Shock/SIRS/MODS Flashcards
What are the four different stages of shock listed in order?
initial
compensatory
progressive
refractory
What occurs during the initial phase of shock?
decreased CO
ineffective tissue perfusion
lactic acidemia - anaerobic metabolism used due to lack of oxygen, causes more cellular damage when built up
USUALLY VITALS SIGNS ARE RELATIVELY NORMAL, HARD TO DIAGNOSE AT THIS STAGE
What are the compensatory mechanisms that our body has to fight against shock? 3 things.
SNS activation - increases CO and BP through adrenal medulla stimulation making norepinephrine entering the bloodstream causing vasoconstriction, increaseed myocardial contractility, and increased HR
Endocrine response -
- ADH is secreted by posterior pituitary which increases venous return to heart and therefore preload
- -ACTH increases secretion of glucocorticoids increases BG
Renin-angiotensin-aldosterone - renin stimulates angiotensin release, ACE converts to angiotensin II, which stimulates vasoconstriction and stimulates aldosterone release, which tells kidneys to conserve water and sodium and kick out potassium
What does our body initially do in the compensatory phase of shock to combat the lactic acidosis?
hyperventilation.
What does someone in compensatory shock look like clinically?
increased HR, BP, RR, normal CO
What is going on at a cellular level during the progressive stage of shock?
anaerobic metabolism proves ineffective for metabolic needs
sodium-potassium pumps begin to fail - cell swells
energy production stops
oxygen utilization fails
autodigestion occurs due to digestive enzymes leaking from swollen cell
What can happen when the CNS, hematologic, pulmonary, renal, and GI systems begin to fail through shock?
CNS - cardiac and respiratory depression, thermoregulatory failure, vasodilation if SNS fails
Hematologic - DIC in response the inflammation in system
pulmoary - ARF
Renal - ATN
GI - ischemia and failure due to vasoconstriction
Describe the refractory stage of shock, what can occur within it?
This is where the shock becomes unresponsive to therapy and eventually MODS develops.
This is the irreversible stage of shock, death occurs.
At least how many organs have to be failing to be considered MODS?
2
What are the different classifications of shock?
Hypovolemic
cardiogenic
Distributive: anaphylactic, neurogenic, and septic
What is the definition of hypovolemic shock, is this a common form of shock?
lack of circulating volume leads to decreased tissue perfusion
THIS IS THE MOST COMMON FORM OF SHOCK
What is the difference between absolute and relative hypovolemic shock?
absolute is the literal decrease in the amount of fluid available (blood loss & dehydration)
refractory is fluid shifting from intravascular to extravascular space (burns for example)
What are some hemodynamic changes that occur from hypovolemic shock?
decreased preload
decreased CO
decreased CI
SvO2 decreased (<60%)
increased SVR
In hypovolemic shock, there are four stages that are based on how much fluid loss has occured. What are the volumes that separate each phase? these correlate with the stages of shock.
1 - <500 - initial
2 - 500-1000 - compensatory
3 - 1000-2000 - progressive
4 - 2000-3000 - refractory
Describe the initial stage of hypovolemic shock, how much fluid has been lost?
<500 lost compensatory mechanisms being used and CO is normal, symptom free
Describe the compensatory stage of hypovolemic shock, how much fluid has been lost at this point?
500-1000ml lost
tachycardia, hypotension, decreased urine output, weak pulse, cool extremities, mild acidosis may be present, narrowed PP
increased SVR, CO REMAINS RELATIVELY NORMAL, BUT BEGINS TO FALL
Describe the progressive stage of hypovolemic shock, how much fluid has been lost at this point usuaully?
1000-2000 lost
same as compensatory, worsened.
include progressive acidosis, neuro symptoms like decreased LOC, tachypnea (acidosis), SvO2 <60, UOP <30ml/h, dysrhythmias may develop, decreased CO and increased SVR
Describe the refractory phase of hypovolemic shock, how much volume has been lost at this point?
2000-3000ml
same as progressive
ADD: decreased oxygen saturations, anuric, mental stupor and possible coma, extreme extremity signs of vasoconstriction, severe acidosis
What is the primary focus of management of hypovolemic shock?
identifying the cause of the fluid loss, stopping it, and increasing circulating volume
What is the first line fluid type used in treating hypovolemic shock?
crystalloid solutions, isotonic solutions are preferred (lactated ringers or 0.9% normal saline) NOT D5W
LR IS CONTRAINDICATED IN RENAL FAILURE CLIENTS
When are colloids and other volume expanders primarily used in the treatment of hypovolemic shock?
usually in the case of blood loss, this includes PRBCs to include the oxygen carry capacity
Are colloid solution recommended for early treatment of hypovolemic shock?
Not usually in the beginning of treatment, usually once stable, in the beginning of treatment the capillary permeability still may be high enough to allow the larger particles of colloid solution to escape the vascular space.
When is autotransfusion a good idea?
chest trauma hemorrhage
How do you mintor fluid replacement therapy?
CVP monitoring (0-8mmHg)
What size IV is preferred for fluid administration for hypovolemic shock, any preference where access is gained?
16 or larger in the AC or central
What are two possible complications of fluid volume replacement, especially if rapid?
hypothermia (fluids may be warmed)
pulmonary congestion (ensure administration is at rate that prevents this)
Nursing management for hypovolemic shock?
`monitor i/o
daily weights
limiting blood samples
maintin invasive lines
positioning
monitor for fluid overload
What are some risk factors for the development of cardiogenic shock?
older age
LVEF <35%
large MI, left ventricular infarct is most common cause
history of DM
previous MI
septal ruptures of heart, papillary muscle rupture, cardiomyopathies, PE, myocarditis, cardiac tamponade
dysrhythmias - brady and tachy
open heart surgery
What are the hemodynamic findings when it comes to cardogenic shock? (SBP, MAP, CI, PAOP, SVR)
SBP <90
MAP <70
CI <2.2L/min/m^2
PAWP >18mmhg
SVR > 1400
What are the signs and symptoms of cardiogenic shock that the client will show that arre unique to this specifiic type of shock? radiography?
S3 S4, crackles, rhonchi, JVD, myocardial ischemia (troponin), respiratory alkalosis, decrease in PaO2 on ABG, rhonchi
Radiographic: enlarged heart, pulmonary congestion
THINK HEART FAILURE
What are some ways the cardiogenic shock can be managed?
increasing contractility - dopamine, epinephrine, levophed, vasopressin
decreasing fluid overload - diuretics
vasodilate - nitro, ace inhibitors,
vasoconstrict - amrinone, mirinone, dobutamine
thrombolytics
cath lab
IABP
What are the two ways anaphylactic shock can occur/?
IgE mediated (initial exposure creates it, then second exposure activates) and anaphylactoid (non IgE, first sures causes reaction)
What are anaphylactoid reactions commonly associated with?
NSAIDS, and aspirin
What is the dosage of epinephrine for anaphylaxis?
1:1000 (1mg/ml), 0.2-0.5ml im or subQ every 5 minutes
What are some specific signs of anaphylaxis?
vasodilation, increased capillary permeability, peripheral vasodilation, excessive mucous secretion, coronary vasoconstriction, smooth muscle constriction in bladder and uterus, urticaria and pruritus
angioedema - face, oral cavity, lower pharynx
respiratory - laryngeal edema, wheezing, stridor, dysphagia, tightness in chest, vomiting, cramping
Management of anaphylaxis?
Overview: remove offending antigen, reverse effects of biochemical mediators, promote adequate tissue perfusion
Mild: oxygen, antihistamine (IM or subQ) MAYBE epi
Severe:
manage AIRWAY AIRWAY AIRWAY
EPI, bronchodilator, corticosteroid, vasoconstrictors, positive inotropes
fluid replacement
What is happening with neurogenic shock?
loss of suppression of sympathetic tone, onset occurs in minutes, can last for weeks
What can cause neurogenic shock?
SPINAL CORD INJURY ABOVE LEVEL OF T6, SPINAL ANALGESIA, SEVERE EMOTIONAL DISTRESS, PAIN, DRUGS
What are the signs and symptoms of neurogenic shock?
hypotension, bradycardia, HYPOTHERMIA (heat loss from excessive vasodilation, warm dry skin, motor/sensory dysfunctions (spinal shock)
decreased CO
duration depends on severity
How do you manage neurogenic shock?
C-spine
Fluid resuscitation (if SBP <90) (UOP<30ml/h, changes in mental status)
vasoconstrictors
warmings/environmental control
pulmonary support
dysrhythmia treatment
if spinal cord injuries require immobilization, what needs to be prevented? through what measures?
DVT
measure calf and thigh, passive rom, ted hose, scd, anticoagulant therapy
why HOB slightly elevated after spinal anaesthesia?
so it doesnt travel up CNS to prevent systemic effects
What are the differences between uncomplicated sepsis, severe sepsis, and septic shock? why are these categories made?
uncomplicated sepsis - SIRS resulting from an infection
Severe sepsis - sepsis associated with organ dysfunction, hypoperfusion, or hypotension
septic shock - sepsis accompanied with persistent hypotension despite adequate fluid resuscitation along with presence of perfusion abnormalities
THESE ARE IN ORDER OF PROGRESSION OF SEPSIS
What are some things that increase the risk of developing septic shock?
extreme of age malnutrition debilitation chronic illness drug or ETOH neutropenia splenectomy multiple organ failure
What are some risk factors for progression of sepsis to severe sepsis?
SBP <110 temp more than 38.2 - 100.76 hypernatremia platelets less than 150 x 10^9 bili more than 30 mechanical ventilation infection present
Does sepsis have a high mortality rate? septic shock?
20% sepsis
70% septic shock
What is the primary cause of sepsis?
= uncontrolled inflammatory response
What does sepsis do to coagulation?
causes clots to form throughout vasculature, eventually running them dry = DIC
impaired fibrinolysis leaves clots in microvasculature increasing ischemia
Other than hypercoagulation, what else does sepsis do?
increased capillary permeability
myocardial depression - cytokines cause this
hypermetabolic state - increased energy consumption, no response to insulin, glycogen stores are used up, switch to anaerobic metabolism = aciosis, EFFECTS LIVER from triglyceride breakdown for ketones to be used in krebs cycle
maldistribution of blood - widespread vasodilation reduces return to heart, vasoconstriction of microcirculation decreased perfusion to vascular beds decreasing tissue perfusion
organ failure - due to ineffective energy sources and blood flow from above mechanisms
What assessment finding might be present in a client experiencing initial sepsis? (hemodynamics included)
decreased RAP and PAOP, decreased SVR and PVR
Increased HR causes a normal CO/CI initially
hypoxemia due to pulmonary vasoconstriction and microemboli
increased immature neutophils (bands)
elevated BG
widened PP
warm,pink skin
bounding pulse
hypoxemia, respiratory alkalosis, metabolic acidosis, crackles
decreased LOC
decreased UOP
temp > 38 or < 36
S/S of secondary stage of sepsis?
decreased CO, Hypotension, vasoconstriction
stupor or coma
skin is cold/clammy
mottling, cyanosis (peripheral)
pulses weak and rapid
shallow respirs abnormal pattern
anuria
What are the goals of management for septic shock?
maximize oxygen delivery to meet demands
halt inflammatory response
prevent progression to MODS
What are specific management techniques for patients experiencing sepsis?
identify the specimen through cultures
ABX therapy (may be hazardous)
vent - keep PaO2 > 70
diet high in protein
labs - WBCs, aPTT, PT, platelet
surgical debridement if wound present
fluids - crystalloid
vasoconstrictors - dobutamine
positive inotropes
temp control
CVP of 8-12 or 12-15 for vented with MAP of 65 or greater
no steroids,no protein C
bg less than 150
Why might sepsis incidents be increasing?
increasing elderly population
increasing debilitated clients
increased patients with underlying disease
overuse of antibiotics
What is SIRS?
systemic inflammatory response syndrom - systemic inflammation, precursor to septic shock
What are the diagnostic criteria for SIRS?
temp >38 or < 36
HR > 90
RR > 20 or PaCO2 <32
WBC >12,000 or < 4,000
TWO OR MORE MUST BE PRESENT
With a infection evident through a blood culture or tissue sample along with SIRS present is called what?
Sepsis
What does the progression of sepsis result in?
MODS
What is MODS?
presence of altered function in two or more organs in an acutely ill patient that requires intervention to maintain homeostasis
What is the mortality rate of MODS?
75%
What are some causes of MODS?
uncontrolled SIRS
prolonged release of inflammatory mediators
Which organs are first to be affected by MODS?
lungs, heart, and kidneys
once the first is effected, the likelihood of another being effected increases dramatically
What are some signs of MODS?
neuro: altered LOC, confusion, psychosis
Respir - tachypnea, PaO@ < 70, SaO2 < 90%,
renal - oliguria, anuria, increased CK
CV - tachycardia, hypotension, altered CVP & PAOP
hepatic (late: compensates well) - jaundice, increase enzymes, decreased albumin, increased PT, increased bilirubin, ammonia increase, DIC
hematologic - decreased platelets, increased PT, aPTT, decreased protein C, increased d-dimer, lactic acid elevation
HYPERGLYCEMIA
How do you treat MODS?
hemodynamic support
nutrition
control BG
respiratory support - vent with high PEEP
conserve energy
manage fever
SIMILAR TO TREATMENT OF SEPSIS
What is the resuscitation bundle for sepsis? What timeframe is this for?
lactate measurement
blood cultures from 2 sites prior to antibiotic administration
broad-spectrum antibiotics started
30ml/kg bolus of crystalloid
vasopressors for persistent hypotension
CVP >8
ScvO2 > 70%
THIS IS USED IN THE FIRST 6 HOURS
following the lactate measure during the resuscitation bundle for sepsis, what is the bolus amount given for a value of >4 or for someone with hypotension?
30ml/kg ASAP
