Shock/SIRS/MODS

Question 1

What are the four different stages of shock listed in order?

Answer 1

initial
compensatory
progressive
refractory

Question 2

What occurs during the initial phase of shock?

Answer 2

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

Question 3

What are the compensatory mechanisms that our body has to fight against shock? 3 things.

Answer 3

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

Question 4

What does our body initially do in the compensatory phase of shock to combat the lactic acidosis?

Answer 4

hyperventilation.

Question 5

What does someone in compensatory shock look like clinically?

Answer 5

increased HR, BP, RR, normal CO

Question 6

What is going on at a cellular level during the progressive stage of shock?

Answer 6

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

Question 7

What can happen when the CNS, hematologic, pulmonary, renal, and GI systems begin to fail through shock?

Answer 7

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

Question 8

Describe the refractory stage of shock, what can occur within it?

Answer 8

This is where the shock becomes unresponsive to therapy and eventually MODS develops.

This is the irreversible stage of shock, death occurs.

Question 9

At least how many organs have to be failing to be considered MODS?

Answer 9

2

Question 10

What are the different classifications of shock?

Answer 10

Hypovolemic

cardiogenic

Distributive: anaphylactic, neurogenic, and septic

Question 11

What is the definition of hypovolemic shock, is this a common form of shock?

Answer 11

lack of circulating volume leads to decreased tissue perfusion

THIS IS THE MOST COMMON FORM OF SHOCK

Question 12

What is the difference between absolute and relative hypovolemic shock?

Answer 12

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)

Question 13

What are some hemodynamic changes that occur from hypovolemic shock?

Answer 13

decreased preload

decreased CO

decreased CI

SvO2 decreased (<60%)

increased SVR

Question 14

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.

Answer 14

1 - <500 - initial

2 - 500-1000 - compensatory

3 - 1000-2000 - progressive

4 - 2000-3000 - refractory

Question 15

Describe the initial stage of hypovolemic shock, how much fluid has been lost?

Answer 15

<500 lost compensatory mechanisms being used and CO is normal, symptom free

Question 16

Describe the compensatory stage of hypovolemic shock, how much fluid has been lost at this point?

Answer 16

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

Question 17

Describe the progressive stage of hypovolemic shock, how much fluid has been lost at this point usuaully?

Answer 17

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

Question 18

Describe the refractory phase of hypovolemic shock, how much volume has been lost at this point?

Answer 18

2000-3000ml

same as progressive

ADD: decreased oxygen saturations, anuric, mental stupor and possible coma, extreme extremity signs of vasoconstriction, severe acidosis

Question 19

What is the primary focus of management of hypovolemic shock?

Answer 19

identifying the cause of the fluid loss, stopping it, and increasing circulating volume

Question 20

What is the first line fluid type used in treating hypovolemic shock?

Answer 20

crystalloid solutions, isotonic solutions are preferred (lactated ringers or 0.9% normal saline) NOT D5W

LR IS CONTRAINDICATED IN RENAL FAILURE CLIENTS

Question 21

When are colloids and other volume expanders primarily used in the treatment of hypovolemic shock?

Answer 21

usually in the case of blood loss, this includes PRBCs to include the oxygen carry capacity

Question 22

Are colloid solution recommended for early treatment of hypovolemic shock?

Answer 22

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.

Question 23

When is autotransfusion a good idea?

Answer 23

chest trauma hemorrhage

Question 24

How do you mintor fluid replacement therapy?

Answer 24

CVP monitoring (0-8mmHg)

Question 25

What size IV is preferred for fluid administration for hypovolemic shock, any preference where access is gained?

Answer 25

16 or larger in the AC or central

Question 26

What are two possible complications of fluid volume replacement, especially if rapid?

Answer 26

hypothermia (fluids may be warmed) pulmonary congestion (ensure administration is at rate that prevents this)

Question 27

Nursing management for hypovolemic shock?

Answer 27

`monitor i/o daily weights limiting blood samples maintin invasive lines positioning monitor for fluid overload

Question 28

What are some risk factors for the development of cardiogenic shock?

Answer 28

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

Question 29

What are the hemodynamic findings when it comes to cardogenic shock? (SBP, MAP, CI, PAOP, SVR)

Answer 29

SBP <90 MAP <70 CI <2.2L/min/m^2 PAWP >18mmhg SVR > 1400

Question 30

What are the signs and symptoms of cardiogenic shock that the client will show that arre unique to this specifiic type of shock? radiography?

Answer 30

S3 S4, crackles, rhonchi, JVD, myocardial ischemia (troponin), respiratory alkalosis, decrease in PaO2 on ABG, rhonchi Radiographic: enlarged heart, pulmonary congestion THINK HEART FAILURE

Question 31

What are some ways the cardiogenic shock can be managed?

Answer 31

increasing contractility - dopamine, epinephrine, levophed, vasopressin decreasing fluid overload - diuretics vasodilate - nitro, ace inhibitors, vasoconstrict - amrinone, mirinone, dobutamine thrombolytics cath lab IABP

Question 32

What are the two ways anaphylactic shock can occur/?

Answer 32

IgE mediated (initial exposure creates it, then second exposure activates) and anaphylactoid (non IgE, first sures causes reaction)

Question 33

What are anaphylactoid reactions commonly associated with?

Answer 33

NSAIDS, and aspirin

Question 34

What is the dosage of epinephrine for anaphylaxis?

Answer 34

1:1000 (1mg/ml), 0.2-0.5ml im or subQ every 5 minutes

Question 35

What are some specific signs of anaphylaxis?

Answer 35

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

Question 36

Management of anaphylaxis?

Answer 36

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

Question 37

What is happening with neurogenic shock?

Answer 37

loss of suppression of sympathetic tone, onset occurs in minutes, can last for weeks

Question 38

What can cause neurogenic shock?

Answer 38

SPINAL CORD INJURY ABOVE LEVEL OF T6, SPINAL ANALGESIA, SEVERE EMOTIONAL DISTRESS, PAIN, DRUGS

Question 39

What are the signs and symptoms of neurogenic shock?

Answer 39

hypotension, bradycardia, HYPOTHERMIA (heat loss from excessive vasodilation, warm dry skin, motor/sensory dysfunctions (spinal shock) decreased CO duration depends on severity

Question 40

How do you manage neurogenic shock?

Answer 40

C-spine Fluid resuscitation (if SBP <90) (UOP<30ml/h, changes in mental status) vasoconstrictors warmings/environmental control pulmonary support dysrhythmia treatment

Question 41

if spinal cord injuries require immobilization, what needs to be prevented? through what measures?

Answer 41

DVT measure calf and thigh, passive rom, ted hose, scd, anticoagulant therapy

Question 42

why HOB slightly elevated after spinal anaesthesia?

Answer 42

so it doesnt travel up CNS to prevent systemic effects

Question 43

What are the differences between uncomplicated sepsis, severe sepsis, and septic shock? why are these categories made?

Answer 43

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

Question 44

What are some things that increase the risk of developing septic shock?

Answer 44

``` extreme of age malnutrition debilitation chronic illness drug or ETOH neutropenia splenectomy multiple organ failure ```

Question 45

What are some risk factors for progression of sepsis to severe sepsis?

Answer 45

``` 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 ```

Question 46

Does sepsis have a high mortality rate? septic shock?

Answer 46

20% sepsis 70% septic shock

Question 47

What is the primary cause of sepsis?

Answer 47

= uncontrolled inflammatory response

Question 48

What does sepsis do to coagulation?

Answer 48

causes clots to form throughout vasculature, eventually running them dry = DIC impaired fibrinolysis leaves clots in microvasculature increasing ischemia

Question 49

Other than hypercoagulation, what else does sepsis do?

Answer 49

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

Question 50

What assessment finding might be present in a client experiencing initial sepsis? (hemodynamics included)

Answer 50

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

Question 51

S/S of secondary stage of sepsis?

Answer 51

decreased CO, Hypotension, vasoconstriction stupor or coma skin is cold/clammy mottling, cyanosis (peripheral) pulses weak and rapid shallow respirs abnormal pattern anuria

Question 52

What are the goals of management for septic shock?

Answer 52

maximize oxygen delivery to meet demands halt inflammatory response prevent progression to MODS

Question 53

What are specific management techniques for patients experiencing sepsis?

Answer 53

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

Question 54

Why might sepsis incidents be increasing?

Answer 54

increasing elderly population increasing debilitated clients increased patients with underlying disease overuse of antibiotics

Question 55

What is SIRS?

Answer 55

systemic inflammatory response syndrom - systemic inflammation, precursor to septic shock

Question 56

What are the diagnostic criteria for SIRS?

Answer 56

temp >38 or < 36 HR > 90 RR > 20 or PaCO2 <32 WBC >12,000 or < 4,000 TWO OR MORE MUST BE PRESENT

Question 57

With a infection evident through a blood culture or tissue sample along with SIRS present is called what?

Answer 57

Sepsis

Question 58

What does the progression of sepsis result in?

Answer 58

MODS

Question 59

What is MODS?

Answer 59

presence of altered function in two or more organs in an acutely ill patient that requires intervention to maintain homeostasis

Question 60

What is the mortality rate of MODS?

Answer 60

75%

Question 61

What are some causes of MODS?

Answer 61

uncontrolled SIRS prolonged release of inflammatory mediators

Question 62

Which organs are first to be affected by MODS?

Answer 62

lungs, heart, and kidneys once the first is effected, the likelihood of another being effected increases dramatically

Question 63

What are some signs of MODS?

Answer 63

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

Question 64

How do you treat MODS?

Answer 64

hemodynamic support nutrition control BG respiratory support - vent with high PEEP conserve energy manage fever SIMILAR TO TREATMENT OF SEPSIS

Question 65

What is the resuscitation bundle for sepsis? What timeframe is this for?

Answer 65

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

Question 66

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?

Answer 66

30ml/kg ASAP