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443: Advanced Concepts > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What are the causes of cardiogenic shock?

A

anything effecting the ability of the heart to beat efficiently

MI
cardiomyopathy
blunt cardiac injury
severe systemic or pulmonary HTN
cardiac tamponade
myocardial depression from metabolic problems
pericarditis
arrhythmias

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2
Q

What are the manifestations of cardiogenic shock?

A

tachycardia, hypotension, narrowed pulse pressure, pallor and cool, clammy skin, decreased cap refill, anxiety, confusion, agitation, decreased UO

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3
Q

What is the interprofessional goal for cardiogenic shock?

A

restore blood flow to myocardium by restoring balance between oxygen supply and demand

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4
Q

What types of drugs can be used for cardiogenic shock?

A

nitrates
diuretics
vasodilators
beta-adrenergic blockers

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5
Q

What are the causes of hypovolemic shock?

A

loss of intravascular fluid volume (absolute): hemorrhage, GI loss, fistula drainage, diabetes insipidus, hyperglycemia, diuresis

fluid volume moves into extravascular space d/t increased capillary permeability (relative): burns

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6
Q

What are manifestations of hypovolemic shock?

A

loss of SNS response: increased HR, CO, RR; decreased SV, CVP, pulmonary artery wedge pressure

anxiety
tachypnea
decreased UO

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7
Q

What is the interprofessional goal for hypovolemic shock?

A

stopping loss of fluid and restoring circulating volume

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8
Q

What are the types of distributive shock?

A

neurogenic, anaphylactic, septic

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9
Q

What are the causes of neurogenic shock?

A

can occur within 30 min of spinal cord injury or spinal anesthesia and can last up to 6 wks

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10
Q

What are the manifestations of neurogenic shock?

A

hypotension
bradycardia
inability to regulate body temperature (poikilothermia) resulting in heat loss
dry skin

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11
Q

What types of drugs are used for neurogenic shock?

A

vasopressors and atropine
fluid resuscitation

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12
Q

What are the cause of anaphylactic shock?

A

acute life-threatening hypersensitivity rxn

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13
Q

What are the manifestations of anaphylactic shock?

A

massive vasodilation, release of vasoactive mediators, increase capillary permeability, respiratory distress d/t laryngeal edema or bronchospasms: anxiety, confusion, dizziness, sense of impeding doom, angina, incontinence, angioedema, wheezing, stridor, flushing, pruritis, uticaria

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14
Q

What are the interprofessional care goal for anaphylactic shock?

A

maintain patent airway

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15
Q

What drugs are used for anaphylactic shock?

A

nebulizers
aerosolized epi
aggressive fluid replacement (IV corticosteroids if it doesn’t help)

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16
Q

What is the cause of septic shock?

A

systemic inflammatory response to documented or suspected infection

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17
Q

What are manifestations of septic shock?

A

tachypnea/hyperventilation initially (results in respiratory alkalosis which will turn into respiratory acidosis)
decreased UO
altered neurological status
GI dysfunction: bleeding, paralytic ileus

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18
Q

What is the interprofessional management goal of septic shock?

A

fluid replacement to restore perfusion

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19
Q

What are the drugs used for septic shock?

A

vasopressors (IV corticosteroids backup)
antibiotics (should start within 1st hour)
PPIs (stress ulcer prophylaxis)
LW heparins (DVT prophylaxis)

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20
Q

What are the causes of obstructive shock?

A

physical obstruction to blood flow causing decreased CO

restricted diastolic filling of right ventricle from compression
abdominal compartment syndrome: abdominal pressure compresses inferior vena cava thus decreasing venous return to heart
PE
right ventricular thrombi causing outflow obstruction

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21
Q

What are manifestations of obstructive shock?

A

decreased CO
icnreased afterload
variable left ventricular filling pressure
JVD
pulses paradoxus (exaggerated fall in bp during inspiration by greater than 10mmHg)
any manifestations of right sided HF

22
Q

What is the interprofessional care goal for obstructive shock?

A

early recognition and treatment

23
Q

What is the primary goal of drug therapy for shock? Examples of drug types used

A

correction of decreased tissue perfusion

sympathomimetic (mimic SNS)
vasopressor (if unresponsive to fluid resuscitation)
vasodilator (decrease afterload)

24
Q

What is the initial assessment and treatment for chemical, small and large thermal, inhalation, and electrical burns?

A

chemical: brush solid particles off skin and use water lavage

small thermal: cover with clean, cool, tap water and dampened towel

large thermal: check pulses, elevate burnt limb aove heart to decrease pain and aid in reduction of swelling, cool burns for no more than 10 minutes, do not immerse or pack with ice (causes vasoconstriction which will worsen with injury

inhalation: watch signs for respiratory distress

electrical: will see entry and exit point wounds

25
What are the subsequent assessments for chemical, inhalation (upper and lower airway), and electrical burns?
chemical: tissue destruction may continue up to 72hrs after chemical injury inhalation: needs continual monitoring for 24 to 48hrs upper: swelling may be massive and onset rapid, eschar and edema may compromise breathing lower: pulmonary edema may not appear until 12 to 48 hrs after burn and will manifest as ARDS electrical: at risk for dysrhythmias/ cardiac arrest (may occur right away or 24hrs after injury), severe metabolic acidosis, and myoblobinuria (can lead to ATN)
26
What are the classifications and manifestations of the depths of burns?
superficial partial thickness: involves epidermis, don't blister but are painful, dry, red, and blanchable, may develop a little or some worsening pain and erythema over 3 to 4 days superficial deep partial thickness: develops within 24hrs, painful, blanchable, pink to cherry red, wet, shiny with serous exudate, blisters, can take up to 2 to 3 wks deep partial thickness: painful, blister, wet, waxy, or dry, patchy cheesy white or red, blanchable, may take up to 9 wks to heal, may cuase hypertrophic scarring full thickness: eschar is usually intact, skin is waxy white to leathery grey or charred, dry and inelastic, nonblanchable, no vesicles or blisters
27
What are typical clues for smoke inhalation burns?
presence of facial burns singed nasal hair hoarseness, painful swallowing darkened oral and nasal membranes carbonaceous sputum hx of being burned in enclosed space clothing burns around neck and chest if oropharynx and/or larynx: redness, blistering, edema of tissues
28
What are the initial medical concerns after a major burn?
hypovolemic shock: caused by a massive shift of fluids out of blood vessels as a result of increased capillary permeability edema: d/t increased capillary permeability, HCT increases and blood becomes more viscous, this along with edema increases peripheral resistance colloidal osmotic pressure decreases as capillary permeability increases causing loss of protein from vascular space resulting in more fluid shifting out of vascular space and into interstitial spaces airway management fluid resuscitation wound care drugs: analgesic and sedative, tetanus, antimicrobial agents
29
How is fluid resuscitation managed?
colloids are held for the first 12 to 24 hrs post burn to allow for capillary permeability to return to normal/ near normal (allowing colloids to actually stay within vasculature) parkland formula: 4mL of LR per kg per percentage TBSA burned, give first half over 8 hrs and second half over next 16 hrs
30
How is TBSA calculated?
front of head and neck = 4.5 back of head and neck = 4.5 front of an arm = 4.5 back of an arm = 4.5 front upper torso = 9 front stomach = 9 back of upper torso = 9 back of stomach area = 9 genitals = 1 front of a leg = 9 back of a leg = 9
31
What are the nutritional needs of those with major burn injuries?
needed if intubated or TBSA burnt>20% early and aggressive nutritional support within hours of burn hypermetabolic state: resting metabolic expenditure may be increased by 50 to 100% above normal, caloric needs are about 5000 kcal/day
32
What are nursing considerations for those with circumferential burns?
burns may cause circulation problems distal to burn may develop compartment syndrome with direct damage to muscle and subsequent edema (may need escharotomies)
33
What are infection prevention measures done for burn patients?
tetanus: d/t likelihood of anerobic bacterial infection antimicrobials: topical (silver sulfadizaine, mafenide acetate), systemic agents not typical given (unless sepsis occurs) d/t little to no blood supply to eschar
34
What are early manifestations of ARDS?
dyspnea, tachypnea, cough, restlessness chest auscultation may be normal or may be fine, scattered crackles mild hypoxemia and respiratory alkalosis d/t hyperventilation chest XR may be normal or minimal scattered interstitial infiltrates edema may not show until 30% increase in fluid content in lungs
35
What are late manifestations of ARDS?
pulmonary function tests reveal decreased lung volumes, functional residual capacity, and compliance tachycardia, diaphoresis, changes in mental status, cyanosis, pallor diffuse crackles and coarse crackles hypoxemia despite increased FiO2
36
What are direct lung injuries? Examples?
injuries that directly affect lung tissue aspiration viral or bacterial infections (ie. pneumonia) chest trauma mechanical ventilation
37
What are indirect lung injuries? Examples?
injury to body that indirectly cause an inflammatory response in lungs sepsis (most common cause, may be direct or indirect depending on where it originates) severe mass trauma mass blood transfusions (antibody rxn) pancreatitis
38
What are the three phases of ARDS? Patho?
exudative: injury occurs to lungs leading to acute inflammatory response, usually occurs on days 1-7, damage to vascular endothelium causing capillary permeability and then the formation of intrapulmonary shunt and results in atelectasis proliferative: systemic inflammation leading to increased capillary permeability and fluid of vascular space leaking into tissues, usually occurs 1-2 wks after injury fibrotic: lung is remodeled by collagenous and fibrous tissues, may take 6 to 12 months to fully recover
39
What are complications of ARDS?
GI: stress ulcers, bleed pulmonary: barotrauma, subcutaneous emphysema renal failure DVT psychological
40
What are the diagnostic testing of ARDS?
bilateral patchy infiltrates on CXR abnormal central venous or pulmonary artery pressures initial increased CO but as hypoxemia, hypercapnia, and acidosis becomes more severe CO will decrease bronchoalveolar lavage has high protein content
41
What are three hallmarks of ARDS?
bilateral patchy infiltrates on CXR no s/s of HF no improvements in PaO2 despite increasing oxygen delivery (refractory hypoxemia)
42
What medications are used for ARDS?
antibiotics: sepsis sedation, neuromuscular blocks and analgesics: comfort, decrease respiratory effort diuretic: edema inotropes and vasopressures: increase cardiac output
43
What are the key nursing interventions for patients with ARDS?
prevention of complications (infections, aspiration, skin breakdown, contractures, nutrition, stress ulcers, renal failure) provide support allow disease time to resolve
44
What are symptoms of insomnia
long sleep latency (difficulty falling asleep) fragmented sleep (frequent waking) prolonged nighttime awakenings nonrestorative sleep
45
How is the sleep/wake cycle regulated?
suprachiasmatic nucleus (SCN) in hypothalamus is synchronized through light (strongest time cue) detectors in retina and will regulate neurotransmitters for sleep/wake
46
What is insufficient sleep associated with?
increased BMI increased insulin resistance impaired cognitive function
47
What is OSA?
partial or complete upper airway obstruction and reduced tone during sleep that lasts 10 to 90 seconds apneic period may include: hypoxemia and hypercapnia
48
What are manifestations of OSA?
frequent arousals during sleep insomnia excessive daytime sleepiness witnessed apneic episodes snoring morning headache irritability personality changes
49
What are complications of OSA?
HTN poor concentration/memory impotence depression
50
How is an OSA diagnosis made?
medical and sleep hx PSG

443: Advanced Concepts (6 decks)

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