NURS 415/N313R_MedSurg_Exam_1_SG-1

Ch. 17 – Fluid, Electrolyte, and Acid-Base Imbalances Terminology Related to Body Fluid Chemistry - Anion  ion that carries a negative charge - Cation  ion that carries a positive charge - Electrolyte  substanc ...

Ch. 17 – Fluid, Electrolyte, and Acid-Base Imbalances Terminology Related to Body Fluid Chemistry - Anion  ion that carries a negative charge - Cation  ion that carries a positive charge - Electrolyte  substance that dissociates in solution into ions (i.e. and molecule of NaCl becomes Na and Cl) - Nonelectrolyte  substance that does not dissociate into ions in solution (i.e. glucose and urea) - Osmolality  a measure of the total solute concentration per kilogram of solvent - Osmolarity  a measure of the total solute concentration per liter of solution - Solute  substance that is dissolved in a solvent - Solution  homogenous mixture of solutes dissolved in a solvent Distribution of Body Fluids - Water & electrolytes in the body  60% of body weight o Older adults  45-55% o Infant  70-80%  Both of these groups are at a higher risk for fluid-related problems - Body fluids constantly move  distributed through different compartments - Intracellular Fluids  fluid within the cell o 2/3rds of the body water is located within the cells  40% of body weight - Extracellular Fluids  fluid away from or outside of the cell o Interstitial Fluid  in between cells o Intravascular  inside blood vessel, but outside of cells (i.e. plasma, the fluid in blood) o Transcellular  fluid located inside a cavity or structure (i.e. intraocular or CSF) - Water is necessary in the regulation of body temperature, lubricating joints and membranes, and acts as a medium for food digestion Electrolytes - Electrically charged particles or elements that dissolves or dissociates in water - Cation  positively charged ions (sodium, potassium, calcium, and magnesium) - Anion  negatively charged ions (bicarbonate, chloride, and phosphate) o Most proteins bear a negative charge and are thus anions - Electrolyte Composition of Fluid Compartments: o The overall concentration of the electrolytes is approx the same in the two compartments (ECF v. ICF), but specific ions differ o ICF  most prevalent cation is potassium, anion is phosphate o ECF  most prevalent cation is sodium, anion is bicarbonate Processes that Influence Body Fluid Movements - Electrolytes move according to their concentration and electrical gradients toward the areas of lower concentration and toward areas with the opposite charge - Osmosis  movement of water between two compartments separated by a semipermeable membrane (a membrane permeable to water but not to a solute) o Movement of fluid from an area of less solute concentration to an area of high solute concentration  more dilute (more water) compartment to more concentrated compartment (less water) o Stops when concentration differences disappear or when hydrostatic pressure builds and is sufficient to oppose any further movement of water o Colloid Osmotic Pressure (oncotic)  drawing power created by albumin; protein molecules attract water, pulling fluid from the tissue space to the vascular space o Hydrostatic Pressure  the force within a fluid compartment; pressure of a volume of fluid against a wall (i.e. BP) - Diffusion  the movement of molecules from an area of high concentration to one of low concentration o Net movement of molecules stops when the concentrations are equal in both areas o Membrane but be permeable o Facilitated diffusion  moves molecules from an area of high concentration to one of low concentration; passive and requires not energy other than that of the concentration gradient - Filtration  water and diffusible substances move together due to a difference in fluid pressure (i.e. urin formation via renal tubules and capsule) o Movement from greater pressure to less pressure - Capillary hydrostatic pressure and interstitial oncotic pressure cause the movement of water out of the capillaries. Plasma oncotic pressure and interstitial hydrostatic pressure cause the movement of fluid into the capillary. - Accumulation of fluid in the interstitium (edema) occurs if venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic pressure rises. - Decreased oncotic pressure is seen when the plasma protein content is too low  renal disorders, liver disease, malnutrition - Trauma, burns, and inflammation can damage capillary walls and allow plasma proteins to accumulate in the interstitium  increased oncotic pressure draws fluid into the interstitium and holds it there - Fluid is drawn into the plasma space whenever there is an increase in the plasma osmotic or oncotic pressure  administration of colloids, dextran, mannitol, or hypertonic solutions Type of Solution According to Concentration - Hypotonic Solution  solution of lower osmotic pressure that regularly gives up fluid and water - Hypertonic Solution  solution with higher osmotic pressure o 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 Factors Affecting the Regulation of Body Fluids - Fluid Intake  regulated by thirst mechanisms (based on sodium levels in the blood) o Older adults experience a decrease in the thirst mechanism resulting in decreased fluid intake - Hormonal Regulation o ADH  stimulated by change of osmolality in blood or a decrease in circulating blood volume; increase in concentration stimulates pituitary to release ADH  Acts in the renal distal and collecting tubules causing water reabsorption o Aldosterone  adrenal gland; increase in potassium stimulates aldosterone release  Potassium excites tissue  too much can cause too much excitement and effect CO  Goal of aldosterone is to attract and reabsorb sodium  Enhance sodium retention and potassium excretion  The secretion of aldosterone may be stimulated by decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule o Renin  kidneys; stimulates less kidney perfusion to decrease BP; released when kidney perfusion is decreased secondary to decrease in BP  Angiotensin I & II  vasoconstriction, II stimulates aldosterone to contain Na and helps volume, BP & mentation to increase  ACE Inhibitors prevent vasoconstriction and aldosterone to increase blood volume action  Angiotensin is acted on by the rennin to form angiotensin I, which converts to angiotensin II, which stimulates the adrenal cortex to secrete alodosterone - Fluid Output Regulation  exemplified by kidney o Skin, lungs and GI  insensible water loss – 500-600 ml/day; about 400 ml from the lungs  The book says normally 600-900 ml/day is lost  The amount of water loss is increased by accelerated body metabolism, which occure with increased body temperature and exercise. - Electrolyte Intake Disturbances in F&E - Electrolyte Imbalances o Sodium  90% contained in ECF; main concern is water regulation  Function  main cation of the ECF and plays a major role in maintaining the concentration and volume; primary determinant of ECF osmolality  Also important in the generation and transmission of nerve impulses and the regulation of acid-base balance  Normal value  135-145 meq/L  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 • 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 • Manifestations: dehydration of cells (especially seen in brain cells) o Decreased ECF Volume  restlessness, agitation, twitching, seizures, coma, intense thirst; dry, swollen tongue, sticky mucous membranes, postural hypotension, decreased CVP, weight loss, weakness, lethargy o 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 • 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 • Manifestations: cellular swelling and first manifested in CNS o 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 o Normal or Increased ECF volume  headache, apathy, confusion, muscle spasms, seizures, coma, nausea, vomiting, diarrhea, abdominal cramps, weight gain, increased BP, increased CVP o Potassium  main electrolyte intracellularly – 98%  Function  critical for many cellular metabolic functions; neuromuscular and cardiac function, also regulates intracellular osmolality and promotes cellular growth  Normal Value  3.5-5.0 meq/L  90% of potassium intake is eliminated by the kidneys  if kidney function is significantly impaired, toxic levels of potassium maybe retained  Potassium moves into cells during the formation of new tissues and leaves the cell during tissue breakdown  Hyperkalemia  increased cellular excitability • Caused by: o Excessive potassium intake  excessive or rapid parenteral administration, potassium-containing drugs, potassium-containing salt substitute o Shift of potassium out of cells  acidosis, tissue catabolism (fever, sepsis, burns), crush injury, tumor lysis syndrome o Failure to eliminate potassium  renal disease, potassium-sparing diuretics, adrenal insufficiency, ACE inhibitors (these drugs reduce the kidney’s ability to excrete potassium) o Can also be caused by giving expired blood (hemolysis) • Manifestations: Initially pt may experience cramping leg pain followed by weakness or paralysis of skeletal muscles o Irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyperkalemia sudden or severe o ECG changes  tall, peaked T wave, prolonged PR interval, ST segment depression, loss of P wave, widening QRS, V fib, ventricular standstill o Hypokalemia  decreased cellular excitability  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  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 - Fluid Imbalances o 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  NOT dehydration (dehydration refers to loss of pure water alone without corresponding loss of sodium)  Decrease in circulating blood volume  decrease in BP  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  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 o 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  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  Causes: • Excessive isotonic or hypotonic fluids, heart or renal failure, primary polydipsia, SIADH, cushing syndrome, long-term use of corticosteroids  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 - Osmolar Imbalances o Hyperosmolar  body fluid that is too concentrated (lots of solute) – blood is so concentrated that cell shrinks by osmosis  DM (increased blood sugar) – increased concentration  Give hypotonic solution  ½ NS o Hyposmolar  water excess, cell can potentiall swell Factors Affecting F&E Imbalance - Age  very young are made of mostly fluids and dehydrate easily; very old can easily get dehydrated r/t decreased senses - Illness  acute illness, surgery, burns, CHF, resp. disorders, renal disease - Environmental factors  heat, extreme temperature, sweating - Diet - Lifestyle  smoking, alcohol intake - Medications Common Laboratory Studies - CBC o Hematocrit  amount of RBCs in whole blood; if pt is overly hydrated, hematocrit with decrease; dehydrated, hematocrit will increase - ABG - Serum Electrolytes Level Nursing Therapeutics/Plan of Care - 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. - Enteral replacement of F&E loss  GI, oral fluids, g-tube - 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). o 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! - Parenteral replacement of F&E  IV fluids - Medication  lasix o Lasix - increase potassium rich foods o Spironolactone – watch potassium rich foods o Potassium sparing  HR, ECG  increase HR, irregularities (arrhythmia could be indicator) o Potassium wasting  slow HR - I&O Monitoring Example of IV Solutions TABLE 17-18 Composition and Use of Commonly Prescribed Crystalloid Solutions Solution Tonicity Glucose (g/L) Indications and Considerations 5% Isotonic, but physiologically hypotonic 50 • Provides free water necessary for renal excretion of solutes • Used to replace water losses and treat hypernatremia • Provides 170 calories/L • Does not provide any electrolytes 10% Hypertonic 100 • Provides free water only, no electrolytes • Provides 340 calories/L 0.45% Hypotonic 0 • Provides free water in addition to Na+ and Cl− • Used to replace hypotonic fluid losses • Used as maintenance solution, although it does not replace daily losses of other electrolytes • Provides no calories 0.9% Isotonic 0 • Used to expand intravascular volume and replace extracellular fluid losses • Only solution that may be administered with blood products • Contains Na+ and Cl− in excess of plasma levels • Does not provide free water, calories, other electrolytes • May cause intravascular overload or hyperchloremic acidosis 3.0% Hypertonic 0 • Used to treat symptomatic hyponatremia • Must be administered slowly and with extreme caution because it may cause dangerous intravascular volume overload and pulmonary edema 5% in 0.225% Isotonic 50 • Provides Na+, Cl−, and free water • Used to replace hypotonic losses and treat hypernatremia • Provides 170 calories/L 5% in 0.45% Hypertonic 50 • Same as 0.45% NaCl except provides 170 calories/L 5% in 0.9% Hypertonic 50 • Same as 0.9% NaCl except provides 170 calories/L Ringer's solution Isotonic 0 • Similar in composition to plasma except that it has excess Cl−, no Mg2+, and no HCO3− • Does not provide free water or calories • Used to expand the intravascular volume and replace extracellular fluid losses Lactated Ringer's (Hartmann's) solution Isotonic 0 • Similar in composition to normal plasma except does not contain Mg2+ • Used to treat losses from burns and lower Gl • May be used to treat mild metabolic acidosis but should not be used to treat lactic acidosis • Does not provide free water or calories 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 - Ideal fluid replacement for a pt with an ECF volume deficit - Ex: LR  contains sodium, potassium, chloride, calcium, and lactate (the precursor of bicarbonate) in about the same concentrations as those of the ECF o Contraindicated in the presence of lactic acidosis because of the body’s decreased ability to convert lactate to bicarbonate - Monitor for signs of fluid overload  #1 is pulmonary edema - Be careful giving to CHF or HTN pts - Don’t give to pts with pH greater than 7.5 - Don’t give LR to pts with liver disease  they can’t metabolize lactate - D5W  don’t give to pts with increased ICP – water causes swelling Hypertonic  initially raises the osmolality of ECF and expands it - Useful in treatment of hypovolemia and hyponatremia - The higher osmotic pressure draws water out of the cells into the ECF - Increased risk of intravascular fluid volume excess  monitor BP, lung sounds, and serum sodium levels frequently - Do not give in any condition that may cause cellular dehydration  diabetes Wound care  irrigate with NS, not water  water causes cell to swell - NS causes cell to shrink and promote wound healing Foley  inflate balloon with only sterile water  NaCl with crystallize Ch. 18, 19, 20 – Perioperative Nursing Concepts Define the three stages of perioperative nursing: - Preoperative  from the decision of having the surgical intervention until the patient is on the OR table o Scope of Nursing Activities  Establish a baseline evaluation  medical hx, allergies, etc.  Arranging consults  cardiopulmonary clearance (can pt tolerate effects of anesthesia?)  Providing education/ Health teachings  what to expect after surgery - Intraoperative  on the OR table and ends with admission to the post anesthesia care unit (PACU) o Scope of Nursing Activities  Providing patient with safety  pt still groggy and confused, change in F&E, BP, side rails up, provide warmth  Maintaining aseptic environment  Ensuring proper function of equipment  double check all equipment  Providing specific instruments  Proper documentation  Providing emotion support  Assisting in positioning of patient  Act as scrub nurse, circulating nurse, RNFA - Post-Operative  from PACU admission until the follow-up evaluation in the clinical setting or home o Scope of Nursing Activities  Maintaining airway  Monitoring VS  Assessing the effects of anesthesia  Assessing for complication  bleeding, check dressing  Providing comfort and pain relief  Promote recovery  Initiating teaching, follow up care and referral for discharge Surgical Classification - Diagnostic  determination of the presence and/or extent of pathology (i.e. lymph node biopsy or bronchoscopy) - Currative  elimination or repair of pathology (i.e. removal of a ruptured appendix or benign ovarian cyst) - Palliation  alleviation of symptoms without cure (i.e. cutting a nerve root to remove symptoms of pain, or creating a colostomy to bypass an inoperable bowel obstruction) - Prevention  examples include removal of a mole before it becomes malignant or removal of the colon in a patient with familial polyposis to prevent cancer - Exploration  surgical examination to determine the nature or extent of a disease - Cosmetic improvement  examples include repairing a burn scar or changing breast shape Degree of Urgency - Emergency  immediate – life threatening - Urgent  prompt attention – within 24-30 hours surgery must be performed - Required  needs to have surgery, but can wait weeks to months - Elective  non-catastrophic, but should have surgery (i.e. hernia) - Optional  cosmetic Describe a Comprehensive Preoperative Assessment to Identify Surgical Risk Factors - Goals of the assessment are to: o Determine the psychologic status of the patient in order to reinforce the use of coping strategies during the surgical experience o Determine physiologic factors that are directly or indirectly related to the surgical procedure that may contribute to operative risk factors o Establish baseline data for comparison in the intraoperative and postoperative period o Identify and document the surgical site and/or side on which the surgical procedure will be performed o Identify prescription medications and OTC drugs and herbs that have been taken by the patient that may affect surgical outcome o Confirm that the results of all preoperative laboratory and diagnostic tests are documented in the patient’s record and communicated to appropriate personnel o Identify cultural and ethnic factors that may affect the surgical experience o Determine if the patient has received adequate information from the surgeon to make an informed decision to have surgery and that the consent form is signed and witnessed Physiologic Assessment of the Preoperative Patient Cardiovascular System •Identify acute or chronic problems; focus on presence of angina, hypertension, heart failure, recent history of myocardial infarction. •Auscultate and palpate baseline pulses: apical, radial, and pedal for rate and characteristics (compare one side to the other). •Inspect and palpate for presence of edema (including dependent areas), noting location and severity. •Inspect and palpate neck veins for distention. •Take baseline blood pressure in both arms. •Identify any drug or herbal product that may affect coagulation (e.g., aspirin, ginkgo, ginger). •Review laboratory and diagnostic tests for cardiovascular function. •Identify patients with pacemakers and/or implantable defibrillators. Respiratory System •Identify acute or chronic problems; note the presence of infection or chronic obstructive pulmonary disease (COPD), asthma. •Assess history of smoking, including the time interval since the last cigarette and the number of pack-years. (Remember that although smoking should be discouraged preoperatively, it may be difficult for patients to stop during this time of anxiety.) •Auscultate lungs for normal and adventitious breath sounds. •Determine baseline respiratory rate and rhythm, and regularity of pattern. •Observe for cough, dyspnea, and use of accessory muscles of respiration. Neurologic System •Determine orientation to time, place, and person. •Identify presence of confusion, disorderly thinking, or inability to follow commands. •Identify past history of strokes, transient ischemic attacks or nervous system diseases (e.g., Parkinson's disease, multiple sclerosis). Urinary System •Identify any preexisting disease. •Determine ability to void. Prostate enlargement may affect catheterization during surgery and ability to void postoperatively. •If necessary, note color, amount, and characteristics of urine. •Review laboratory and diagnostic tests for renal function. Hepatic System •Inspect skin color and sclera of eyes for any signs of jaundice. •Review past history of substance abuse, especially alcohol and IV drug use. •Review laboratory and diagnostic tests for liver function. Integumentary System •Assess mucous membranes for dryness and intactness. •Determine skin status; note drying, bruising, or breaks in surface. •Inspect skin for rashes, boils, or infection, especially around the planned surgical site. •Assess skin moisture and temperature. •Inspect the mucous membranes and skin turgor for dehydration. Musculoskeletal System •Examine skin/bone pressure points. •Assess for presence of any pressure ulcers. •Assess for limitations in joint range of motion and muscle weakness. •Assess mobility, gait, and balance. •Assess for presence of joint pain. Gastrointestinal System •Determine food and fluid intake patterns and any recent weight loss. •Weigh and measure patient. •Assess for the presence of dentures and bridges (loose dentures or teeth may be dislodged during intubation). Immune System •Identify any immunodeficiency or autoimmune disorders. •Assess for use of corticosteroids or other immunosuppressant drugs. Identify Health Factors that Affect the Patient Preoperatively - Nutritional Status/Fluid  correct malnutrition prior to surgery o Obesity stresses both the cardiac and pulmonary systems and makes access to the surgical site and anesthesia administration more difficult  predisposes pt to wound dehiscence, wound infection, and incisional herniation postoperatively - Drug/Alcohol Use  may affect anesthesia o Alcohol intoxication  NG tube and lavage in case of emergency - Respiratory Status  surgery can be postponed in case of respiratory infection o Stop smoking 4-8 weeks before surgery; must have completely abstained from smoking for at least 24 hours prior to surgery o The presence of an upper airway infection may result in the cancellation or postponement of elective surgery b/c the existing infection will place the patient at an increased risk of bronchospasm, laryngospasm, decreased O2 sat, and problems with respiratory secretions o The pt with a hx of asthma or COPD is at high risk for postoperative pulmonary complications, which include hypoxemia and atelectasis - Cardiovascular Status  O2 sat, fluid status o Uncontrolled BP?  reschedule until under control o Recent MI or pacemaker, consult cardiologist prior to surgery o Hx of congenital, rheumatic, or valvular heart disease  antibiotic prophylaxis may be given before surgery to decrease the risk of bacterial endocarditis o Hx of HTN  the ACP may administer vasoactive drugs to maintain adequate BP during surgery - Hepatic/Renal Function  are they able to excrete medication? o Renal dysfunction is associated with a number of alterations, including F&E imbalances, coagulopathies, increased risk for infection, and impaired wound healing. o A decrease in renal function may contribute to an altered response to drugs and unpredictable drug elimination o The liver detoxifies many anesthetics and adjunctive drugs o Hepatic dysfunction  may put pt at increased risk for clotting abnormalities and adverse responses to medications - Endocrine Function  hypoglycemic secondary to NPO status o Pts with DM are especially at risk for adverse effects of anesthesia and surgery  hypoglycemia, hyperglycemia, ketosis, cardiovascular alterations, delayed wound healing, and infection are common complications o Hyper/Hypothyroidism  increased surgical risk b/c of alterations in metabolic rate - Immune Function  allergies (esp. latex) o Corticosteroids used in immunosuppressive doses may be tapered before surgery  impairment of the immune system can lead to delayed wound healing and increased risk for post op infections - Previous Medication Use  discontinue herbal meds 2-3 weeks before o Stop Aspirin 7-10 before surgery to prevent bleeding - Psychosocial Factors  anxiety, fear – both of which affects health teaching - Spiritual/Cultural Beliefs Health History in a Preop Patient Health Perception–Health Management Pattern •What has the doctor explained to you about your surgery? •Have you had surgery before?* •Have you or any family members ever experienced any problems with anesthesia?* •Do you smoke?* If yes, how many packs daily? For how many years? •Do you have any chronic illnesses?* •Are you taking any medications?* Are you allergic to any foods or medications?* •What is your usual use of alcohol? Nutritional-Metabolic Pattern •What is your usual or present height and weight? •Have you had a recent weight gain or loss?* •Do you have any food preferences or dislikes?* •Do you have any difficulty chewing or swallowing?* •Do you take vitamins?* Supplements?* •Do you have any problems healing?* •Do you have a history of liver problems?* Elimination Pattern •Do you experience any problems with constipation?* •Do you experience any problems with urinary elimination?* Activity-Exercise Pattern •Do you have a history of high blood pressure or cardiac disease?* •Do you have any history of dyspnea, coughing, hemoptysis, COPD, or asthma?* •Do you presently have an upper respiratory infection?* •Do you have any musculoskeletal problems that might affect positioning during surgery or activity level after surgery?* •Do you have any limitation in mobility of your neck?* •Do you require any special equipment for ambulation?* Sleep-Rest Pattern •Describe any problems you have with sleeping. •Do you use sleeping pills?* •Do you snore? Cognitive-Perceptual Pattern •Do you wear glasses, contact lenses, or a hearing aid?* •How would you describe your pain tolerance? •What methods have you found effective for pain relief? Self-Perception–Self-Concept Pattern •How do you feel about having this surgery? •Have you experienced any changes in the way you feel about yourself or your body?* Role-Relationship Pattern •Will this surgery create any problems in your usual roles or relationships?* •Will you have the support you feel you need following discharge? Sexuality-Reproductive Pattern •Do you expect this surgery to have any impact on your usual sexual activity?* Coping–Stress Tolerance Pattern •How do you feel about this surgery? Value-Belief Pattern •Do you have a conflict between your planned surgery and your value or belief system? Identify Legal and Ethical Considerations Related to Informed Consent - 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 Describe Preoperative Nursing Measures that Decrease the Risk for Infection and other Post-Op Complications - 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 Describe the Immediate Preoperative Preparation of the Patient - 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 Describe the Interdisciplinary Approach to the Care of the Patient During Surgery 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 Describe the Principles of Surgical Asepsis - 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 Identify the Use of Nursing Process for Optimizing Patient Outcomes During the Intraoperative Period - Room Preparation  ensure privacy, safety, and prevention of infection - Transferring the Patient  apply monitor leads, BP cuff, and pulse ox, IV catheter if not already in place - Scrubbing, Gowning, and Gloving  to eliminate dirt, skin oil, and transient microorganisms; to decrease the microbial count as much as possible; and to inhibit rapid rebound growth of microorganisms - Basic Aseptic Technique  to prevent infections - Assisting the Anesthesia Care Provider  remain at pts side to ensure safety and to assist the ACP - Safety Considerations  surgical time-out - Positioning the Patient  secure extremities, provide adequate padding and support, and obtain sufficient physical or mechanical help to avoid unnecessary straining of self or patient - Preparing the Surgical Site  reduce the number of organisms available to migrate to the surgical wound Describe the Role of the Nurse in Ensuring Patient Safety During the Intraoperative Period Potential Intraoperative Complications - Nausea/Vomiting  turn head to side - Anaphylaxis  latex, adhesives - Hypoxia/Respiratory Complications  occlusion of airways – check VS and tubing to make sure nothing is kinked - Hypothermia  OR is cold, infusions, open up body, decrease in glucose metabolism secondary to anesthesia – monitor temp, ECG, VS. change wet sheets - Malignant Hyperthermia  rare, inherited muscular disorder that is chemically induced by anesthesia o Hx of cramping, family hx o Earliest sign  tachycardia (150+ BPM) o Last sign  increased body temp that develops rapidly (increasing 2-4 degrees q5 min) can raise up to 104 o D/C anesthetic if this happens - DIC (Disseminated Intravascular Coagulation)  life threatening thrombus formation in microcirculation o Manifestations  bleeding – all clotting factors have been used in microcirculation Identify Common Postoperative Problems and Their Management Complications and Causes Mechanisms Manifestations Interventions Airway Obstruction Tongue falling back Muscular flaccidity associated with ↓ consciousness and muscle relaxants Use of accessory muscles Snoring respirations ↓ Air movement Patient stimulation Jaw thrust Chin lift Artificial airway Retained thick secretions Secretion stimulation by anesthetic agents Dehydration of secretions Noisy respirations Coarse crackles Suctioning Deep breathing and coughing IV hydration Chest physical therapy Laryngospasm Irritation from endotracheal tube or anesthetic gases Most likely to occur after removal of endotracheal tube Inspiratory stridor (crowing respiration) Sternal retraction Acute respiratory distress O2 Positive pressure ventilation IV muscle relaxant Lidocaine Corticosteroids Laryngeal edema Allergic drug reaction Mechanical irritation from intubation Fluid overload Similar to laryngospasm O2 Antihistamines Corticosteroids Sedatives Possible intubation Hypoxemia Atelectasis Bronchial obstruction caused by secretions or ↓ lung volumes ↓ Breath sounds ↓ O2 saturation Humidified O2 Deep breathing Incentive spirometry Early mobilization Pulmonary edema ↑ Hydrostatic pressure ↓ Interstitial pressure ↑ Capillary permeability Crackles Infiltrates on chest x-ray Fluid overload ↓ O2 saturation O2 therapy Diuretics Fluid restriction Pulmonary embolism Thrombus dislodged from peripheral venous system; lodged in pulmonary arterial system Acute tachypnea Dyspnea Tachycardia Hypotension ↓ O2 saturation O2 therapy Cardiopulmonary support Anticoagulant therapy Aspiration Inhalation of gastric contents Bronchospasm Atelectasis Crackles Respiratory distress ↓ O2 saturation O2 therapy Cardiac support Antibiotics Bronchospasm ↑ Smooth muscle tone with closure of small airways Wheezing Dyspnea Tachypnea ↓ O2 saturation O2 therapy Bronchodilators Hypoventilation Depression of central respiratory drive Medullary depression from anesthetics/opioids/sedatives Shallow respirations ↓ Respiratory rate/apnea ↓ PaO2 ↑ PaCO2 Stimulation Reversal of opioids/benzodiazepines Mechanical ventilation Poor respiratory muscle tone Neuromuscular blockade Neuromuscular disease As above Reversal of paralysis Mechanical ventilation Mechanical restriction Tight casts, dressings, positioning, and obesity preventing lung expansion As above Elevate head of bed Repositioning Loosen dressings Pain Shallow breathing to prevent incisional pain As above Complaints of pain Guarding behavior Opioid analgesic therapy in reduced dose PaCO2, Partial pressure of arterial carbon dioxide; PaO2, partial pressure of arterial oxygen. Postoperative Nursing Management - PACU o Pt may remain in PACU for 4-6 hours o VS q15 min o Nurse should anticipate type of surgery, anesthesia, and pt needs o Soft colored lighting o Nurse should be good w/ physical exam – know s/s o 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 Hemmorrhage/ 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 Blood Transfusion - Indications for transfusions o Improve circulating blood volume  major blood volume loss, change in mentation o Increase O2 carrying-capacity of blood  PRBCs improve O2 carrying capacity o Replace clotting factors and/or platelets  mostly for pts with chemo or who have cancer of the blood - Types of Transfusions o Whole blood  seldom given; only given when more than 60% of blood is lost or in an emergency (if no time to match, will give type O) o Packed Red Blood Cells (PRBCs)  250-350 ml recommended if hematocrit is < 21% or hemoglobin < 7-8 g; 1 unit of blood can increase Hgb 1 gm and Hct 4% o Platelets  don’t worry about compatibility or crossmatching o Fresh Frozen Plasma (FFP)  ABO blood typing and crossmatching b/c antibodies are in plasma – 200-250 ccs o Autologous  pt donates to themselves; prevents complications b/c its you own – can be stored pre=op for 2 years in frozen condition  Good for rare blood type or people with multiple antibodies - Pre-Transfusion Testing  donated blood needs to be tested first o Infectious Diseases  west nile, HIV, syphilis o ABO & Rh  Rh (-) vs. Rh (+) o Antibody Screen o Crossmatching  check for agglutination (clotting o Donated blood is tested against recipients blood for compatibility - Potential Complications o Acute Hemolytic Reaction  d/t ABO incompatibility; occurs within first 50-100 ccs given  S/S  severe headache, chest pain, fever, chills, tachycardia  Stop transfusion immediately  Bleeding and shock, back pain  Can cause acute renal failure or DIC o Delayed Hemolytic Reaction  d/t incompatibility of some antigen groups (Rh factor) – can take several weeks  S/S same as above  Not immediate; S/S occur in lesser degree o Allergic Reaction  most common; antibodies react to donor plasma or antigen  S/S  itchiness, fever, chills  Stop transfusion immediately o Circulatory Overload  happens when you give blood too fast – no contractility EF is low o Infection  infectious disease o DIC  result from massive treatment from trauma – especially when blood isn’t being crossmatched (esp. in emergency) o Hyperkalemia  when giving old blood and blood is being lysed – lysed blood gives of K+  Arrhythmia  Check K+ level before transfusion o Hypothermia  warm blood before administration - Transfusion Procedure o Pre-Transfusion  Consent  IV site and cannula size  16 0r 18  NS IVF with Y-type tubing  dextrose and LR can hemolyse the RBCs  Request from blood bank (must give within 30 minutes upon its arrival)  VS  take before treatment as baseline  Pre-Medicate  benadryl or Tylenol; has to be on order; given to pts who have had a hx of rxn  Confirm blood compatibility  2 RNs along w/ identity of pt and blood o During Transfusion  VS  especially during first 15 minutes; stay with patient until first 50 ccs are infused; then take VS hourly and instruct pt to report any signs of rxn  Infusion rates  run slowly at first; no treatment more than 4 hours; generally given over 2 hours (if more than 2 hours, support yourself with a doctors order) o Post-Transfusion Care  Give rest of NS per doctors order o Documentation o Blood transfusion can only be used on an IV pump if indicated by a doctor o BP cuff can be used to push blood in quicker but be sure BP cuff doesn’t exceed 300 mg/Hg  Used for emergency, place around bag Ch. 34 – Coronary Artery Diseases Some Review Terminology: - Preload  the volume of blood in the ventricles at the end of diastole, before the next contraction - Afterload  the peripheral resistance against which the left ventricle must pump - Stroke Volume  amount of blood that leaves the LV (SV x 60 = CO) Coronary Artery Disease - A type of blood vessel disorder that is included in the general category of atherosclerosis - Affects the coronary arteries resulting to atherosclerosis or hardening of the arteries due to fatty deposits - Heart attack  leading cause of Cardiovascular disease death and death in general - 1.1 million  estimated Americans will have MI in 2003 - 460,000  will die, half of them before reaching the hospital - Atherosclerosis  begins as soft deposits of fat that harden with age Theories of Atherogenesis - Endothelial Injury  endothelium of the artery is damaged due to chemical irritants in the blood o Can be injured as a result of tobacco use, hyperlipidemia, HTN, diabetes, hyperhomocysteinemia, and infection causing a local inflammatory response - Lipid Infiltration  lipids enter into the endothelium resulting in inflammation and trauma - Aging  blood vessel hardens and loses elasticity - Thrombogenic  RBCs, platelets, and lipids stick in intimal layer and builds up over time - Vascular Dynamics - Inflammation  results from infectious stimuli o C-reactive protein (CRP), a nonspecific marker of inflammation, is increased in many patients with CAD o Chronic exposure to even minor elevations of CRP can trigger the rupture of plaques and promote the oxidation of low-density lipoprotein (LDL) cholesterol, leading to increased uptake by macrophages in the endothelial lining 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 higher risk to develop CAD  Nicotine causes catecholamine release (epinephrine, norepinephrine)  cause increased HR, peripheral vasoconstriction, and increased BP  These changes increase the cardiac workload, necessitating greater myocardial oxygen consumption  Nicotine also increases platelet adhesion, which increases the risk of emboli formation  The effects of an increased cardiac workload, combined with the oxygen depleting effect of carbon monoxide, significantly decreases the oxygen available to the myocardium  Carbon monoxide may also be a chemical irritant  endothelial injury o Physical Inactivity  Physically active people have increased HDL levels, and exercise enhances fibrinolytic activity thus reducing the risk of clot formation  Exercise training for those who are physically inactive decreases the risk of CAD through more efficient lipid metabolism, increased HDL2 production, and more efficient oxygen extraction by the working muscle groups, thereby decreasing the cardiac workload  Physically active persons are seldom obese and can achieve a 5-10 mm Hg drop in their BP, thus reducing three risk factors in CAD o Obesity  Weight 30% more than standard weight  BMI higher than 30  Obese persons are thought to produce increased levels of LDLs and triglycerides, which are strongly implicated in atherosclerosis  Obesity is often associated with HTN, and increased insulin resistance  As obesity increases, the heart size grows, causing increased myocardial oxygen consumption - Modifiable Contributing Risk Factors o Diabetes Mellitus  2-4 times greater risk  Because the person with diabetes has an increased tendency toward connective tissue degeneration and endothelial dysfunction, it is thought that this is condition may account for the tendency toward atheroma development  Diabetic pts also have alterations in lipid metabolism and tend to have high cholesterol and triglyceride levels o Metabolic Syndrome  Refers to a cluster of risk factors for CAD including obesity, elevated triglycerides, HTN, abnormal serum lipids, and an elevated fasting blood glucose o Psychologic States  Type-A personality often creates stress and tension making them more prone to MI’s  Depressed pts have elevated levels of circulating catecholamines that may contribute to endothelial injury and inflammation, and platelet activation  Stress  SNS stimulation and its effect on the heart (increased HR  intense force of myocardial contraction  increased myocardial oxygen demand) are generally considered to be the physiologic mechanism by which stress predisposes to the development of CAD  Stress-induced mechanisms can cause elevated lipid and glucose levels and alterations in blood coagulation, which can lead to increased atherogenesis o Homocysteine  A sulfur-containing amino acid produced by the breakdown of the essential amino acid methionine which is found in dietary protein  High levels (>12-15) possibly contribute to atherosclerosis by: • Damaging the inner lining of blood vessels • Promoting plaque build up • Altering the clotting mechanism to make clots more likely to occur Major Clinical Manifestations of CAD - Angina Pectoris  chest pain - Acute Coronary Syndrome  develops when ischemia is prolonged and not immediately reversible - Sudden Cardiac Death  unexpected death from cardiac problems o An abrupt disruption in cardiac function, producing an abrupt loss of CO and cerebral blood flow o Death usually occurs within one hour of the onset of acute symptoms (i.e., angina, palpitations) o Majority of cases caused by acute ventricular dysrhythmias (V. tach, V. fib) Types of Angina - Symptom of CAD - Angina is the clinical manifestation of reversible myocardial ischemia o Myocardial ischemia occurs when the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen o Either an increased demand for oxygen or a decreased supply of oxygen can lead to myocardial ischemia o The primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis (75% or more obstructed for ischemia to occur) o On the cellular level, the myocardium becomes hypoxic within the first 10 seconds of coronary occlusion  with total occlusion of the coronary arteries, contractility ceases after several minutes depriving the myocardial cells of oxygen and glucose for aerobic metabolism o Anaerobic metabolism begins and lactic acid accumulates  myocardial nerve fibers are irritated by the increased lactic acid and transmit a pain message to the cardiac nerves and upper thoracic posterior nerve roots (the reason for referred cardiac pain to the left shoulder and arm) - Chronic Stable Angina  chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms o Unpleasant feeling, often described as a constrictive, squeezing, heavy, choking, or suffocating sensation o Most pain appears substernally, but the sensation may occur in the neck or radiate to various locations, including the jaw, shoulders, and down the arms o The pain usually lasts for only a few minutes (3-5) and commonly subsides when the precipitating factors is relieved  Precipitating factors  physical exertion, temperature extremes, strong emotions, consumption of heavy meal, tobacco use, sexual activity, stimulants, and circadian rhythm patterns  Can be controlled with medication - Silent Ischemia  asymptomatic o Pts with diabetes have an increased prevalence of silent ischemia that is thought to be related to diabetic neuropathy affecting the nerves that innervate the cardiovascular system - Nocturnal Angina and Angina Decubitus o Nocturnal  occurs at night but not necessarily when the person is in the recumbent position or during sleep o Angina decubitus  chest pain that occurs only while the person is lying down and is usually relieved by standing or sitting  Abdominal contents push up and restrict lung expansion decreasing oxygen content resulting in angina - Prinzmetal’s Angina  variant angina o Often occurs at rest, usually in response to spasm of a major coronary artery o Rare but frequently seen in pts with a history of migraine headaches and Raynaud’s phenomenon - Unstable Angina  chest pain that is new in onset, occurs at rest, or has a worsening pattern o Unpredictable emergency Chronic Stable Angina Prinzmetal's Angina Unstable Angina Etiology Myocardial ischemia, usually secondary to CAD Coronary vasospasm Rupture of thickened plaque, exposing thrombogenic surface Characteristics • Episodic pain lasting 5-15 min • Provoked by exertion • Relieved by rest or nitroglycerin • Occurs primarily at rest • Triggered by smoking • May occur in presence or absence of CAD • New-onset angina • Angina of increasing frequency, duration, or severity • Occurs at rest or with minimal exertion • Pain refractory to nitroglycerin 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 Complications of MI - Dysrhytmias  most common complication of MI (80%) o Caused by any condition that affects the myocardial cell’s sensitivity to nerve impulses, such as ischemia, electrolyte imbalances, and SNS stimulation o The intrinsic rhythm of the heartbeat is disrupted, causing a fast HR, a slow HR, or an irregular beat - Heart Failure  complication that occurs when the pumping power of the heart has diminished o HF occurs initially with subtle signs such as mild dyspnea, restlessness, agitation, or slight tachycardia - Cardiogenic Shock  occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Diagnostic Studies for Angina - Chest X-ray  taken to look for cardiac enlargement, aortic calcifications, and pulmonary congestion - ECG  can detect rhythm of heart, activity of pacemaker, conduction abnormalities, position of heart, size of atria and ventricles, presence of acute injury, and history of MI - Laboratory Test o Serum Lipids o Cardiac Markers  cardiac enzymes o CRP  marker of inflammation that can predict risk of cardiac disease and cardiac events, even in patients with normal lipid values - Treadmill Exercise Testing  increases demand for O2 and visualizes how heart is coping. Continual monitoring of vital signs and ECG rhythms for ischemic changes are important in the diagnosis of left ventricular function and CAD - Nuclear Imaging (IV Injection of Radioisoptope)  It supplies information about myocardial contractility, myocardial perfusion, and acute cell injury, and looks at cold spots - PET Scan  uses two radionuclides. Nitrogen-13-ammonia is injected IV first and scanned to evaluate myocardial perfusion. A second radioactive isotope, fluoro-18-deoxyglucose, is then injected and scanned to show myocardial metabolic function. In the normal heart, both scans will match, but in an ischemic or damaged heart, they will differ - Coronary Angiography  study involves injection of radiopaque contrast medium directly into coronary arteries by same procedure as for cardiac catheterization. It is used to evaluate patency of coronary arteries and collateral circulation. - Echocardiogram  transducer that emits and receives ultrasound waves is placed in four positions on the chest above the heart. Transducer records sound waves that are bounced off the heart. Also records direction and flow of blood through the heart and transforms it to audio and graphic data that measure valvular abnormalities, congenital cardiac defects, wall motion, ejection fraction, and cardiac function. Diagnostic Studies for MI - Patient History  pain, risk factors, and health history - ECG  changes in ST segment. The ECG often reveals the time sequence of ischemia, injury, infarction, and resolution of the infarction - Serum Cardiac Marker  important in the dx of MI; when cardiac cells die, their intracellular enzymes are released into circulation o Creatine Kinase (CK)  begin to rise 3-12 hours after an MI, peak in 24 hours, and return to normal within in 2-3 days  The CK enzymes may be fractioned into bands, including the MB band (CK-MB) which is specific to myocardial cells and can help quantify myocardial damage o Troponin  a myocardial muscle protein released into circulation after myocardial injury  Highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than CK-MB  Troponin rises as quickly as CK (3-12 hours), peak at 24-28 hours, and return to baseline over 5-14 days 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) 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 Nursing Therapeutics/Plan of Care Angina - Health Promotion  aimed to decrease risk factors - Acute Interventions o Administration of Oxygen  check to make sure machine is running and is not kinked o Monitor VS, ECG, heart sounds o Give nitrate followed by narcotic analgesic o Position for comfort  30-45 degree angle  Stomach or abdominal contents are being pushed down by gravity  facilitates more lung expansion - Ambulatory/ Home Care o Pt assurance  can still lead a productive life  Pt feels invalid? Use open ended questions o Health teaching  diet, weight management, exercise program o Counseling  signs of anxiety, depression, worry MI - Acute Interventions o Pain  nitrate, morphine administration, use pain scale  Also look for physiologic signs  increased HR and BP  Check bladder too if pt is sedated o Monitoring  ECG, arrhythmia, ventricular fib (most common and lethal arrhythmia) o Rest and comfort o Control anxiety o Emotional and behavioral reactions o Physical assessment  neck vein engorgement  heart is not emptying  think CHF, which is a complication of MI - Ambulatory/ Home Care o Patient teaching o 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 o For uncomplicated MI, ambulate the pt by day 3 o Physical exercise  rhythmic, repetitive activity that still works muscles (isotonic exercise – ROM) o Resumption of Sexual activity  use matter of fact approach  Remain neutral – talk about taking prophylactic nitroglycerin, walking  7-10 days post uncomplicated MI  Not advisable after a heavy meal or consumption of alcohol  Should be able to clime 2 flights of stairs w/o signs of chest pain or dyspnea  Stress to avoid anal intercourse  No Viagra post MI Ch. 35 – Heart Failure Heart Failure  an abnormal clinical condition involving impaired cardiac pumping - Results in vasoconstriction and fluid retention - Also results in diminished cardiac output and cardiac congestion - Associated with a number of cardiovascular diseases  long-standing HTN, CAD, and MI 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 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) Complications of CHF - Pleural Effusion  results from increasing pressure in the pleural capillaries. A transudation of fluid occurs from these capillaries into the pleural space - Dysrhythmias  enlargement may cause an alteration in the normal electrical pathway - Left Ventricular Thrombus  enlarged LV and decreased CO combine to increase the chance of thrombus formation in the LV - Hepatomegaly  especially associated with RV failure; the liver lobules become congested with venous blood  the hepatic congestion leads to impaired liver function eventually leading to death of liver cells, fibrosis, and cirrhosis - Renal Failure  secondary to decreased CO Classification of Heart Failure  based on a person’s tolerance to physical activity NYHA Functional Classification of Heart Disease ACC/AHA Stages of Heart Failure Class I No limitation of physical activity. Ordinary physical activity does not cause fatigue, dyspnea, palpitations, or anginal pain. Class II Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in fatigue, dyspnea, palpitations, or anginal pain. Class III Marked limitation of physical activity. Usually comfortable at rest. Ordinary physical activity causes fatigue, dyspnea, palpitations, or anginal pain. Class IV Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of angina may be present even at rest. If any physical activity is undertaken, discomfort is increased. Stage A Patients at high risk of developing left ventricular dysfunction because of the presence of conditions that are strongly associated with the development of HF. Stage B Patients who developed structural heart disease that is strongly associated with the development of HF but who have never shown signs of HF. Stage C Patients who have current or prior symptoms of HF associated with underlying structural heart disease. Stage D Patients with advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions. Diagnostic Studies TABLE 35-6 COLLABORATIVE CARE: Acute Decompensated Heart Failure and Pulmonary Edema Diagnostic History and physical examination ABGs, serum chemistries, cardiac enzymes, BNP level, liver function tests Chest x-ray Hemodynamic monitoring 12-lead ECG Echocardiogram Nuclear imaging studies (see Table 32-7) Cardiac catheterization Stress Test Collaborative Therapy Treatment of underlying cause High Fowler's position O2 by mask or nasal catheter; BiPAP BP, HR, RR, urinary output at least q1hr Continuous ECG and pulse oximetry monitoring Hemodynamic monitoring (e.g., intraarterial BP, PAWP, CO) Drug therapy: diuretics IV (furosemide [Lasix]); nitroglycerin IV; morphine IV; nesiritide (Natrecor); inotropic therapy (see Table 35-9) Daily weights Possible cardioversion (e.g., atrial fibrillation) Endotracheal intubation and mechanical ventilation Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device) - EF can be measured using echocardiography and/or nuclear imaging studies - EF can be used to differentiate between systolic and diastolic HF  important for treatment TABLE 35-7 COLLABORATIVE CARE: Chronic Heart Failure Diagnostic History and physical examination Determination of underlying cause Serum chemistries, cardiac enzymes, BNP level, liver function tests Chest x-ray 12-lead ECG Echocardiography Exercise stress testing Nuclear imaging studies (see Table 32-7) Hemodynamic monitoring Cardiac catheterization Collaborative Therapy Treatment of underlying cause Oxygen therapy at 2-6 L/min by nasal cannula Rest-activity periods Drug therapy (see Table 35-9) Daily weights Sodium-restricted diet Circulatory assist devices (e.g., ventricular assist device) Cardiac resynchronization therapy with internal cardioverter-defibrillator Cardiac transplantation Drug Therapy - 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 Nursing Therapeutics/ Plan of Care 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) o Ambulatory Home Care  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 Ch. 36 – Dysrhythmias and ECG Interpretation Conduction System Review - Specialized nerve tissue responsible for creating and transporting the electrical impulse, or action potential - The impulse initiates depolarization and subsequently cardiac contraction - Electrical impulse is initiated by the SA node (the pacemaker of the heart) and travels through the muscle fibers of the atria by internodal pathways and cell-to-cell conduction  mechanical contraction of the atria follows the depolarization of the cells - The electrical impulse travels from the atria to the AV node, moves through the bundle of his and the left and right bundle branches  the action potential then diffuses widely through the walls of both ventricle by means of Purkinje fibers  synchronized ventricular contraction - The cardiac cycle starts with depolarization of the SA node  climaxes with ejection of blood  ends with repolarization when the contractile fiber cells and the conduction pathway cells regain their resting polarized condition - Cardiac muscle cells have a compensatory mechanism that makes them unresponsive or refractory to restimulation during the action potential  during systole there is an absolute refractory period during which cardiac muscle doesn’t respond to any stimuli  after this period, cardiac muscle gradually recovers its excitability and a relative refractory period occurs by early diastole ECG Review - P  begins with the firing of the SA node and represents depolarization of the fibers of the atria (atrial contraction) o Duration 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 - Irregurlary Irregular rhythm  P waves are constantly irregulary/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 cause 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' Ch. 37 – Inflammatory and Structural Heart Disorders - Valvular Heart Disease  functional alteration of one or more valves of the heart due to stenosis and regurgitation o Because of the 4 valves there can be 8 different diagnoses - Stenosis  constriction or narrowing o Can be due to hardening o So narrow, it doesn’t close completely, allowing leakage o In a stenotic valve, the valve orifice is smaller, impeding the forward flow of blood and creating a pressure gradient difference across and open valve o The degree of the stenosis is seen in the pressure gradient differences  the higher the gradient, the greater the stenosis - Regurgitation  insufficiency that permits leakage or backward flow through the incompetent valve; blood goes back and forth o Incomplete closure of the valve leaflets results in the backward flow of blood o In a normal heart, blood coming out of the atrium causes the valve to open  as the ventricle fills, the valve closes - Cardiac output decreases, LV has to work harder trying to compensate for decreased CO  CHF evolves - Valvular disorders occur in children and adolescents primarily from congenital conditions such as tricuspid atresia, pulmonary stenosis, and aortic stenosis. Mitral Valve Stenosis  shortening, thickening of the (mitral) valve - Most cases result from rheumatic heart disease o Due to mostly infection or complication of streptococcal infection o Tonsils are the first structures that filter microorganisms in your system  if your immune system is already weak, the microorganism multiples and creates a colony o It begins to circulate and goes to the valves of the heart o It eventually heals but creates a scar resulting in stenosis - Patho: o Rheumatic carditis causes scarring of the valve leaflets and the chordae tendineae  contractures and adhesions develop between the commissures (the junctional areas)  stenosic mitral valve takes on a “fish mouth” shape because of the thickening and shortening of the valve structures o These structural deformities cause obstruction of blood flow and create a pressure difference between the LA and LV during diastole o LA pressure and volume elevation cause increased pulmonary vasculature pressure and subsequent hypertrophy of the pulmonary vessels o Chronic mitral stenosis  pressure overload occurs in the LA, the pulmonary bed, and the RV - Less common causes are congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus - Manifestations: o Exertional dyspnea  due to reduced lung compliance o Fatigue and palpitations  from atrial fibrillation due to cardiac hypertrophy (ventricle enlarges because of constant compensation; atria enlarges because of constant backflow of blood) o Heart sounds include a loud first heart sound and a low-pitched, rumbling diastolic murmur (best heard at the apex with a stethoscope)  murmur caused by turbulence of blood passing through a narrow passageway o Hoarseness  from atrial enlargement pressing on the laryngeal nerve o Hemoptysis  from pulmonary HTN o Chest pain  from decreased CO o Seizures or stroke  from emboli that can arise from blood stasis in the LA Mitral Valve Regurgitation  backward flow of blood from LV to LA - Mitral valve function depends on intact mitral leaflets, mitral annulus, chordae Tendineae, papillary muscles, LA, and LV  any defect in any of these structures can result in regurgitation - Allows blood to flow backward from the LV to LA due to incomplete valve closure during systole - LV and LA both work harder to preserve an adequate CO - Causes: o MI o Chronic rheumatic heart disease o Mitral valve prolapse o Ischemic papillary muscle dysfunction o Inflammatory  due to the damage from the valve lifting and due to infection o Degenerative o Infective o Structural/congenital  it just doesn’t close or fit together - Manifestations: o Chronic MR:  Atrial enlargement, ventricular dilatation, and eventual ventricular hypertrophy resulting from additional volume load  Weakness, fatigue, palpitations, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema  secondary to LV failure  Systolic murmur  due to accentuated LV filling o Acute MR  LA and ventricle do not abruptly dilate  Pulmonary edema and shock  due to sudden increase in pressure and volume that is transmitted to the pulmonary bed  Thready peripheral pulses, cool clammy extremities  secondary to decreased CO Mitral Valve Prolapse  abnormality of the mitral valve leaflets and the papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the LA during systole - Etiology  unknown - Most patients asymptomatic for their entire lives - Characteristic  murmur from regurgitation that gets more intense through systole Aortic Valve Stenosis  causes obstruction of flow from the LV to the aorta during systole - Results in LV hypertrophy and increased myocardial oxygen consumption because of the increased myocardial mass - As the disease progresses and compensatory mechanisms fail, reduced CO leads to pulmonary HTN and HF - Mitral valve disease often accompanies this when occurs secondary to rheumatic fever - Causes: o Congenital o Older patients  usually a result of rheumatic fever or senile fibrocalcific degeneration - Manifestations: o Symptoms develop when the valve orifice becomes about one third its normal size o Symptoms include classic triad  angina, syncope, and exertional dyspnea o Systolic crescendo-decrescendo murmur Aortic Valve Regurgitation  retrograde blood flow from the ascending aorta into the LV during diastole, resulting in volume overload - LV initially compensates for chronic AR by dilation and hypertrophy - Myocardial contractility eventually declines and blood volumes increase in the LA and pulmonary bed  pulmonary HTN and RV failure - Causes: o Result of primary disease of the aortic valve leaflets, the aortic root, or both o Acute AR  trauma, IE, or aortic dissection  Life-threatening emergency o Chronic AR  result of rheumatic heart disease, a congenital bicuspid aortic valve, syphilis, or chronic rheumatic conditions - Manifestations: o Acute AR  sudden signs of cardiovascular collapse (severe dyspnea, chest pain, and hypotension) o Chronic AR  water hammer pulse (a strong, quick beat that collapses immediately)  Generally remains asymptomatic or years and is seen with exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea only after considerable myocardial dysfunction has occurred TABLE 37-13 Clinical Manifestations of Valvular Heart Diseases Clinical Manifestations Mitral valve stenosis Dyspnea on exertion, hemoptysis; fatigue; palpitations; loud, accentuated S1; low-pitched, rumbling diastolic murmur; atrial fibrillation on ECG Mitral valve regurgitation Acute—generally poorly tolerated, with fulminating pulmonary edema and shock developing rapidly; new systolic murmur Chronic—weakness, fatigue, exertional dyspnea, palpitations; an S3 gallop, holosystolic or pansystolic murmur Mitral valve prolapse Palpitations, dyspnea, chest pain, activity intolerance, syncope; midsystolic click, late or holosystolic murmur Aortic valve stenosis Angina, syncope, dyspnea on exertion, heart failure; normal or soft S1, diminished or absent S2, systolic crescendo-decrescendo murmur, prominent S4 Aortic valve regurgitation Acute—abrupt onset of profound dyspnea, chest pain, left ventricular failure and shock Chronic—fatigue, exertional dyspnea, orthopnea, PND; water-hammer pulse; heaving precordial impulse; diminished or absent S1, S3, or S4; soft decrescendo high-pitched diastolic murmur, Austin-Flint murmur, systolic ejection click Tricuspid and pulmonic stenosis Tricuspid—peripheral edema, ascites, hepatomegaly; diastolic low-pitched, decrescendo murmur with increased intensity during inspiration Pulmonic—fatigue, loud midsystolic murmur 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 - 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 Ch 38 – Vascular Disorders Aortic Aneurysm - Out pouchings or dilations of the arterial wall - May involve the aortic arch, thoracic aorta, and/or abdominal aorta o Most aneurysms found in abdominal aorta below the level of the renal arteries - The larger the aneurysm, the greater the risk of rupture - Patho: o The dilated aortic wall becomes lined with thrombi that can embolize, leading to acute ischemic symptoms in distal branches o Primary causes:  Atherosclerosis  plaques deposit beneath the intima causing degenerative changes in the media leading to loss of elasticity, weakening, and eventual aortic dilation • When the high pressure gets to be too much, an out pouching forms  Genetic predisposition  Penetrating or blunt trauma  Infection - Classifications: o True Aneurysm  one in which the wall of the artery forms the aneurysm, with at least one vessel layer still intact  Fulsiform aneurysm  circumferential and relatively uniform in shape  Saccular aneurysm  pouch like with a narrow neck connecting the bulge to one side of the arterial wall o False Aneurysm  not an aneurysm, but a disruption of all layers of the arterial wall resulting in bleeding that is contained by surrounding structures  May result from trauma or infection, or occur after peripheral artery bypass graft surgery at the site of the graft to artery anastomosis  May also result from arterial leakage after removal of cannulae such as upper or lower extremity catheters and intraaortic balloon pump devices - Manifestations: o Often asymptomatic because the blood still flows through  Becomes symptomatic when the delivery at the distal part no longer receives oxygen o Deep, diffuse chest pain that may extend to the interscapular area o Hoarseness  a result of pressure on the recurrent laryngeal nerve o Dysphagia  pressure on esophagus o Distended neck veins and edema of the head and arms  caused by decreased venous return if aneurysm presses on superior vena cava o Pulsatile mass in the periumbilical area  never touch pulsation (can result in another out pouching or rupture) o Audible bruit  from the turbulence of blood in the structure o Pain, abdominal or back  r/t compression of nearby anatomic structures o Discomfort with or without alteration of bowel elimination  from bowel compression - Complications: o Rupture/Bleeding/Death o Grey Turner’s Sign  severe back pain secondary to rupture occurring into the retroperitoneal space o If rupture occurs anteriorly into the abdominal cavity, most pts font survive long enough to get to the hospital  die from massive hemorrhage - Collaborative Care o Goal  prevent rupture of aneurysm  If aneurysm is < 4 cm  conservative treatment (i.e., no lifting etc…anything that can increase abdominal pressure, basic lifestyle modifications)  Greater that 5-6 cm  surgical repair - Nursing Therapeutics: o Decrease risk factors associated with atherosclerosis o Pre-op  support and teaching o ICU care post surgery o Maintain BP  an adequate BP is important to maintain graft patency  Prolonged hypotension may result in graft thrombosis  Severe HTN may cause undue stress on the arterial anastomoses, resulting in leakage of blood or rupture at the suture lines o 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 o Prevention of infection/ ABT  the development of a prosthetic vascular graft infection is a relatively rare but potentially life-threatening complication o Prevention of paralytic ileus  through early ambulation – start with isometric movements (sitting in bed and letting their legs dangle before letting them walk) o 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 o 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 o Avoid heavy lifting 4-6 weeks post op o Monitor for S/S of infection