seen in disease states such as dilated cardiomyopathy  DCM is a condition in which poor systolic function (weakened muscle function) is further compromised by dilated LV walls that are unable to relax  Pts often have extremely poor EF (< 35%), high pulmonary pressures, and biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity)  Can be caused acutely by an MI or chronically from worsening cardiomyopathy or HTN  Body’s response is low CO to mobilize its compensatory mechanisms to maintain CO and BP - Compensatory Mechanisms o Sympathetic Nervous System Activation  Often the first mechanism triggered in response to an inadequate SV and CO  resulting in an increased release of catecholamines  increased HR and contractility which improves CO, and peripheral vasoconstriction  Increases the myocardium’s need for O2 over time and increases the workload of the already failing heart  Vasoconstriction causes an immediate increase in preload, which may initially increase CO  and increase in venous return to heart, which is already volume overloaded, actually worsens ventricular performace o Neurohormonal Response  Decreased kidney perfusion  release of renin  which converts angiotensinogen to angiotensin  angiotensin I is then converted to angiotensin II  causing the adrenal cortex to release aldosterone (resulting in sodium and water retention) and increase peripheral vasoconstriction (increases BP)  renin-angiotensin-aldosterone system (RAAS)  Low CO causes a decrease in cerebral perfusion pressure  posterior pituitary secretes ADH  increases water reabsorption in the renal tubules, causing water retention and therefore increased blood volume (adding to the already volume overload)  Endothelin is produced by vascular endothelial cells and is stimulated by ADH, catecholamines, and angiotensin II  results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy  Proinflammatory cytokines are released by cardiac myocytes in response to various forms of cardiac injury  further depresses cardiac function by causing cardiac hypertrophy, contractile dysfunction, and myocyte cell death  Together, these factors result in an increase in cardiac workload, myocardial dysfunction, and ventricular remodeling (hypertrophy of the cardiac myocytes) o Ventricular Dilation  enlargement of the chambers of the heart  Occurs when pressure in the heart chambers (usually LV) is elevated over time  The muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole  Frank-Starling Law  the degree of stretch is directly related to the force of the contraction  Initially, this increased contraction leads to increased CO and maintenance of arterial BP and perfusion  Eventually, this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively  decreasing CO o Ventricular Hypertrophy  an increase in the muscle mass and cardiac wall thickness in response to overwork and strain  Generally follows persistent or chronic dilation and thus further increases the contractile power of the muscle fibers  increased CO and maintenance of tissue perfusion  Hypertrophic heart muscle has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation, and is prone to ventricular dysrhythmias CHF/MI  remember assessment, risk factors, and prioritizing nursing action MI  Acute Interventions - Pain  nitrate, morphine administration, use pain scale o Also look for physiologic signs  increased HR and BP o Check bladder too if pt is sedated - Monitoring  ECG, arrhythmia, ventricular fib (most common and lethal arrhythmia) - Rest and comfort - Control anxiety - Emotional and behavioral reactions - Physical assessment  neck vein engorgement  heart is not emptying  think CHF, which is a complication of MI Collaborative Care for MI - Initial management is best accomplished in ICU - Fibrinolytic Therapy  produce an open artery by lysis of thrombus to reperfuse the myocardium o Urokinase  enzymes used to dissolve clot - Cardiac Catherization  balloon or stent placement that suppresses the occlusion and allows blood to flow - Drug Therapy: o IV Nitroglycerin  drip to continuously create vasodilation  Potential for hypotension  maintain pt safety (SR up, bed low, etc.)  Used to decrease preload and afterload while increasing the myocardial O2 supply o Antiarrhythmic drugs o Morphine Sulfate  decreases demand of blood to heart  Pain, sedative effects decrease metabolism therefore decreasing O2 demand and anxiety levels  Vasodilator o Beta Blocker  Reduce myocardial oxygen demand by reducing HR, BP, and contractility o ACE Inhibitors  Help prevent ventricular remodeling and prevent or slow the progression of HF  Decreases cardiac demand and workload and decreases afterload o Stool Softeners  Prevents straining and the resultant vagal stimulation from the Valsalva maneuver  Vagal stimulation produces bradycardia and can provoke dysrhythmias - Nutritional Therapy o Low-salt, low-saturated-fat, and low-cholesterol Collaborative Care for Angina - Aimed at decreasing oxygen demand and/or increasing oxygen supply - Continued emphasis on the reduction of risk factors - Drug Therapy o Use of nitrates initial therapeutic intervention o Antiplatelet Aggregation Therapy (first line of treatment)  Aspirin, Ticlid, Plavix o Nitrates  can give max of 3 times in 5 minute intervals  Sublingual  relieve pain in 3 minutes and last 30-60 minutes (20-45 minutes stated in class)  Nitroglycerin Ointment  3-6 hour prophylaxis  Transdermal controlled  maintains steady plasma levels within the therapeutic range during 24 hours  Long-Acting Nitrates  IV nitroglycerin  Take prophylactic nitrate 5-10 minutes before activity  r/t supply and demand  Nitrates dilate peripheral blood vessels and dilate coronary arteries and collateral vessels o B – Adrenergic Blockers  Decrease sympathetic nervous system stimulation  decreasing HR and demand for O2 o Calcium Channel Blockers  Decreased systemic vascular resistance and afterload in periphery  Cause smooth muscle relaxation and relative vasodilation of coronary systemic arteries, thus increasing blood flow - Percutaneous Coronary Intervention (PCI)  insertion of a catheter equipped with an inflatable tip to the coronary artery resulting to vessel dilation - Stent Placement  imbedded w/ antiplatelets o Expandable mesh like structures designed to maintain vessel patency by compressing the arterial walls and resisting vasoconstriction - Atherectomy - Laser Angioplasty - Myocardial Revascularization (CABG) Nursing Therapeutics/ Plan of Care  CHF Acute CHF - Goal  improve LV function by decreasing intravascular volume, decreasing venous return (preload), decreasing afterload, improving gas exchange and oxygenation, decreasing CO2, and reducing anxiety o Decrease Intravascular Volume  reduces venous return to the LV, reducing preload, allowing the overfilled LV to contract more efficiently and improve CO  increases LV function, decreases pulmonary vascular pressures, and improves gas exchange  Use of diuretics  loop o Decrease Venous Return  decreasing preload reduces the amount of volume returned to the LV during diastole  use high-fowler’s with feet horizontal or hanging at bedside (causes pooling and decreases venous return  IV nitroglycerin (vasodilator used to reduce circulating volume by decreasing preload and lso increasing coronary artery circulation by dilating the coronary arteries) o Decrease Afterload  (the amount of work the LV has to produce to eject blood into the systemic circulation) if afterload is reduced, the CO of the LV improves and thereby decreases pulmonary congestion  IV sodium nitroprusside (Nipride) is a potent vasodilator that reduces preload and afterload  drug of choice for patient with pulmonary edema because of its rapid onset of action and potent effects on the vascular system  by reducing both preload and afterload, myocardial contraction improves, increasing CO and reducing pulmonary congestion.  Morphine sulfate dilates both the pulmonary and systemic blood vessels reducing preload and afterload o Improve Gas Exchange and Oxygenation  morphine, oxygen o Improve Cardiac Function  digitalis o Reduce Anxiety Chronic CHF - Goal  treat underlying cause, maximize CO, provide treatment to alleviate symptom o Administer O2 o Monitor O2 by ABG or pulse ox o Allow physical and emotional rest o Drug Therapy  ACE Inhibitor  significant increase in CO  Diuretic Therapy  mobilize fluid, reduce preload  Inotropic drugs  digitalis  Vasodilators  Beta Blockers  directly block the negative effects of the SNS on the failing heart o Dietary Therapy  Sodium restriction (2 gm sodium diet)  avoid/limit milk, cheese, bread, cereal, canned foods  Diet education  Weight management  Fluid restriction (if there is renal insufficiency) Drug Therapy  CHF - Morphine IV  decrease preload and afterload, decreases O2 demand, decreases anxiety - Diuretic Therapy  mobilize edematous fluid, reduce pulmonary venous pressure, and reduce preload reducing blood volume returned to the heart and improving cardiac function - Digitalis  positive inotropic agent directed at improving cardiac contractility to increase CO, decrease LV diastolic pressure, and decrease SVR - Nitroglycerin  decrease preload by increasing venous capacitance, dilating the pulmonary vasculature, and improving arterial compliance  cause vasodilation by acting directly on the smooth muscle of the vessel wall - Daily Weight - Cardioversion - Endotracheal Intubation/ Mechanical Ventilation - Sodium Restricted Diet Right vs Left CHF  S/S, nursing interventions Types of CHF - Left-Sided Heart Failure  most common form of HF o Results from LV dysfunction, which prevents normal blood flow and causes blood to back up into the LA and into the pulmonary veins o Increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then alveoli, which is manifested as pulmonary congestion and edema - Right-Sided Heart Failure o Causes a backup of blood into the RA and venous circulation  JVD, hepatosplenomegaly, vascular congestion of the GI tract, and peripheral edema o Primary cause of RHF  left-sided HF; left-sided failure results in pulmonary congestion and increased pressure in the blood vessels of the lung (pulmonary HTN)  eventually, chronic pulmonary HTN (increased RV afterload) results in right-sided hypertrophy and failure o Cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease) can also cause RHF o RV infarction may also cause isolated RV failure Clinical Manifestations of CHF - Acute CHF o Pulmonary edema  lung alveoli become filled with serosanguineous fluid (most commonly caused by acute LV failure secondary to CAD) o Increased RR and Decreased PaO2  increase in the pulmonary venous pressure caused by decreased efficiency of the LV  engorgement of the pulmonary vascular system  lungs become less compliant, and there is increased resistance in the small airways. Lymphatic system also increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. o Severe Tachypnea (interstitial edema)  if pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the intertsitial space than the lymphatics can drain o Alveolar Edema  occurs if the pulmonary venous pressure increases further causing the tight alveoli lining cells to be disrupted and allowing a fluid containing RBCs to move in to the alveoli o Increased PaCO2 (Acidemia)  as the disruption become worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid  worsening ABG values o Agitation o Cyanosis, pale, clammy, and cold skin  secondary to vasoconstricion o Severe dyspnea, orthopnea o Wheezing, coughing o Frothy, blood tinged sputum o Crackles, wheezes , rhonchi - Chronic HF o Fatigue  caused by a decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia o Dyspnea  caused by increased pulmonary pressures secondary to interstitial and alveolar edema o Paroxysmal Nocturnal Dyspnea (PND)  occurs when the patient is asleep; caused by the reabsorption of fluid from dependent body areas when the patient is recumbent o Tachycardia  diminished CO increases SNS stimulation, which increases HR o Edema  fluid overload o Nocturia  when the person lies down at night, fluid movement from the interstitial spaces back into the circulatory system is enhanced causing renal blood flow and diuresis o Skin Changes  tissue capillary oxygen extraction is increased causing dusky, cool, and diaphoretic skin o Behavioral Changes  cerebral circulation is impaired secondary to decreased CO; restlessness, confusion, and decreased attention span or memory are often observed o Chest Pain  due to decreased coronary perfusion from decreased CO and increased myocardial work Right-Sided Heart Failure Left-Sided Heart Failure Signs RV heaves Murmurs Jugular venous distention Edema (e.g., anterior tibias, medial malleoli, scrotum, sacrum) Weight gain ↑ HR Ascites Anasarca (massive generalized body edema) Hepatomegaly (liver enlargement) LV heaves Pulsus alternans (alternating pulses: strong, weak) ↑ HR PMI displaced inferiorly and posteriorly (LV hypertrophy) ↓ PaO2, slight ↑ PaCO2 (poor O2 exchange) Crackles (pulmonary edema) S3 and S4 heart sounds Pleural effusion Changes in mental status Restlessness, confusion Symptoms Fatigue Anxiety, depression Dependent, bilateral edema Right upper quadrant pain Anorexia and GI bloating Nausea Weakness, fatigue Anxiety, depression Dyspnea Shallow respirations up to 32-40/min Paroxysmal nocturnal dyspnea Orthopnea (shortness of breath in recumbent position) Dry, hacking cough Nocturia Frothy, pink-tinged sputum (advanced pulmonary edema) Health teachings  valvular replacement, or valvular heart defect, CHF, MI (discharge planning) Ambulatory/ Home Care  MI - Patient teaching - Anticipatory Guidance  preparing the pt and family for what to expect in course of recovery in order to make patient feel a sense of control - For uncomplicated MI, ambulate the pt by day 3 - Physical exercise  rhythmic, repetitive activity that still works muscles (isotonic exercise – ROM) - Resumption of Sexual activity  use matter of fact approach o Remain neutral – talk about taking prophylactic nitroglycerin, walking o 7-10 days post uncomplicated MI o Not advisable after a heavy meal or consumption of alcohol o Should be able to clime 2 flights of stairs w/o signs of chest pain or dyspnea o Stress to avoid anal intercourse o No Viagra post MI Ambulatory Home Care  CHF - Teach pt the physiologic changes of CHF - Encourage to take medications regularly - Teach pt to take his/her own pulse  to know under what circumstances drugs should be withheld and a health care provider consulted - Alert on sign and symptoms of hypo/hyperkalemia  if diuretics that deplete or spare potassium are being used - Discuss energy saving and energy efficient behaviors Management of Valvular Heart Disease - Prevent recurrent rheumatic fever or infective endocarditis  prophylactic antibiotic therapy - Focused on preventing exacerbations of HF, acute pulmonary edema, thromboembolism, and recurrent endocarditis - If manifestations of HF present  vasodilators, positive inotropes, beta blockers, diuretics, and low-sodium diet - Anticoagulant therapy is used to prevent and treat systemic or pulmonary embolization and is also used prophylactically in patients with A. fib - Dysrhythmias  treated with digoxin, antidysrhythmic drugs, or electrical cardioversion - Beta blockers may be used to slow the ventricular rate in pts with A. fib Nursing Therapeutics  Valvular Heart Disease - Prevent acquired rheumatic valvular disease - Prevent recurrent infection through antibiotics  prophylactic treatment should continue for life in individuals who develop rheumatic heart disease o Additional prophylaxis is necessary if a patient with known rheumatic heart disease has dental or surgical procedures involving the upper respiratory, GI, or GU tract - Hospitalization due to CHF and arrhythmia - Exercise plan to increase cardiac tolerance  strenuous physical activity should be avoided because damaged valves may not be able to handle the demand for an increase in CO o Restrict activities that regurlarly produce fatigue and dyspnea - Smoking cessation  may increase incidences of respiratory and upper respiratory infections - Assist in planning ADLs  emphasis on conserving energy, setting priorities, and taking planned rest periods Collaborative Care  Aneurysm - Goal  prevent rupture of aneurysm o If aneurysm is < 4 cm  conservative treatment (i.e., no lifting etc…anything that can increase abdominal pressure, basic lifestyle modifications) o Greater that 5-6 cm  surgical repair Nursing Therapeutics  Aneurysm - Decrease risk factors associated with atherosclerosis - Pre-op  support and teaching - ICU care post surgery - Maintain BP  an adequate BP is important to maintain graft patency o Prolonged hypotension may result in graft thrombosis o Severe HTN may cause undue stress on the arterial anastomoses, resulting in leakage of blood or rupture at the suture lines - O2 Supply  if any reason the oxygen level decreases, the heart will want to work harder, therefore increasing pressure and increasing the tension on the suture line resulting in an eruption - Prevention of infection/ ABT  the development of a prosthetic vascular graft infection is a relatively rare but potentially life-threatening complication - Prevention of paralytic ileus  through early ambulation – start with isometric movements (sitting in bed and letting their legs dangle before letting them walk) - Monitor peripheral perfusion status  a decreased or absent pulse in conjunction with a cool, pale, mottled, or painful extremity may indicate embolization of aneurismal thrombus or plaque, or graft occlusion - Monitor renal perfusion  urine output – one cause of decreased renal perfusion is embolization of a fragment of thrombus or plaque from the aorta that subsequently lodges in one or both of the renal arteries - Avoid heavy lifting 4-6 weeks post op - Monitor for S/S of infection Nursing diagnosis  especially CAD patient Clinical Manifestations of CAD - Angina o Appears substernally, in the neck, radiate to jaw, shoulder and down to the arm - Myocardial Infarction o Pain is severe, immobilizing, not relieved by rest or nitrate administration o Described as heaviness, pressure, tightness, burning, crushing (remember, pt will state in laymans terms) o Occurs as a result of sustained ischemia, causing irreversible myocardial cell death o 80-90% of all acute MIs are secondary to thrombus formation  when a thrombus develops, perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis  contractile function of the heart stops in the necrotic area(s) o Most MIs involve some portion of the LV o Commonly occurs in the morning hours and usually lasts for 20 minutes or more o Pts with diabetes are more likely to experience silent MIs due to cardiac neuropathy and present with atypical symptoms (i.e., dyspnea) o An older patient may experience change in mental status, SOB, pulmonary edema, dizziness, or a dysrhythmia o Additional clinical manifestations:  Sympathetic nervous system stimulation  increased SNS stimulation results in release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels (expect skin to be ashen, clammy, and cool to touch)  Increased HR and BP initially secondary to release of catecholamines  Later, BP may drop because of decreased CO  Decreased renal perfusion may occur (secondary to decreased CO) and decrease urine output  Crackles may be noted in the lungs, persisting for several hours to several days, suggesting LV dysfunction  JVD, hepatic engorgement, and peripheral edema may indicate RV dysfunction  N/V can result from reflex stimulation of the vomiting center by the severe pain • Can also result from vasovagal reflexes initiated from the area of the infracted myocardium  Fever may also occur as a systemic manifestation of the inflammatory process caused by myocardial cell death Developmental Stages of CAD - Fatty Streak  earliest lesion of atherosclerosis o Can be seen as early as 15 years old o Characterized by lipid filled smooth muscle - Raised Fibrous Plaque  beginning of progressive changes of arterial wall o Platelets start to accumulate leading to thrombus formation o Narrowing of artery seen as early as 30 years of age o Once endothelial injury has occurred, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intima o The fatty streak is eventually covered by collagen forming a fibrous plaque that appears grayish or whitish o These plaques can form on one portion of the artery or in a circular fashion involving the entire lumen o The result is a narrowing of the vessel lumen and a reduction in blood flow to the distal tissues - Complicated Lesion  final stage in the development of atherosclerotic lesion o Most dangerous  little to no circulation to organ o As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration, and rupture o Once the integrity of the artery’s inner wall has become compromised, platelets accumulate in large numbers, leading to a thrombus o Plaque can consist of lipids or platelet aggregation o The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery o Calcium deposits make it worse  can’t scrape out o Activation of the exposed platelets causes expression of glycoprotein IIb/IIIa receptors that bind fibrinogen o This, in turn, leads to further platelet aggregation and adhesion, further enlarging the thrombus - Ischemia  death of tissue CAD Risk Factors - Non-Modifiable Risk Factors o Age, Gender, and Ethnicity  Highest among white, middle-aged men  After age 65, the incidence in men and women equalizes although cardiovascular disease causes more deaths in women than men  CAD is present in African American women at rates higher than their white counterparts  Women tend to manifest CAD 10 years later in life than men o Family history and Genetics  Some congenital defects in coronary artery walls predispose the person to the formation of plaques  Familial hypercholesterolemia, and autosomal dominant disorder, has been strongly associated with CAD at early ages - Modifiable Major Risk Factors o Elevated Serum Lipids  The risk of CAD is associated with a serum cholesterol level of more than 200 mg/dl or a fasting triglyceride level of more than 150 mg/dl  High serum HDL levels are desirable and low serum HDL levels are considered a risk factor for CAD  HDLs carry lipids away from arteries and to the liver for metabolism • HDL lower than 35 mg/dl is considered a major risk factor • HDL levels can be increased by physical activity, moderate alcohol consumption, and estrogen administration  LDLs contain more cholesterol than any of the other lipoproteins and have an affinity for arterial walls • Elevated LDL levels correlate most closely with and increased incidence of atherosclerosis and CAD • Persons with no or only one risk factor  LDL goal is < 160 mg/dl • Persons at high risk  LDL goal is < 70 mg/dl  Lifestyle factors that can contribute to elevated triglycerides include high alcohol consumption, high intake of refined carbohydrates and simple sugars, and physical inactivity • When a high triglyceride level is combined with a high LDL level, a smaller, denser LDL particle is formed, which favors deposition on arterial walls  often seen in people with insulin resisitance (type 2 DM) o Hypertension  BP greater than or equal to 140/90 mm Hg  The stress of a constantly elevated BP increases the rate of atherosclerotic development  shearing stress that causes endothelial injury  Atherosclerosis causes narrowed, thickened arterial walls and decreased the distensibility and elasticity of vessels  More force is required to pump blood through diseased arterial vasculature, and this increased force is reflected in higher BP  This increased workload is also manifested by left ventricular hypertrophy and decreased SV with each contraction o Tobacco Use  2-6 times