Week 12: Shock, SIRS & MODS Flashcards

1
Q

SHOCK, SIRS, MODS

A

-Shock decreased tissue perfusion
SIRS – Systemic Inflammatory Response Syndrome
MODS- Multiple organ dysfunction syndrome

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2
Q

Shock

A

-Syndrome characterized by decreased tissue perfusion & impaired cellular metabolism
-Results in an imbalance between the supply of and the demand for oxygen and nutrients
Classified As:
-LOW FLOW: low blood flow
-DISTRIBUTIVE: maldistribution of blood flow

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3
Q

Shock: Classifications (Low Flow)

A

Cardiogenic
-Related to the heart
Hypovolemic
-Massive tissue injury
-Hemorrhage

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4
Q

Shock : Classifications (Distributive)

A

Neurogenic
-Related to spinal cord
Anaphylactic
-Severe allergic reaction
Septic
-infection

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5
Q

Shock Low Flow (Cardiogenic Shock)

A

Systolic or diastolic dysfunction of the pumping action of the heart resulting in compromised cardiac output

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6
Q

Shock Low Flow (Hypovolemic Shock)

A

-Occurs when intravascular fluid volume is lost and the remaining volume is inadequate to fill the vascular space
ABSOLUTE: fluids leave the body
RELATIVE: fluid shifts from the vascular space into the interstitial or intracavitary space (third spacing)

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7
Q

SHOCK LOW FLOW MANIFESTATIONS

A

-Tachycardia
-Hypotension
-Pulmonary congestion
-Decreased renal perfusion

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8
Q

SHOCK LOW FLOW PHYSICAL EXAM

A

-Tachypnea
-Pale, cool, clammy skin
-Decreased capillary refill time
-Anxiety, confusion, agitation
-Decreased urinary output

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9
Q

SHOCK DISTRIBUTIVE (NEUROGENIC SHOCK)

A

-Hemodynamic phenomenon that can occur within 30mins of a spinal cord injury at the T5 vertebra or above & lasts up to 6wks
-Results in a massive vasodilation without compensation caused by the loss of SNS vasoconstrictor tone
-This massive vasodilation leads to a pooling of blood in the blood vessels

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10
Q

SHOCK NEUROGENIC MANIFESTATION

A

-Hypotension
-Bradycardia
-Temperature dysregulation

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11
Q

SHOCK NEUROGENIC PHYSICAL EXAM

A

-Heat loss
-Potential for hypothermia
-Skin is warm and dry

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12
Q

SHOCK DISTRIBUTIVE (ANAPHYLACTIC SHOCK)

A

-Acute, life-threatening allergic reaction to a substance
-Causes massive vasodilation with fluid shifting from the vascular to interstitial space: EDEMA
Respiratory distress
-Laryngeal
-Severe bronchospasm
-Circulatory failure

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13
Q

SHOCK ANAPHYLACTIC MANIFESTATIONS

A

-Angioedema
-Swelling of lips and tongue
-Wheezing and stridor
-Flushing
-Pruritus and urticaria
-Sense of impending doom

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14
Q

SHOCK DISTRIBUTIVE (SEPSIS)

A

Sepsis:
-systemic inflammatory response to a documented or suspected infection

Severe Sepsis:
-sepsis complicated by organ dysfunction, hypoperfusion, or hypotension

The body’s response to infection is exaggerated
↑ inflammation ↑ coagulation ↓ fibrinolysis

Septic Shock
-Develops in the presence of sepsis with hypotension despite fluid resuscitation

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15
Q

SHOCK SEPTIC

A

-The clinical presentation of sepsis is complex, and no single specific symptom
-↑CO: stresses myocardium
-Tachycardia
-Tachypnea

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16
Q

SHOCK SEPTIC MANIFESTATION

A

-Fever
-Hyperglycemia
-Edema
-Hypotension
-Oliguria
-Decreased capillary refill

Respiratory failure is common (85%)
A.) Patient hyperventilates to compensate
B.) Respiratory alkalosis
C.) Respiratory acidosis

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17
Q

Stages of Shock

A

1.) INITIAL STAGE:
-Occurs at a cellular level & not usually clinically apparent
-Metabolism changes from aerobic to anaerobic, causing lactic acid build-up (waste product)
-Lactic acid must be removed by the liver.
-However, this process requires oxygen, which is unavailable because of the ↓ in tissue perfusion

2.) Compensatory
3.) Progressive
4.) Refractory

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18
Q

Stages: Compensatory

A

The body activates compensatory mechanisms in an attempt to:
-overcome the increasing consequences of anaerobic metabolism
-to maintain homeostasis
You begin to see the body’s response to the imbalances in oxygen supply & demand

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19
Q

Stages: Compensatory

A

One of the first clinical signs of shock is hypotension, which occurs because of ↓CO & narrowing of the pulse pressure:
a.) Baroreceptors in carotid & aorta activate the SNS
b.) Stimulates vasoconstriction
c.) Releases epinephrine & norepinephrine
d.) Blood flow to heart & brain is maintained
e.) Blood diverted away from kidneys, GI tract, skin, & lungs

A multisystem response to decreasing tissue perfusion is initiated in the compensatory stage of shock

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20
Q

Stages: Progressive

A

-The progressive stage of shock begins as compensatory mechanisms fail
-In this stage, aggressive interventions are necessary to prevent MODS
-Distinguishing feature of this stage is continued ↓ cellular perfusion & resulting altered capillary permeability
-Interstitial edema
-Anasarca (general swelling of the whole body)
-Changes in the client’s mental status are important findings in this stage

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21
Q

STAGES PROGRESSIVE (PULMONARY SYSTEM)

A

-Blood flow is already reduced
-Arterioles constrict
-Edema
-Bronchoconstriction
-Impaired gas exchange

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22
Q

STAGES PROGRESSIVE (CARDIOVASCULAR SYSTEM)

A

-CO falls
-Hypotension
-↓ perfusion to coronary, cerebral & peripheral arteries
-Weakening of peripheral pulses
-Ischemia of distal extremities
-MI, dysrhythmias
-Acute tubular necrosis: AKI

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23
Q

STAGES PROGRESSIVE (GI SYSTEM)

A

-↓ blood supply
-Mucosal barrier becomes ischemic
-Ulcers
-GI bleeding
-Liver fails to metabolize drugs & waste: jaundice

Pt is at risk for disseminated intravascular coagulation (DIC) which is abnormal clotting that uses up platelets & clotting factors which then lead to bleeding.

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24
Q

Stages- Refractory

A

Patients demonstrate profound hypotension & hypoxemia
-Exacerbation of anaerobic metabolism
-Accumulation of lactic acid
-Fluids continue to shift out of the vascular space
-Blood pools in the capillary beds r/t constricted venules & dilated arterioles
-Hypotension & tachycardia worsen
-↓ coronary blood flow leads to worsening myocardial depression & further decline in CO
-The failure of the liver, the lungs, and the kidneys results in an accumulation of waste products, such as lactate, urea, ammonia, and carbon dioxide
-In this final stage, recovery is unlikely. The organs are in failure, and the body’s compensatory mechanisms are overwhelmed

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25
Q

Shock Diagnostics

A

-Lactate levels are elevated >4 mmol/L
-12 lead ECG
-Continuous cardiac monitoring
-Continuous pulse oximetry (EAR)
-Arterial pressure

26
Q

Shock Goals of Care

A

-Restoration of adequate tissue perfusion
-Normal vital signs, specifically, MAP greater than 65 mmHg
-Recovery of organ function
-Prevention of progression toward further complications related to prolonged states of hypoperfusion

27
Q

Shock Collaborative Care

A

-Ensure patient airway (may need a ventilator)
-O2 administered to keep sats > 90%
-Optimize mean arterial pressure (MAP) & circulating blood volume with aggressive fluid resuscitation & drugs

28
Q

Collaborative Care- Cardiogenic Shock

A

GOAL
restore blood flow to the myocardium by restoring the balance between oxygen supply & demand

-Thrombolytic therapy
-Cardiac catheterization
-Angioplasty with stent implantation
-Emergency revascularization
-CABG
-Valve replacement

29
Q

Collaborative Care- Hypovolemic Shock

A

-Focus on stopping the loss of fluid and restoring the circulating volume
-Fluid resuscitation 3:1: 3 ml of isotonic crystalloid per every 1 ml of estimated blood loss

30
Q

Collaborative Care: Septic Shock

A

-Patients in septic shock require large amounts of fluid replacement to achieve hemodynamic improvement
-Hemodynamic monitoring with a PA catheter or central venous catheter
-Glucose levels <10 mmol/L
-Antibiotics after cultures are obtained
-Stress ulcer prophylaxis with histamine (H2)-receptor blockers
-DVT prophylaxis with low-dose heparin

31
Q

Collaborative Care: Neurogenic Shock

A

-Loss of sympathetic tone: hypotension & ↓ venous return
-Need to maintain BP & organ perfusion
-Atropine for bradycardia
-Cautious administration of fluids because hypotension not r/t fluid loss

32
Q

Collaborative Care: Anaphylactic Shock

A

-Anaphylaxis can quickly progress to anaphylactic shock within minutes if not treated immediately
-Epinephrine is the 1st line of treatment
-2nd line of tx includes H1-antihistamines (Benadryl) & H2-antihistamines (Zantac) which block the histamine receptors
-Maintain airway: can quickly change r/t laryngeal edema or bronchoconstriction

33
Q

Nursing Assessment

A

-Focus on ABCs & tissue perfusion
-Vital signs
-LOC
-Peripheral pulses
-Capillary refill
-Skin (temp, colour, moisture)
-Urinary output

AS SHOCK PROGRESSES:
-pt’s skin becomes cooler & mottled
-urine output decreases
-peripheral pulses diminish
-neurological status continues to deteriorate

34
Q

Nurse Implementation

A

In order to prevent shock, the nurse must identify patients at risk:
-pts who are older
–pts with debilitating illnesses
–pts who are immuno-compromised
–pts with ↓O2 delivery
–pts with tissue hypoxia
–pts with severe allergies
-any person who sustains surgical or accidental trauma (hemorrhage, spinal cord injury, and other conditions)

35
Q

Nurse Implementation (Neuro Status)

A

-orientation & LOC, should be assessed q1h or more: best indicator of cerebral blood flow
-watch for changes in
* behaviour
* restlessness,
* hyperalertness,
* blurred vision
* confusion,
* paresthesias

36
Q

Nursing Implementation (Cardiovascular Status)

A

-Careful assess’t of HR, CVP, PA pressures q 15 min
-Continuous monitoring of ECG
-Heart sounds: S3 & S4 sounds
-Assess pt’s response to administration of fluids & meds q5-15 mins

37
Q

Nurse Implementation (Respiratory Status)

A

-Monitor resp q15-30mins: rate, depth, rhythm
-Assess breath sounds q1h
-Pulse oximetry: earlobe more accurate during advanced shock
-Interpret ABGs: gives definitive info on
ventilation & O2 status & acid-base balance

38
Q

Nursing Implementation

A

RENAL STATUS: urine output q1h
BODY TEMP: q1h
SKIN:
pallor, flushing, cyanosis diaphoresis, capillary refill
GI: bowel sounds q4h (decreased motility)

39
Q

SIRS & MODS

A

A systemic inflammatory response to a variety of insults, including infection, ischemia, infarction, injury

Characterized by at least 2 of the following:
-Fever
-Edema
-Hypotension
-Tachycardia
-Impaired oxygenation
-Increased WBC count

The failure of 2+ organ systems to such a degree that homeostasis cannot be maintained without intervention
-MODS is a progression from SIRS
-Mortality rate is 70% when three or more organs fail

40
Q

Organ & Metabolic Dysfunction

A

When the inflammatory response is not controlled, the consequences that occur include:
-activation of inflammatory cells
-release of mediators
-direct damage to the endothelium
-hypermetabolism

Organ perfusion may be compromised because of:
-Hypotension
-Decreased perfusion
-Microemboli
-Redistributed or shunted blood flow

41
Q

Organ and Metabolic Dysfunction (Respiratory)

A

-Most commonly affected in MODS
-Inflammatory mediators have a direct effect on the pulmonary vasculature
-Fluid shifts into the alveoli  alveolar edema
-End result is ARDS

42
Q

Organ & Metabolic Dysfunction (Cardiovascular)

A

-myocardial depression & massive vasodilation in response to ↑ tissue demands
Eventually, either:
-the perfusion of vital organs becomes insufficient
-the cells are unable to use oxygen and their function is further compromised

43
Q

Organ & Metabolic Dysfunction (Neuro)

A

-Mental status changes can be an early sign of MODS
Pt can become:
-Confused & agitated
-Combative
-Disoriented
-Lethargic
-Comatose

44
Q

Organ & Metabolic Dysfunction (Renal)

A

↓ perfusion to kidneys
AKI

45
Q

Organ & Metabolic Dysfunction (GI Tract)

A

↓ motility: abdominal distension & paralytic ileus
Blood is shunted away from GI mucosa: ischemic injury (Ulceration & GI bleeding)

46
Q

Metabolic Changes

A

-SIRS & MODS both trigger a hypermetabolic response
-Glycogen, then amino acids, then fatty acids are converted to glucose
* Hyperglycemia
* Insulin resistance
-End result is a catabolic state & lean body mass (muscle) is lost
-May last for days and results in liver dysfunction
-DIC may occur
-Electrolyte imbalances are
* These changes exacerbate mental status changes, neuromuscular dysfunction, and dysrhythmias

47
Q

SIRS & MODS

A

-Without early, goal-directed therapy, the prognosis for patients with SIRS and MODS is poor
-Mortality rates have been as high as 70% to 80% when three or more organs are involved

48
Q

Nursing & Collaborative Care
(Prevention & Treatment of Infection)

A

-Aggressive IPAC strategies to ↓ risk for HAIs
-Host dysfunction may lead to infection

49
Q

Nursing & Collaborative Care
(Maintenance of Tissue Oxygenation)

A

-Hypoxemia frequently occurs in patients with SIRS & MODS
-Interventions aim to ↓ O2 demand and ↑ O2 delivery

50
Q

Nursing & Collaborative Care
(Nutritional & Metabolic Support)

A

-Hypermetabolism: profound weight loss, cachexia & more organ failure
-Enteral or parenteral nutrition
-Tight glycemic control is important
(blood glucose <10 mmol/L)

51
Q

Nursing & Collaborative Care
(Appropriate Support of Individual Failing Organs)

A

-ARDS requires aggressive O2 therapy & ventilator
-Treat DIC
-Dialysis for renal failure

52
Q

Blood Components & Products

A

Red Blood Cells (frozen or packed)
-To ↑ Hb to transport oxygen

Platelets
-Bleeding caused by thrombocytopenia

Plasma (fresh frozen)
-Rich in clotting factors but contains no platelets
-Bleeding caused by deficiency in clotting factors

Cryoprecipitate
-Rich in concentrated clotting factors in less volume
-Replacement for fibrinogen deficiency r/t DIC

53
Q

After A Blood Donation…

A

each unit is centrifuged to create:
-Plasma
-Buffy coat (contains platelets)
-Red blood cells

Each layer is then separated and processed into blood components

54
Q

Blood- Types & Antigens

A

ANTIGENS
-surface proteins found on RBCs – either A or B
-form basis for ABO typing system

ANTIBODIES
-found in the serum of blood types A, B, & O that react with A or B antigens

55
Q

Blood- Rhesus (Rh) Factor

A

Another surface antigen of the RBCs and 2nd important consideration in blood typing
-Those with it are Rh+ (positive)
-Those without it are Rh- (negative)

56
Q

Blood- Putting It Altogether

A

Blood groups must be compatible
A: A, AB
B: B, AB
AB: AB
O: any

BUT Rh must also be considered
NEG: pos or neg
POS: only pos

57
Q

Blood- Putting it Together

A

A blood sample is sent for a “group & screen” and/or “crossmatch”

GROUP
-determines pt’s blood group & Rh status

SCREEN
-for significant antibodies

CROSSMATCH
-compatibility test to ensure no antibodies are present in pt’s sample that will react with blood being prepared for transfusion

58
Q

Blood Component Therapy (Blood Transfusions)

A

If incompatible or mismatched blood is transfused, a transfusion
-Antibodies trigger RBC destruction (hemolysis)
-Reaction can be mild to severe

Positive identification of the blood product and the recipient must be made by the nurse
90% of rxns r/t improper ID

59
Q

Blood Component Therapy

A

Frequently used in managing hematological diseases
Many therapeutic & surgical procedures depend on blood product support
-Because transfusions are not free from hazards, they should be used only if necessary
-Nurses must be careful to avoid developing a complacent attitude about this common but potentially dangerous therapy

60
Q

Blood Transfusions- Nursing Management

A

-Informed consent
-Positive ID of blood product & pt
-Take VS before transfusion
-Stay with pt for the first 15 mins of infusion
(Rxns most likely to occur)
-Re take VS
-Monitor pt q30mins

61
Q

Blood Transfusions- Reactions

A

ACUTE (immediate - 6h)
-Fever
-Allergic reaction (1 in 100)
-Bacterial contamination
-Hemolysis
-Transfusion-associated circulatory overload (TACO) (1 in 100)
-Transfusion-related acute lung injury (TRALI)
-Pulmonary edema

DELAYED (1 - 14 days)
-Hemolysis
-Purpura
-Graft vs host disease
-Infections