Exam #5 Flashcards

1
Q

Shick Patho

A
  • Too little o2 is delivered to the tissues (related to sustained decrease in MAP)
  • can be due to issues with total blood volume, cardiac output, size of the vascular bed

1) compensatory phase: body begins to compensate and move blood to selected areas
- baroreceptors pick up on hypovolemia –> reabsorb sodium and water –> increase osmolarity –> fight or flight –> increased epi/norepi –> vasoconstriction –> blood shunted to brain and heart
- biggest effect is on lungs: blood is shunted to heart and brain
- blood isn’t oxygenated well due to lungs not working well

2) Progressive: if MAP continues to decrease, lactic acid levels and other harmful metabolites increase which damages tissues
- decrease in all organ function, decrease in mental status, decrease co2, decreased o2, change in LOC
- massive capillary permeability, ablumin leaks, edema, alveoli edema –> decreased o2 and respiratory issues
- ileus from decreased blood to the GI tract, necrosis of GI tissue

3) Irreversible: if this continues, MODS occurs
- all organs are damaged, necrosis of brain, DIC, massive bleed out
- MODS

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2
Q

categories of shock

A
  • cardiogenic
  • hypovolemic
  • distributive: neurogenic, anaphylactic, septic
  • obstructive
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3
Q

S/S of shock

A
  • cardio: increased HR but weak pulses (compensating but weak), decreased BP (loss of fluid), low o2 sat (V/Q mismatch in compensatory stage)
  • skin: cool and clammy first (blood shunted to brain and heart), warm/cool/clammy in later stage, pale, cyanotic, mottled
  • respiratory: RR increases but depth is shallow (anarobic metabolism, V/Q mismatch, pulmonary edema, acidotic –> increased RR), decreased pao2 (80-100), decreased sao2
  • renal/urinary: urine output decreased, specific gravity increased (very concentrated urine, fluid retained in body)
  • CNS: in early shock thirst/anxiety/restlessness (decreased o2 to the brain), in later shock confusion/lethargy/coma (organs shut down)
  • musculoskeletal: muscle weakness and pain (arobic to anarobic shift), decreased or absent Deep tendon reflexes
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4
Q

shock lab results

A
  • increased lactic acid: muscle breakdown from anarobic metabolism (if it goes down then it means it’ shifting back to arobic)
  • increased potassium: retention, acidiosis
  • increased BUN/creatinine
  • increased glucose: in early phase, compensatory, fight or flight mode/cortisol
  • increased PaCO2: build up of waste, v/q shunt, decreased RR = co2
  • decreased pao2: shunted to heart and brain
  • decreased PH: acidosis
  • hct/hgb: decreased if hemorrhagic, increased if dehydrated or fluid shift
  • compensitory stage: metabolic acidosis with resp compensation
  • progressive stage: acidosis w/o respiratory compensation
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5
Q

shock DX studies

A
  • no single finding confirms or rules out shock, but changes can support the diagnosis of shock
  • history and physical: car accident, fall, allergies, surgery, illness
  • 12 lead ECG: decreased o2 to heart and brain, dysrhythmias
  • chest xray: pulmonary infiltrates. bleeds
  • pulse ox: hemoglobin may make it look false
  • hemodynamic monitoring: BP, MAP, PAWP (left preload), CVP (right preload)
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6
Q

general shock treatment

A
  • maintain patent airway
  • oxygen to keep 02 > 90%
  • fluids: for septic, hypovolemic and anaphylactic - crystalloids (LR, NS), colloids (blood, blood products, plasmanate, hetastarch, plasma expanders)
  • drugs: prefered via central venous catheter, use drugs if fluids don’t help – vasopressors (dopamine, norepinephrine, make sure pt has enough fluid on board first by monitoring PAWP and CVP), inotropes (dobutamine, primacro) increase cardiac contractility and cardiac output, vasodilators (Tridil, nipride) increase cardiac perfusion
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7
Q

shock nursing care

A
  • prevent: catch pt in compensatory phase, use aseptic technique, promote hydration
  • assess every 15 minutes until shick is controlled then hourly
  • monitor MAP
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8
Q

cardiogenic shock

A
  • direct pump failure, fluid volume is not affected
  • causes: systollic, diastolic or structural problems, dysrhythmias, MI, cardiac arrest
  • assessment: can look like heart failure (left sided = pulmonary edema, right sided = JVD/edema), increased BNP, increased ANP
  • TX: thrmobolytics (break down clots), angioplasty with stenting, CABG, valve replacement, IABP, cardiac transplant. vasodilators, diuretics, beta blockers, inotropes (increase force of contraction)
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9
Q

hypovolemic shock

A
  • total body fluid decreased
  • causes: absolute (actual fluid loss, hemorrhage, comiting, diarrhea, diabetes), relative (fluid shift from vascular space to extravascular space, 3rd spacing - bowl obstruction, burns, ascites, ruptured spleen, pancreatitis, sepsis)
  • assessment: hct/hgb decreased with hemorrhage, hct/hgb increased with dehydration/fluid shift
  • TX: 1st stop loss of fluid and restore circulating volume, 2nd give vaso drugs
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10
Q

Distributive shock

A
  • fluid is shifted from central vascular space, total body fluid volume is normal or increased, loss of vascular tone
  • causes: neural-induced (vasomotor center - spinal cord injury above t6, spinal anesthesia, vasomotor center depression), chemical-induced (anaphylactic - massive vasodilation after being exposed to allergy, septic - infection = massive vasodilation due to inflamm response)
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11
Q

Neurogenic Shock

A
  • injury above T6, loss of vasomotor center
  • assessment: bradycardia with low BP, flaccid paralysis below level of lesion, loss of reflex activity, cool or warm skin (poikilothermia), dry skin
  • TX: depends on the cause, vasopressors (constricts vessels), atropine, give fluids cautiously (not a fluid issues, brain issue), no colloids (not a fluid volume issue just vasomotor issue)
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12
Q

Anaphylactic shock

A
  • allergy to med, food, bug bite, etc
  • assessment: dyspnea, wheezing, stridor, flushing, pruritis, uticaria, swelling of lips, tongue
  • TX: prevention is key, epinephrine (constricts and increases BP), antihistamines (benadryl, stops inflamm), bronchodilators (open airway), aggressive fluid resuscitation with colloids (hetastarch, albumin, dextran), IV corticosteroids (only if low BP persists)
    1st give Epi, then antihistamine, then fluid replacement
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13
Q

Septic Shock

A
  • systemic infection
  • assessment:
    1s phase - hyperdynamic
  • initially everything speeds up, aggressive, agitation
  • vasodilation (skin pink, warm, flushed), increased cellular metabolism, increased fever greater than 104
  • increased HR and BP, bounding pulses
  • WBC with left shift (increased bands)
    2nd phase - hypodynamic
  • sudden onset, rapid decline, poor prognosis
  • skin cool and mottled
  • temp below normal
  • low BP, low CO
  • DIC
  • decreased heart and brain function
  • treatment
  • large amount of fluid replacement (isotonic and colloids)
  • IV abx with cultures
  • vasopressors (norepi, dopamine, vasopressin) when increased PAWP & CVP
  • may need inotropes (dobutamine), increase contractions
  • IV corticosteroids used occasionally
  • xigris (treats systemic infections)
  • in 1st phase, heparin to prevent DIC
  • in 2nd phase, clotting factors (FFP, Cryo) to treat DIC
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14
Q

obstructive shock

A
  • problems that impair the ability of the normal heart muscle to pump effectively , total body fluid volume is not affected
  • causes: tamponade, pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, PE, pulmonary HTN, thoracic tumor, pericarditis – all affect normal blood flow to heart
  • assessment: JVD, pulsus peradoxus (pulse changes with breathing), bradypnea is a late sign
  • TX: early recognition and tx to relieve obstruction - mechanical decompression, radiation/debulking, thrombolytics
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15
Q

SIRS

A
  • systemic inflammatory response syndrome, generalized inflammation in organs remote from the initial insult
  • clinical response to a nonspecific insult of either infectious or noninfectious origin
  • 2 or more of the following variables: Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F), Heart rate of more than 90 beats per minute, Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO 2) of less than 32 mm Hg, Abnormal white blood cell count (>12,000/µL or 10% immature [band] forms)
  • systemic inflammation (doent have to be caused by infection)
  • can be caused by ischemic or necrotic tissue (MI, pancreatitis), endotoxin release, bacteria, trauma, burns
  • S/S: increased temp ( > 100.4), increased HR ( > 90), increased RR ( >20), WBC high or low
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16
Q

MODS

A
  • multiple organ dysfunction syndrome
  • failure of 2 or more organ systems such that homeostasis cannot be maintained without intervention
  • results from SIRS
  • both SIRS and MODS = respiratory is the first system to show symptoms (ARDS), mental status changes, acute kidney injury, hypermetabolic and catabolic state, liver dysfunction (decreased albumin = edema), DIC, electrolyte imbalances
  • S/S of MODS and SIRS = development of ARDS, Myocardial depression, change in neuro status, hyperglycemia, renal hypoperfusion, ATN, mucosal ischemia, GI bleeds, jaundice, hepatic encephalopathy, increased bleeding times, decreased platelet count,
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17
Q

nursing care for MODS and SIRS

A
  • detect early signs of deterioration
  • prevent hospital aquired infections
  • prevent hypoxemia: lungs are first to be affected
  • prevent malnutrition: excess calories needed to promote healing/immunity
  • control blood sugars
  • support failing organs
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18
Q

adrenergic drug indications

A
  • beta 1: heart, increases HR, increases renin release which increases BP
  • beta 2: lungs, bronchodilation, increases glycogenolysis
  • alpha 1: vasoconstriction

1) respiratory: beta 2 adrenergic, bronchodilation - asthma, bronchitis
- exp: albuterol, ephedrine, formoterol, levabuterol, salmeterol
2) topical nasal decongestants: alpha 1 adrenergic - constrict dilated arterioles, reduction of nasal blood flow
- exp: ephedrine, naphazoline, oxymetazoline
3) cardiovascular: used to support CV during cardiac failure or shock, vasoconstrictive
- exp: dobutamine, dopamine, ephedrine, norepinephrine

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19
Q

adrenergic adverse effects

A
  • alpha adrenergic: causes vasoconstriction – headache, restlessness, excitement, insomnia, euphoria, chest pain, hypertension, tachy, palpitations, dysrhythmias
  • beta adrenergic: increases HR and BP – mild tremors, headache, nervousness, dizziness, nausea, vomiting, increased HR, palpitations, fluctuations in BP
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20
Q

Adrenergic Toxicity, management of overdose

A
  • manage symptoms and support the patient
  • majority of adrenergic drugs have a very short hald life and need to be given IV drip
  • two life threatening effects = CNS and CV - seizures (diazepam) and intracranial/systemic hemorrhage (esmolol)
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21
Q

interactions with adrenergic drugs

A
  • alpha and beta drugs given with adrenergic antagonists directly antagonize each other
  • tricyclic antidepressants and MAOIs increase vasopressor effects and can cause acute hypertensive crisis
  • thyroid perparations, synthroid, can caused really bad side effects
22
Q

Dobutamine (dobutrex)

A
  • beta 1 selective vasoactive drug (heart only)
  • IV/continous infusion - very short half life
  • increase cardiac contractility (positive inotropy) - increase CO/SV
  • similar to natural catecholamine
23
Q

dopamine (inotropin)

A
  • IV continuous infusion
  • naturally occuring catecholamine neurotrasmitter
  • potent dopaminergic, beta 1, alpha 1 adrenergic receptor activity
  • low doses = dopaminergic - dilates blood vessels to brain, heart, kidneys and mesentary
  • higher doses = beta 1 - improve cardiac contractility and output
  • highest dosages = alpha 1 - vasoconstriction, increase BP and MAP
  • contraindicated with pheochromocytoma (increase epi/norepi and casues major HTN)
24
Q

epinephrine (adrenaline)

A
  • SQ/IV
  • prototypical nonselective adrenergic agonist (hits both beta and alpha receptors)
  • vasoactive catecholamine
  • low doses = beta 1
  • high doses = alpha 1 and beta 2 (give for anaphylactic shock)
25
Q

Fenoldopam (carlopam)

A
  • peripheral dopamine 1 agonist for high BP, decreases BP with severe HTN
  • stimulates D1 receptors and causes arterolar vasodilation
  • beneficial effects on renal function because it increases renal flow (helps feed organs)
26
Q

midodrine (proamatine)

A
  • alpha 1
  • vasoconstriction of both arterioles and veins resulting in peripheral vasoconstriction
  • primarily indicated for treatment of orthostatic hypotension
  • PO BID or TID 2.5mg -5mg tabs
  • last dose to be given before 1800 (laying down can increase HTN)
27
Q

norepinephrine (levophed)

A
  • continuous IV infusion
  • alpha 1: vasoconstriction
  • beta 1: positive inotropy
  • no beta 2
  • use primarily in treatment of hypotension and shock
  • very serious vasoconstrictor, can cut off blood flow to extremities, renals, GI tract
28
Q

phenylephrine (neo-synepherine)

A
  • alpha adrenergic
  • short term treatment to raise BP in patients in shock
  • vasoconstriction for use in regional anesthestics
  • given with epi when anesthetics are used to keep it localized, constricts vessels
  • if this drug infiltrates it can cause necrosis: assess at leastd every hour
  • phentolymine can be given if the drug infiltrates
29
Q

A&P of burn injuries

A
  • immediate release of catecholamines and other mediators – increase BP and HR, vasoconstrict, disrupted blood flow
  • increased capillary permeability: edema anywhere including the lungs, third spacing, low sodium, hypovolemia, massive fluid shifts
  • decreased perfusion to GI system: paralytic ileus, abd distention, curling’s ulcer (major issue in duodenum, shinted blood to brain and heart)
  • myoglobin and k released from cell damage: acute tubular necrosis kidney damage, high potassium cardiac issues
  • inflamm response, destroyed skin: immunosupression, risk of infection/sepsis, loss of ability to sweat (less ability to fight infections)
  • increased demand on metabolic system: massive catabolism and increased need for calories, icnreased body temp, increased o2 demand
  • RBCs hemolyzing cuasing hemoconcentration: high hct, high hgb, increaesd blood viscosity (sludging)
30
Q

thermal burns

A
  • most common burn injury
  • flame, flash, scald, contact with hot objects
  • can require escharotomy (compartment syndrome)
  • if total body surface is 10% = blanket/sheet around pt, do not put wet sheeton pt (hypothermia), IVs for fluid replacement)
31
Q

chemical burns

A
  • acids, alkalis, organic compounds
  • alkalis are worse than acids
  • remove dry chemicals from skin with dry brush then dulte with water to stop causing tissue destruction
  • dont use neutralizing agents
  • white phosphorous (meth) can ignite when interacting with air
32
Q

smoke/inhalation injuriesq

A
  • suspect for any burns of the head, neck, chest or burn that occured in an enclosed space - damages alveoli, intubation for most pts, increase in pulmonary edema
  • major predictibility of mortalitity in burn pts
  • administer 100% humidified o2 by mask, coug, deep breath, intubate
  • lower airway burn can lead to pumonary edema and ARDS
33
Q

carbon monoxide poisoning

A
  • displaces o2 on the hgb molecule causing carboxyhemoglobinemia and hypoxia
  • cherry red skin, headache, n/v, unconsciousness, changein LOV, 02 sat low
  • burns dont cuase unconsciousness
  • ## give 100% o2
34
Q

electrical burns

A
  • heat causing extensive tissue damage, also to nerves and vessels
  • sparks can ignite clothing too causing thermal burn
  • can cause muscle contractions so strong that bones are broken and falls are caused (always assume C spine injury!)
  • most damage is below the skin (iceburg)
  • can cause cardiac and renal problems (K released from damaged cells, heart issues can occur days later)
  • need EKG and cardiac monitoriung ASAP
35
Q

burn depth

A
  • partial thickness, superficial: 1st degree – no blisters, red, pink, dry, painful, only epidermis, heals in 5 days – sunburn, pain
  • partial-thickness, deep: 2nd degree – blisters, red, shiny, wet, severe pain, edema, includes part of dermis, heals in 1-2 weeks – serous fluid
  • full-thickness: 3rd and 4th degree – color varies, dry, waxy, white, leathery, hard, no pain, all of epidermis and dermis, cannot grow new skin – requires graft
36
Q

rule of 9s

A
  • perineum 1%
  • hand 1%
  • arm 4.5%
  • head 4.5%
  • leg 9%
  • torso 18%
37
Q

phases of burn injury

A

1) emergent: resuscitative care, resolve immediate life-threatening problems, usu lasts 48-72hrs – goal is to secure airway, maintain temp, prevent hypo shock (3rs spacing)
2) acute: diuresis until wound closure, can take weeks to months – goal is to prevent infection, wound care, pain control, optimal nutrition and PT
3) rehab: restorative, overlaps with acute phase and contunues to discharge, 2 weeks - 7/8 months – begins when wounds are healted and pt is abel to do self care, achieve max fxn, gain independence

38
Q

burn care goals

A
  • prevent infection
  • restore fluid balance
  • thermregulation
  • adequate skin integrity
  • restore skin integrity
  • adequae nutrution
  • emotional support
39
Q

burn cardiovascular care

A
  • emergent phase: dysrhythmias, hypovolemic shock, circulation impairment, sludging, VTE, heart failure – treat with escharatomy if necessary to prevent circ impairment, baseline ECG
  • acute phase: same
40
Q

burn respiratory care

A
  • emergent phase: eema, obstruction, constriciton, pulmonary edema, resp infection – tx with chest xray, ABGs, frequent assessment , escaratinym, bronchoscopy, o2, turn cough deep breath, chest PT
  • acute phase: same plus pneumonia
41
Q

burn neuro care

A
  • emergent phase: should not have any nero symptoms unless they have other injuries – falls, co2, major loss of fluid
  • acute phase: odd behaviors, may beed psych services, PTSD
42
Q

burn MSK care

A
  • emergent phase: assess for other injuries (fall), start ROM, positioning is critical
  • acute phase: limited ROM, contractures – tx stretch and move as much as possible, splints, ROM 3 x day, pressure garments,
43
Q

burn renal, urniary care

A
  • emergent phase: ATN, ARF (sludge blood) – tx fluid replacement, maintain urine outful 30-50ml/hr, watch BUN, creatinine, na, specific gravity
  • acute: foley removed
44
Q

Burn F&E care

A
  • emergent: 2 large bore needels, arterial line, warmed LR, hourly output 30-50, watch MAP and BP, no diruetics
  • acute phase: watch electrolutes closely
45
Q

parkland formula

A
  • used first 24 hours post burns
  • (2-4ml LR x pt weight kg x TBSA) = 24 hours of fluid
  • give 1/2 in first 8 hours then the other 1/2 in the last 16 hours
46
Q

burn GI, nutritional care

A
  • emergent phase: watch for paralytic ileus, curlings ulcer, feed early, enteral preferred, NG if paralytic ileus or intubated, test for blood
  • acute: diarrhea, ileus, constipation, curlings ulcer, hyperglycemia – tx give antacids, feed, IV insulin, 5000+ calories a day, TPN, weight daily
47
Q

burn skin wound care

A
  • emergent: not pirotiyt until after airway, circulation and fluid replaceent unless circumferential burn
  • clean and debride
  • elevate burned extremeities (increases fluid to heart, decreases swelling and pain)
  • acute phase: infection, sepsis – hand hygeinine, shower daily, twice daily dressing cange, keep room warm 85, topical abx
48
Q

burn special skin care

A
  • face, ears, head, neck - can get very swollen, limit pressure, no pillows, elevate using rolled twoel under shoulderns
  • hands arm: extend, elevate, spingt
  • perineum: keep as dry and clean as possible, foley
  • PT immediately
49
Q

burn procedures

A
  • excision and grafting: done day 1-2 in OR
  • escharotomy
  • fasciotomy
50
Q

burn meds

A
  • analgesics/sedatives: IV only, opioids, PCA pump, premididate before dressing change
  • tetanus immuniation for everyone
  • antimicrobials: not systemic unless they have positive cultures
  • VTE prophylaxis
  • stress ulcer prophylaxis
51
Q

burn pain mngmt

A
  • continuous pain and tx-induced pain

- meds first: PCA opioids, slow release opioids, arond clock analgesics, anxiolytics,