N176 test 2

  1. thermal burn
    -caused by:
    caused by: flame, flash, scald
  2. chemical burn
    -caused by:
    -what to do:
    • caused by: tissue injury and destruction from necrotizing substances
    • what to do: remove the person from the burning agent - lavage with water
  3. smoke inhalation injury
    -caused by:
    -damage to:
    -3 types:
    • caused by: inhalation of hot air or noxious chemicals
    • damage to: tissues of the respiratory tract
    • 3 types: carbon monoxide poisoning, inhalation injury above the glottis, inhalation injury below the glottis
  4. carbon monoxide poisoning
    -when to suspect
    -how to treat
    • complications: hypoxia, carboxyhemoglobinemia (CO has higher affinity for Hgb than O2 and binds it all preventing RBCs from transporting O2 to tissue), death
    • when to suspect: closed space fire
    • treatment: 100% oxygen
  5. inhalation injury above the glottis
    -how produced
    -signs to look for
    • how produced: usually thermally produced
    • complications: may quickly lead to obstruction
    • signs: singed nasal hair, hoarseness, painful swallowing, drooling, dark oral and nasal membranes
  6. inhalation injury below the glottis
    - result of
    -injury severity
    -hallmark sign
    -definitive diagnosis
    • result of: chemical exposure
    • severity: injury is related to time of exposure
    • complications: may manifest as pulmonary edema 12-24hrs or lead to acute respiratory distress and acute respiratory failure
    • hallmark sign: carbonaceous sputum
    • diagnosis: bronchoscopy
  7. electrical burns:
    -result of:
    -severity depends on:
    • result of: coagulation necrosis caused by intense heat generated by electrical current
    • severity: depends on amount of voltage, tissue resistance, current pathways, surface area in contact with the current, and length of time current flow was sustained
    • infuse: LR IV in order to maintain minimum urine output 75ml/hr
  8. 3 layers of skin and their purpose
    • epidermis: outer protective layer responsible for holding in fluids and electrolytes, regulating heat and protecting the body from infection
    • dermis: contains connective tissue, blood vessels, nerve endings, hair follicles, sweat and sebaceous glands
    • subcutaneous tissues: shock absorber and heat insulator for the underlying muscles, tendons, bones and internal organs
  9. superficial burns
    -layer of skin involved
    • layers: epidermis
    • description: sunburn, pink, no blisters
    • pain: local
    • healing: spontaneous without scars in 3-5 days
  10. partial-thickness burns
    -layer of skin involved
    • layers: epidermis and dermis
    • description: red, whiter for deep partial, moist appearance, formation of blisters
    • pain: local
    • healing: 2-3 weeks, scars depending on depth
  11. full-thickness burns
    -layers of skin involved
    • layers: involves fat, muscle, and bone
    • description: variable - white, waxy, red, brown
    • pain: painless
    • healing: skin can’t heal on its own; weeks to months after removing dead skin and applying graft. prone to contracture and scarring
  12. how to calculate extent of burn
    -rule of nines
    -rule of palms
    • rule of nines: head and neck (9%), arms (9%), anterior trunk (18%), posterior trunk (18%), legs (18%), perineum (1%)
    • rule of palms: patients hand surface area=1%
  13. burns to hands, feet, joints, and eyes
    make self-care difficult and jeopardize future function
  14. burns to ears, nose, buttocks and perineum are susceptible to
  15. CV response to burns
    -capillary refill
    • third space fluid shift
    • decdreased CO
    • increased systemic vascular resistance
    • vasoconstriction
    • hypotension
    • tachycardia
    • prolonged capillary refill
    • impaired microcirculation and increased viscosity
  16. pulmonary response to burns
    -lung sounds
    • release of vasoconstrictive agents
    • airway edema
    • soot tinged sputum
    • increased RR and WOB
    • crackles and/or stridor
    • voice hoarseness
  17. renal response to burns
    -blood flow
    -urine output
    -tubular cells
    • hypovolemia and redistribution of blood flow to vital organs leads to decreased glomerular filtration rate
    • oliguria
    • acute tubular necrosis
  18. GI response to burns
    • response due to hypovolemia
    • impaired gastric motility and paralytic ileus
    • stress ulcers leading to Curling's ulcer
  19. metabolic response to burns
    • secretion of cortisol and glucagon to support tissue repair
    • hyperglycemia
    • hypermetabolism
  20. emergent phase of burns
    -start and finish
    • the period of time required to resolve the immediate problems resulting from burn injury
    • starts with fluid loss and edema and ends with fluid mobilization and diuresis
    • usually lasts 24-48hrs
    • care focuses on airway management, fluid therapy, and wound care
  21. airway management in the emergent phase of burns
    • intubation within 1-2hrs if burns to the face
    • extubate after 3-6 days, unless inhalation injury
    • escharatomies is circumferential full thickness burns of the chest or neck or trunk
    • high fowlers
    • 100% oxygen with PEEP and bronchodilators
  22. fluid therapy in the emergent phase of burns
    -volume calculation
    -what fluids
    -best indicator of adequate fluid volume
    • immediately start 2 large bore IVs
    • fluid resuscitation indicated if >15% TBSA burned
    • Parkland formula for fluid volume: 4cc LR per %TBSA burned per kg patient weight - 1/2 within the first 8hrs, 1/4 in 2nd 8hrs, and 1/4 in 3rd 8hrs
    • fluids used: NS, LR, D5 NS, albumin
    • best indicator of adequate fluid volume resuscitation: adequate urine output
  23. wound care in emergent phase of burns
    -types of graphs
    • when: not addressed until the ABCs and fluid replacement have been established
    • how: debridement to remove necrotic skin
    • complications: infection is the most serious threat to further injury and survival
    • goal: coverage of burn wounds
    • graph types: may come from the patient (autograph) and be permanent, may come from cadavers (allograph) or porcine (heterography) and be temporary
  24. special care areas with burns
    -hands and arms
    • face: no dressings
    • eyes: rinses and drops, early ophthalmologist examination
    • hands and arms: extended and elevated with pillows and slings to minimize edema, splints and ROM to hands and feet to maintain functional positions and prevent contractures
    • ears: no pressure
    • perineum: extra care to keep clean and dry, use a Foley - infection prevention
  25. nutritional therapy during emergent phase of burns
    -how much
    • fluid replacement takes priority over nutritional needs
    • when bowel sounds return 48-72hrs, oral intake can be started with clear liquids
    • hypermetabolic state - metabolic expenditure may be increased 50-100% above normal
  26. acute phase of burns
    -starts and ends with
    • starts with mobilization of extracellular fluid and subsequent diuresis and ends when the burned area is completely covered by skin grafts or when the wounds are completely healed
    • diuresis from fluid mobilization occurs and the pt is no longer grossly edematous
    • bowel sounds return
    • necrotic tissue begins to slough
    • partial-thickness wounds heal from the edges and full-thickness wounds must be covered by skin grafts
  27. lab values during acute phase of burns
    • hyponatremia: hydrotherapy, GI drainage, water intoxication
    • hypernatremia: following successful fluid replacement
    • hypokalemia: hydrotherapy, vomiting, diarrhea, GI suction
    • hyperkalemia: renal failure, deep muscle injury
  28. complications of the acute phase of burns
    • immunity: infection - sepsis
    • neuro: not unless hypoxia
    • muscular: decreased ROM and contractures
    • GI: paralytic ileus and Curling's ulcer
    • endocrine: hyperglycemia
  29. collaborative management during acute phase of burns
    • wounds: daily observation, cleansing, debridement
    • pain: management - opioids q1-3hrs, combo drugs - morphine with haloperidol
    • PT/OT: passive and active ROM, custom-fitted splints
    • nutrition: calculation of caloric needs, high-protein, high-carb
  30. rehabilitation phase of burns
    -collaborative management: wound care, products, activity, nutrition
    -emotional needs
    • start: begins when the burn wounds are covered with skin or healed and the patient is able to resume a level of self-care activity
    • healing: wounds heal by primary intention or by grafting, mature healing within 6-24 months
    • complications: skin and joint contractures, hypertrophic scarring
    • collaborative management: both patient and family to learn how to care for wounds, use an emollient water-based cream, emphasize importance of exercise, high-calorie/high-protein diet
    • importance of reestablishing the patient's independence
  31. MAP
    -measurement of
    -affected by
    • measurement of organ perfusion
    • MAP=systolic + 2x diastolic /3
    • total blood volume, cardiac output, size of the vascular bed
  32. cellular changes during shock
    • decreased tissue perfusion
    • reduces oxygen delivery to cells
    • cells increase anaerobic metabolism
    • produces pyruvic acid
    • is converted to lactic acid
    • accumulates in the cells causing acidosis
    • decreases cellular pH
    • release of digestive enzymes
    • destruction of cell membrane and digestion of cellular contents
  33. shock management
    • maintain patent airway
    • adequate oxygenation
    • IV access
    • fluids to maintain BP and CO
    • peripheral pulse assessment
    • assess organ perfusion
  34. initial stage of shock
    • <10 MAP decrease
    • slight HR increase
    • increases lactate
  35. compensatory stage of shock
    • BP: <10-15 MAP, but adequate for organ perfusion
    • HR: 100-150
    • skin: vasoconstriction - cool, pale, moist
    • pulse: rapid, weak, thready
    • urine: <30ml/hr
    • LOC: restless, confused, agitated, responsive
    • respirations: >20/min - to blow off CO2 from acidosis
    • bowel: hypoactive, mild distension
    • pupils: dilated, but reactive to light
    • labs: acidosis, hyperkalemia
  36. progressive stage of shock
    • BP: <20 MAP - inadequate organ perfusion
    • HR: >150
    • skin: cold, cyanotic, mottled
    • pulse: extremely weak and thread, may be absent
    • urine: <20ml/hr
    • LOC: no longer responsive
    • respirations: rapid and shallow, moist crackles
    • bowel: absent, ileus to develop, possible bleed
    • pupils: dilated, sluggish response to light
    • labs: severe acidosis, hyperkalemia, hypoxemia, organ failure - inc Cr and BUN, inc LDH, AST, ALT, inc lactate
  37. refractory stage of shock
    • BP: hypotension despite vasopressors and fluid
    • HR: varies, dysrhythmias common, myocardial ischemia noted on ECG
    • skin: cold, mottled, pettechiae with DIC, edema, 3rd spacing
    • pulse: absent
    • urine: anuria
    • LOC: obtunded to coma
    • respirations: ventilator dependent
    • bowel: absent
    • pupils: dilated and unresponsive
    • labs: acidosis, hyperkalemia, MODS DIC (inc PT, PTT, FSP, dec fibrinogen)
  38. causes of neurogenic shock
    • pain
    • anesthesia
    • spinal cord injury (85% above T1)
    • head trauma
  39. clinical manifestations of neurogenic shock
    -constriction vs dilation
    -venous return
    -tissue perfusion
    • loss of sympathetic tone
    • vasodilation
    • decreased venous return
    • decreased CO
    • decreased tissue perfusion
    • hypotension
    • bradycardia
  40. management of neurogenic shock
    • stabilize the spinal cord
    • airway
    • treat hypotension and bradycardia
    • fluid resuscitation - with caution because cause of shock is not hypovolemia
    • temperature control - monitor hypothermia
  41. distributive shock
    -3 types
    -characterized by: venous, arterial, capillary permeability, microcirculation, tissue perfusion
    • neurogenic, anaphylactic, septic
    • intravascular volume is maldistributed within the circulatory network because of alterations in blood vessels - may be neural or chemical induced loss of vascular tone
    • venous vasodilation (decreased venous return, decreased preload), arterial vasodilation (decreases afterload, decreases BP), increased capillary permeability (decreased circulating volume, increased blood viscosity, increased interstitial edema), excess coagulation and impaired fibrinolysis (decreased microcirculatory blood flow), decreased tissue perfusion
  42. causes of anaphylactic shock
    • allergy
    • drugs
    • contrast media
    • transfused blood and blood products
    • insect stings - second sting has anaphylactic reaction
  43. clinical manifestations of anaphylactic shock
    • massive vasodilation
    • hives
    • laryngeal edema
    • bronchial constriction
    • cardiovascular collapse
    • respiratory failure
    • loss of consciousness
  44. management of anaphylactic shock
    • prevention
    • CPR
    • respiratory management
    • identify and remove causative agent
    • epinephrine IM
    • fluids
    • Benadryl and solumedrol
  45. signs of organ dysfunction
    • neuro: GCS<14 or altered LOC
    • cardiac: SBP<90 or drop of >40 from baseline, MAP<65, increased HR, arrhythmias, decreased capillary refill, mottling, decreased perfusion
    • respiratory: SaO2<90% on room air, hypoxemia, tachypnea, alveolar edema, ARDS
    • GI: absent bowel sounds, paralytic ileus, GI bleed, translocation of bacteria
    • GU: urine output <0.5ml/kg/hr x2hrs or Cr increased >0.5 above baseline
    • labs: lactate>2mmol/L, platelets <100,000, INR>1.5, bilirubin >4
  46. patho of hypovolemic shock
    • total body fluid is decreased due to hemorrhage or dehydration
    • decreased intravascular volume
    • decreased venous return
    • decreased ventricular filling
    • decreased stroke volume
    • decreased CO
    • inadequate tissue perfusion
  47. causes of hypovolemic shock
    • absolute loss of fluid: hemorrhage (loss of whole blood or plasma from thermal injuries or exudative lesions), GI (vomiting, diarrhea, NG suction), renal (diuretics, diabetes insipidus, hyperglycemic osmotic diuresis)
    • relative fluid shifts: internal hemorrhage, pool of fluid in interstitial space, increased capillary permeability (3rd spacing)
  48. clinical manifestations of hypovolemic shock
    • severity is related to the amount of blood lost
    • appearance: cool, pale, diaphoretic, tachy
    • hemodynamics: tachycardia, decreased CO, CVP, PCWP, SV, increased SVR
    • neuro: thirsty, decreased LOC
    • pulmonary: tachypnea
    • renal: decreased urine output
    • temperature: decreased from inadequately warmed banked blood
    • labs: decreased H&H (full effect in 3-6hrs), serum osmolarity, K, Ca, platelets
  49. goals of hypovolemic shock management
    • maintain O2 carrying capacity
    • restore circulating intravascular volume
    • increase tissue perfusion
    • increase venous return to R side of the heart
  50. what to monitor during hypovolemic shock management
    • ABP
    • PAP
    • CVP
    • ABGs
    • lactate
    • H&H
    • electrolytes
    • osmolarity
    • coagulation panel
  51. interventions for hypovolemic shock
    • ensure patent airway
    • stop fluid loss
    • 2 IVs
    • HOB 30deg, elevate feet
    • frequent VS
    • crystalloids: replace 3ccs for every cc estimated blood loss
    • replace fluid quickly - pressure bag or rapid infuser - caution with age extremes
  52. when to transfuse with hypovolemic shock
    • Hgb<8%
    • >30% EBL
    • volume of crystalloids >50ml/kg
    • goal Hct 35%, CVP 8-12
  53. if fluid resuscitation for hypovolemic shock is unsuccessful
    • vasoconstrictors
    • dopamine
    • epinephrine
    • norepinephrine
    • phenylephrin
  54. complications of fluid resuscitation for hypovolemic shock
    -if compensatory actions fail
    • fluid volume overload (especially with age extremes)
    • no LR for liver patients
    • if compensatory actions fail: give ablumin
    • RBC - increase oxygen carrying capacity
    • FFP - controls clotting
    • platelets - control bleeding
  55. EBL and needed infusion
    pulse pressure=36
    urine output=30-35
    CNS=slightly anxious
    • mild blood loss = 15%
    • transfuse: LR, NS, or albumin
  56. EBL and needed infusion
    HR >100
    pulse pressure=30
    urine output=25-30
    CNS=mildly anxious
    • moderate blood loss = 20%
    • transfuse: LR, NS, or albumin
  57. EBL and needed infusion
    HR >120
    pulse pressure=20
    urine output=5-15
    CNS=anxious/ confused
    • severe blood loss = 30%
    • transfuse: LR + blood
  58. EBL and needed infusion
    HR >140
    BP <50 systolic
    pulse pressure=10
    RR >35
    urine output=scant to none
    • profound blood loss = 40%
    • transfuse: LR + blood
  59. pathophysiology of cardiogenic shock
    • left ventricular failure
    • myocardial disease, depression or disruption
    • decreased stroke volume, decreased CO
    • resulting in inadequate O2 delivery, tissue ischemia
  60. causes of cardiogenic shock
    • cardiac arrest
    • MI
    • dysrhythmias
    • valvular changes
    • bacterial or viral cardiomyopathies
    • pericardial tamponade
    • cardiac injury from trauma
    • sepsis
    • shock
  61. clinical manifestations of cardiogenic shock
    • CV: increased PCWP > 18, increased HR, MAP<60, SBP<80, rapid thread pulses, increased capillary refill, SVR>1200 dynes
    • dysrhythmias: SVT, VT, sinus brady, AVB
    • respiratory: increased rate, shallow, pulmonary edema with dyspnea and increased secretions, decreased PaO2, decreased pH, decreased HCO2
    • renal: decreased urine output
    • integumentary: cool, mottled, clammy
    • neuro: impaired
    • GI: thirst, n/v
    • labs: hypoxemia, metabolic acidosis, hypocapnia, lactic acidosis, hypo- or hyperkalemia, increased Cr/BUN
  62. management of cardiogenic shock
    -drug therapies
    -supportive therapies
    -circulatory assist
    • goals: to improve CO and improve tissue perfusion
    • ensure oxygenation: PaO2>80, ventilation PRN, PEEP if FiO2>70%, Hgb>10
    • circulation: restore blood flow to myocardium with thrombolytics, PCI with stenting CABG, reduce workload
    • drugs: diuretics (reduce preload), beta blockers (-lol), digoxin, dopamine, dobutamine, epinephrine, norepinephrine (Levo), NTG (Trindil), nipride, thrombolytic therapy
    • supportive therapy: to correct dysrhythmias
    • circulatory assist devices: IABP (intraaortic balloon pump to decrease workload of the LV), LVAD (left ventricular assist device)
  63. diagnostic value
    -C-reactive protein
    -troponin I
    -troponin T
    • c-reactive protein: >20
    • CK-MB: >5
    • troponin I: >0.4
    • troponin T: >0.1
    • myoglobin: >110
  64. B-type natriuretic protein
    -diagnostic value
    • indicates heart failure
    • secreted by the LV after volume expansion
    • heart failure if 360-380+
    • higher number indicates more severe injury
  65. stress tests
    • to stimulate the myocardium and identify location of injury
    • stress echocardiography, dobutamine stress test
  66. echocardiogram
    • to assess cardiac structures, especially wall motion and valve function; can give good estimate of ejection fraction (normal=65-70%)
    • transesophageal echocardiography (TEE) - posterior view of cardiac structures
    • dobutamine stress echocardiogram
  67. nuclear cardiography
    -technetium pyrophosphate
    • technetium pyrophosphate: accumulates in damaged tissue and is used to detect "hot spots"
    • thallium: damaged or ischemic tissue does not take up thallium so it is used to detect "cold spots"
  68. electrophysiology studies
    -what and why
    • an invasive procedure where programmed electrical stimulation is used to induce lethal dysrhythmias in patients at risk for sudden death
    • indications: prolonged SVT unresponsive to cardioversion and meds, V-tach, V-fib
    • procedure: catheters to the heart looking for ectopic focus.  MD may ablate the pathway and stimulate again to see if it worked
  69. UA
    • unstable angina
    • PCI usually not indicated; not candidates for thrombolytics
  70. NSTEMI
    • non ST segment elevation myocardial infarction
    • manifestations: increased cardiac biomarkers, ECG changes, T wave inversion, ST depression
    • treatment: no thrombolytics, may require PCI
  71. STEMI
    • ST segment elevation myocardial infarction
    • treatment: prompt reperfusion, assess for thrombolysis PCI or CABG
  72. rapid diagnosis and management of ACS to reduce complications
    • O2
    • apsirin
    • nitroglycerin - vasodilator, will drop BP and CO
    • 12 lead ECG
    • cardiac biomarkers, repeat in 6-12 hours
    • CXR
    • history/risk assessment
  73. low risk for UA and NSTEMI
    • no intermediate or high risk factors, but at least one of the following:
    • new onset chest pain not prolonged
    • normal ECG during cp
    • normal cardiac biomarkers
    • no PCI
  74. intermediate risk for UA and NSTEMI
    • 1 of the following:
    • cp>20 minutes
    • T wave inversion
    • Q waves
    • elevated cardiac biomarkers
    • >70years old
    • possible PCI
  75. high risk for UA and NSTEMI
    • 1 of the following:
    • angina
    • ischemia at rest
    • cp>20 at rest
    • new ST depression
    • recurrent angina
    • CHF s/s
    • <40% ejection fraction
    • SBP<100
    • HR>100 or <60
    • VT
    • prior CABG
    • >75 years old
    • prompt PCI
  76. STEMI treatment
    • requires reperfusion
    • O2, monitor, IV
    • aspirin, nitro, morphine
    • fibrinolytic therapy or PCI
    • beta blockers - slow HR, decrease myocardia O2 demand
    • heparin
    • anti-platelet meds
    • ACE inhibitors
    • insulin
    • MgSo4
    • Ca Channel blocker
  77. fibrinolytic therapy
    -patient selection
    • goal: reperfusion by reversing the thrombotic component of the coronary occlusion in order to limit infarct size, maintain LV function and improve long term survival
    • patient selection: recent onset (6hrs) of chest pain and acute MI sxs, ECG with AMI ST segment elevation
    • drugs: TPA, streptokinase, APSAC, retaplase
  78. UA and NSTEMI treatment
    • O2, ECG, IV
    • aspirin, nitro
    • beta blockers
    • morphine
    • heparin
    • anti platelets meds
    • Ca channel blockers
    • ACE inhibitors
    • bed rest
  79. percutaneous transluminal angioplasty (PTCA) and stent
    -clinical improvement
    • procedures: involves dilation of stenotic or occluded coronary artery using a balloon tipped catheter to deploy a stent to open an occluded coronary artery
    • clinical improvement: resolution of chest pain, ST segments, increased exercise tolerance and normalized myocardial perfusion on thallium stress tests
  80. percutaneous transluminal angioplasty (PTCA) and stent
    -post management
    • post management: distal pulses, resolution of sxs, hydration (dye can be hard on kidneys), frequent VS, anticoagulation status, cardiac enzymes (sudden elevation from washout phenomenon)
    • complications: clot may throw (CVA), excessive bleeding, bradycardia (may need atropine)
  81. coronary artery bypass graft surgery (CABG)
    -post-op complications
    • procedure: the patient is placed on cardiopulmonary bypass to provide oxygen circulation and hypothermia during induced cardiac arrest.  the bypasses are created and the heart is rewarmed slowly.
    • complications: low CO syndrome (inotropes or IABP - levo, nicardipine, dopamine, dobutamine), hypertension (r/t hypothermia - can rupture graft sutures), hypotension (grafts can collapse), dysrhythmias, air emboli to the brain, bleeding, pericardial tamponade (esp with graft rupture), renal dysfunction
  82. off pump coronary artery bypass (OPCAB)
    "beathing heart" surgery
    -post-op care
    • procedure: stabilization device applied to target vessel decreases blood flow to the vessel - reanastamosis must be done within 20 min
    • complications: myocardial ischemia, hemodynamic instability, decreased O2, arrhythmias, postpericardiotomy syndrome (fever, pleuritic chest pain, friction rub, pleural effusion, tamponade - treated with NSAIDS)
  83. minimally invasive direct coronary arterial bypass (MIDCABG)
    • indication: single lesion or a lesion on LAD artery
    • procedure: several small incisions between the ribs, the L IMA vein is attached to a still beating heart below the lesion. no bypass
    • recovery: ICU x6hrs, hospitalization x2-3days
  84. arrhythmias after MI
    -why occurs
    -drug of choice for VT/VF
    • occurs in 80% of all MI patients
    • due to ischemic injury and changes in the excitability, conduction and refractory periods of myocardial cells
    • if only a few, considered benign after infarct
    • amiodarone is the drug of choice for VT/VF
    • VT/VF with anterior wall MIs
    • PVCs may preced VT or VF
    • tachydysrhythmias with anterior MIs
    • PACs=early warning sign for CHF
  85. pacemakers
    • indications: failure of the heart to initiate or conduct an electrical impulse at a rate adequate to maintain perfusion
    • device: emits an electrical impulse that produces a wave of depolarization in the myocardium
    • function: must sense the ability of the heart to initiate an impulse, if HR is not adequate, the pacemaker will fire, causing depolarization or capture
    • teaching: dry for 1 week, avoid magnets, no golf or contact sports, take pulse
  86. implanted cardiovertor defibrillator (ICD)
    • indications: survivors of cardiac arrest, medication resistant ventricular dysrhythmias
    • device: 3 lead system implanted in chest cavity
    • function: capable of sensing the patients HR, cardioversion, defibrillation and pacing
    • teaching: lay down when ICD fires, defibrillate PRN, call doc within 24 hours of shock, deactivate with magnet before CT scan
  87. structural defects after acute MI
    -papillary muscle rupture
    -ventricular septal rupture
    -ventricular aneurysm
    • papillary muscle rupture: prolonged ischemia around mitral valve, valves fail suddenly - loud murmur, sudden BP drop
    • ventricular septal rupture: due to prolonged ischemia to the intraventricular septum, end result is biventricular failure from shunting through the defect - pulmonary congestion, systemic edema
    • ventricular aneurysm: thin walled noncontractile outpouchings of the ventricle - holosytolic thrust, ST elevation, thromboembolism - post-mordem classic presentation=linear cyanosis
  88. pericarditis
    -what is it
    • inflammation of the pericardial sac that often involves the diaphragm
    • onset: occures 2-4 days after MI
    • symptoms: pleuritic pain (generalized, constant, gradual onset) made worse with deep breathing and supine position, low grade fever, elevated WBC/ESR/CRP,
    • managment: relief with sitting up and leaning forward and shallow breaths, PAIN RELIEF, aspirin, cholchicine (for gout/inflammation), NSAIDS, tylenol
    • complications: pericardial effusion (fluid in pericardium increases with no rise in intrapericardial pressure), pericardial tamponade (fluid in pericardium with a rise in intrapericardial pressure) - Beck's triad: hypotension, muffled heart sounds, paradoxical pulse
  89. Dressler syndrome
    • pericarditis with effusion and fever 1-4 weekds after MI or open heart surgery
    • treated with corticosteroids
  90. hemodynamic alterations after AMI
    • heart failure
    • pulmonary edema
    • cardiogenic shock
  91. pulmonary edema
    • presentation: dyspnea, anxiety, cyanosis, chest pain, pink frothy sputum, air hunger, crackles
    • patho: myocardial injury, LV failure, increased pulmonary venous pressure, leak of fluid into interstitial space, pulmonary edema, interferance with gas exchange
  92. pulmonary edema management
    -gas exchange
    -mode of mechanical ventilation
    • decrease intravascular volume: diuretics
    • decrease venous return (preload): legs down to decrease venous capitance
    • decrease afterload: vasodilation - nitro, nicardipine - to decrease SVR
    • improve gas exchange and oxygenation: bronchodilator
    • increase CO: positive inotrope - dopamine, dobutamine (less affect on HR)
    • ventilation: BIPAP
  93. cardiogenic shock
    • pump failure syndrome
    • comibnation of hypoperfusion and pulmonary edema
    • more than 40% of LV has been infarcted
  94. cardiogenic shock assessment
    • hemodynamic: inc SVR, dec CO, dec SVO2
    • neuro: restlessness, confusion, apathy, anxiety
    • CV: inc HR, dec BP, rapid thready pulse, arrhythmias
    • pulmonary: severe dyspnea, tachypnea, crackles
    • renal: decreased urine output
    • GI: decreased bowel sounds, n/v
    • radiographic: enlarged cardiac silhouette
    • diagnostic: inc cardiac biomarkers, inc glucose, inc BUN/Cr
  95. management of cardiogenic shock
    -myocardium O2
Card Set
N176 test 2
n176 test 2