Shock

Question 1

compensation in shock

Answer 1

in response to shock, body triggers neuro-endocrine responses to overcome ineffective circulating blood volume
chemo and baro receptors alert hypothalamus to activate SNS releasing massive aount of norepinephrine, epinephrine and cortisol (initiating compensatory mechanisms)

Question 2

what are the compensatory mechanisms?

Answer 2

increased HR- to deliver needed o2 rapidly
increased glycolysis- increase availabilty of glucose for energy
decreased UO- to conserve fluid volume
decreased blood flow to organs- allow more blood flow to vital organs
decreased intestinal peristalsis- shunt blood to vital organs
cool skin- to prodce peripheral vasoconstriction to shunt blood to vital organs
diaphoresis- release heat as by-product of metabolism

Question 3

compensatory (shock)- what does cortisol levels do?

Answer 3

cortisol levels are increased which cause insulin resistance which triggers hepatic glycogenolysis resutling in increased glucose availability for energy
it also alters metabolism so energy is available

Question 4

shock process

Answer 4

endocrine system activated to decrease o2 delivery by increasing blood volume during stress.
stress occurs- hypothalamus realeases ACTH which stimulate cortisol which causes increase insulin resistance resulting in increased glucose
ADH, aldosterone and cortisol increase sodium and water whcih increases intravascular space. CO increases in response to venous return , RAAS is activated to increase blood volume , renin is excreted and angiotensin converts 1 to 2 causing vasoconstriction which increases BP by increasing afterload

Question 5

stages of shock: initial

Answer 5

decreased CO and tissue perfusion occur
decreased o2 delivery to cells result in anaerobic metabolism and develop lactic acidosis

Question 6

stages of shock: compensatory

Answer 6

neuro-endocrine responses are activated to restore CO and o2 delivery
these mechanisms try to restore o2 delivery and CO redistributing blood flow and restoring blood volume

Question 7

stages of shock: progressive

Answer 7

occurs when compensatory mechanisms cannot restore homeostasis and treatment not instituted
results in major organ dysfunction
continued low blood flow, poor tissue perfusion, inadequate o2 delivery, build up of metabolic wastes all overtime lead to MODS

Question 8

stages of shock: refractory

Answer 8

final stage
cell destruction is severe
profound hypotension develops + patient remains hypoxemic despite therapy - leading to body failure + death

Question 9

assessment of shock

Answer 9

ABGs
Lactate (over 5mmol/L is acidic, type A: impaired tissue o2, type B: normal tissue o2 but elevated metabolic acids)
base excess and base deficit ( amount of base required to titrate 1L of arterial blood to normal pH of 7.40, reflects metabolic acid-base status based on amount of HCO3 present, normal +2 to -2. the higher the # the the more acidic and shock is present
venous o2 saturation (SvO2 measure amount of o2 uploaded into tissues before venous blood returns to lungs for reoxygenation, provides info on balance of o2 supply and demand, normal hgb 60-80%, low = prolbem with o2 deliver or increased demand
gastric tonometry- NG tube samples gastric mucosa CO2 level + pH. when pH drops , gastric perfusion worsens = CO2 accumulates
doppler ultrasonography- for high acuity pts, transthoracic vs transesophageal
pulse contour analysis- determine CO with estimating SV

Question 10

interventions to optomize Oxygen delivery

Answer 10

o2 therapy: improves o2 delivery to hypoxic tissues
nasal canula or mask- to conscious/breathing/adequate ABGs pts
intubation with mechanical ventilation- to mod-severe shock pts + unconscoius or resp distress
monitor o2 level- too high can impaire innate immune response and increase infectious complication + tissue damage
IV fluids to restore tissue perfusion
crystalloids (NS/RL) resores interstitial and intravascular volume increasing preload and CO
Colloids (albumin, plasma expanders like dextrose/starches) expands circulating volume and remain in circulation longer then crystalloids
blood or blood products (PRBCs) - given when need to provide adequate hgb concentration and increase o2 carrying capacity or maintain adequate circulating volume
Vasopressors- consider when volume resus not sufficient

Question 11

interventions to decrease oxygen consumption

Answer 11

decrease body work - compensatory hyperventilation occurs causes high muscle effort causing resp distress- mechanical ventilation can help with this
neuromuscular blocking agent (pancuronium, vecuronium) to paralyze muscles eliminating voluntary muscle activity which allows o2 to be redirected for use in heart. REQUIRES intubation and mech vent prior to giving bc they paralyze resp muscles
sedation- (propofol/diprivan) - quickly induces deep sedation, short half life
benzodiazepine used for sedation to control anxiety + longer half life
reduce pain and anxiety- analgesics, anxiolytics
maintain normothermia- antipyretics, cooling with fan, cool blanket, ice pack. watch for shivering (increases metabolism and o2 consumption)
maintain normal glucose levels- stress-induced hyperglycemia- IV insulin given if above 180mg/dL on 2 occasions

Question 12

vasoactive drugs for shock treatment

Answer 12

vasoactive drugs alter blood vessel diameter through vasodilation or constriction
these are initiated when fluid resus have failed to perfuse
combining positive inotropic drugs with vasopressors/vasodilators can be more beneficial

Question 13

vasopressors

Answer 13

cause peripheral vasoconstriction and increase systemic BP through constricting peripheral vasculature
classified as adrenergic agonists (sympathomimetics) they activate adrenergic receptors mimicking SNS stimulation
catecholamines (norepi and dopamine- activate alpha and beta receptors, short duration, don’t cross BBB) vs noncatecholamines (phenylephrine- activates alpha receptors, long duration, cross BBB)
includes- norepinephrine, dopamine, vasopressin, phenylephrine, epinephrine
Alpha receptors- cause vasoconstriction and increases BP. can cause HTN, tissue ischemia/necrosis, tach or bradycardia
beta receptors- increases HR and force of contraction resulting in increase CO. can cause Tachycardia, dysrhythmias, angina
given in small dose increments IV

Question 14

vasopressin

Answer 14

also known as ADH
secreted by pituitary gland in response to decreased blood volume or pressure
causes water conservation decreasing UO and increasing intravascular water and systemic vasoconstriction
used: second line for ppl who need increase MAP and are not responsive to norepinephrine (catecholamine)

Question 15

inotropes

Answer 15

manipulates heart contractility and CO
negative inotropes decrease contractility
positive inotropes increase contractility force and HR (given w/ shock pts) - ex. digoxin (cardiac glycoside), sympathomimetics (dopamine, dobutamine) and phosphodiesterase (milrinone)

Question 16

vasodilators

Answer 16

reduces preload + afterload to improve CO and o2 delivery
peripheral arterial vasodilators decrease SVR by decreasing afterload causing ventricles to have less resistance
only given to pts with adequate fluid volume
nitroglycerin is one- it relaxes muscles of vessels by converting to NO
SE = hypotension and reflex tachycardia

Question 17

vasoactive drugs - nursing implications

Answer 17

IV vasoactive drugs are incompatible with most other drugs
wean in small increments to avoid destabilization of pts hemodynamic status
monitor hemodynamic status- art line, pulm art line, CVC, cardiac output
during titration- monitor HR, BP, MAP q5min till therapeutic level acheived
monitor oxygenation- color, temp, pulses, ABGs, lactate, SvO2, base excess/deficit
SE- local tissue ischemia/necrosis, so CVC is preferred. if infiltration occurs stop drug and contact HCP
antidote for infiltration/extravasation = phentolamine
do not suddenly cessation - will result in rapid drop in BP and worsening shock

Question 18

distributive shock

Answer 18

involve impaired o2 bc of altered blood flow distribution;
smooth muscle becomes incapable of constricting for 1 or 2 reasons: 1) endothelial insult (septic/anaphylactic shock) or 2) loss of sympathetic nervous system response (neurogenic shock)
massive vasodilation occurs causing huge expansion to intravascular compartemnt with no increase volume of circulating blood resulting in hypovolemia = hypotension

Question 19

distributive shock

Answer 19

involve impaired o2 bc of altered blood flow distribution;
smooth muscle becomes incapable of constricting for 1 or 2 reasons: 1) endothelial insult (septic/anaphylactic shock) or 2) loss of sympathetic nervous system response (neurogenic shock)
massive vasodilation occurs causing huge expansion to intravascular compartment with no increase volume of circulating blood resulting in hypovolemia = hypotension

Question 20

septic shock

Answer 20

characterized by altered fluid volume related to vasodilation , increased capillary permeability and maldistribution of circulating volume (some organs receive blood, some don’t)
systemic response to infection triggers series of cellular events. as pathogens invade bloodstream, they stimulate release of inflammatory mediators that impair microvasculature and cause cell dysfunction resulting in increased capillary permeability and vasodilation
perfusion abnormalities = lactic acidosis, oliguria, ALOC

Question 21

sepsis criteria

Answer 21

infection and SIRS criteria: presence of two or more of:
temp greater then 38.3 or less then 36
HR >90bpm
RR>20b/m
C reactive protein 2 or more deviation greater than normal
procalcitonin 2 or more deviations greater then normal
WBC >20,000/mL or <4,000/mL or greater than 10% immature bands

Question 22

early compensatory stage s+s

Answer 22

compensatory mechanisms activated causing warm skin, CO is normal or high, tachycardia, SV normal, CVP or wedge pressure low, SVR decreased (vasodilation), dBP decreases causing widening pulse pressure

Question 23

compensatory mechanisms fail stage S+S

Answer 23

myocardial depressant and hypoxemic effects result and tissue hypoperfusion develops

Question 24

late stage S+S

Answer 24

extremities cold and mottling, lactate levels increase, ScvO2 decreases and tissue perfusion becomes increasingly compromised

Question 25

treatment of septic shock

Answer 25

admin antibiotics within 1 hour, blood cultures should be obtained prior to initiating antibiotics
obtain serum lactate levels (if >4mmol/L means significant tissue hypoperfusion + needs immediate fluid resus)
fluid resus- goal = CVP > 8mmHg, MAP >65, releive hypotension
medication-given if failure to restore o2 and releive hypotension vasopressor (norepinephrine) to increase MAP by vasoconstriction (1st line to treat unresponsive fluid resus pt), dobutamin (symathomimetic inotrope) 2nd line to improve CO and perfusion

Question 26

inflammatory response review

Answer 26

inflammation is localized immunological response to tissue injury (foreign material, trauma, allergens, extreme heat/cold, infection)
its a defense mechanism for protecting body restoring homeostasis and tissue repair

Question 27

inflammatory response: sequence of events

Answer 27

cells injury occurs, mast cells initiate inflammatory processes by releasing chemical mediators (bradykinin, histamine, prostaglandins) resulting in vascular events that trigger local vasodilation and increase vascular permeability
immune system activated which triggers chemotaxis and migration of immun cells to site of injury to destroy offending agent and clean the site in order to prepare for healing and reestablish homeostasis

Question 28

inflammatory response: symptoms

Answer 28

inflammation results from activation of chemical mediators
-localised S+S = redness, heat, welling, pain, loss of function
-systemic S+S = elevated leukocyte count, fever, malaise, anorexia

Question 29

endothelium

Answer 29

provides barrier and chemical support to vascular system and inflammatory system
is a thin single cell layer that is in inner lining of all veins/arteries, it directly interfaces with blood flowing by and acts a selective permeable barrier
they respond to local cell environment like trauma, bacteria, stress
insult to endothelium can alter homeostasis and constribute to SIRS and organ dysfunction

Question 30

when is endothelium activated

Answer 30

when bacteria invade tissues, endothelial cells are activated and release chemical mediators which stimulate inflammatory response + recruit WBC to area and promote clotting to contain the infection
during inflammation endothelial cells undergo necrosis and apoptosis or programmed cell death as the tissues are repaired
endothelium promotes adhesion and migration of WBC, alters vasomotor tone, increases permeability, induces thrombin generation/formation and triggers apoptosis

Question 31

SIRS

Answer 31

not a disease
its a proinflammatory response precipitated by a non specific insult (infectious or noninfectious)
causes = trauma, infection, major surgery, acute pancreatitis, burns, sepsis most common
risks = older age, organ dysfunction, malnutrition, immunosuppressed, compromised gut integrity, obesity
can progress to MODS when it is overwhelmed + cannot compensate/ manage widespread inflammation which compromises organ function

Question 32

SIRS symptoms

Answer 32

when patients have any 2-4 of these:
-temp >38 or <36
- Tachycardia (>90bpm)
-RR >20bpm or PaCO2 <32
-WBC count >12,000 or <4000, or rgeater than 10%immature bands
oher = decreased UO, ALOC

Question 33

MODS

Answer 33

progressive dysfunction or 2 or more organ systems that persist beyond 24hours
occurs as result of severe insult that initiates inflammatory response
mechanism - widespread endothelial injury with release of cytokines and other molecules from endothelial cells

Question 34

primary MODS pathway

Answer 34

develops first 72hrs of admission
direct initiating event causing primary inflammatory response (injury, hemorrhage, hypoxemia)
result of inadequate o2 delivery to cells + failure of microcirculation to remove metabolic end products as more cells die, organ dysfunction and failure occur

Question 35

secondary MODS pathway

Answer 35

involves host response to toxins that occur within context of SIRS rather then direct response that initiates insult
onset - later (weeks after initial acute insult)
second insult reactivates primary inflammatory response (primary MODS) at an exaggerated level

Question 36

MODS patho changes include

Answer 36

uncontrolled systemic inflammation, tissue hypoxia, unregulated apoptosis, microvascular coagulopathy

Question 37

MODS patho changes: uncontrolled systemic inflammation

Answer 37

SIRS is in almost all MODS pts
large # of proinflammatory mediators are initiated = systemic inflammatory response
proinflammatory mediators increase capillary permeability resulting in edema in organs like ARDS in lungs + cerebral edema in brain
these mediators also cause release of NO from endothelial cells resulting in vasodilation
neutrophils release O2 radicals + proteolytic enzymes and increase vascular permeability

Question 38

MODS patho changes: tissue hypoxia

Answer 38

decreased O2 delivery or reduced cellular use of O2 inhibits normal cell function
hypoxia results from derangement in cellular use of O2 in presence of adequate O2 delivery as result- metabolic shutdown occurs
when cells receive less O2 for ATP production, they cant perform protein synthesis or maintain function of NA-K pump becoming widespread + severe organ function is compromised