Week 12: Shock, SIRS & MODS Flashcards
SHOCK, SIRS, MODS
-Shock decreased tissue perfusion
SIRS – Systemic Inflammatory Response Syndrome
MODS- Multiple organ dysfunction syndrome
Shock
-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
Shock: Classifications (Low Flow)
Cardiogenic
-Related to the heart
Hypovolemic
-Massive tissue injury
-Hemorrhage
Shock : Classifications (Distributive)
Neurogenic
-Related to spinal cord
Anaphylactic
-Severe allergic reaction
Septic
-infection
Shock Low Flow (Cardiogenic Shock)
Systolic or diastolic dysfunction of the pumping action of the heart resulting in compromised cardiac output
Shock Low Flow (Hypovolemic Shock)
-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)
SHOCK LOW FLOW MANIFESTATIONS
-Tachycardia
-Hypotension
-Pulmonary congestion
-Decreased renal perfusion
SHOCK LOW FLOW PHYSICAL EXAM
-Tachypnea
-Pale, cool, clammy skin
-Decreased capillary refill time
-Anxiety, confusion, agitation
-Decreased urinary output
SHOCK DISTRIBUTIVE (NEUROGENIC SHOCK)
-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
SHOCK NEUROGENIC MANIFESTATION
-Hypotension
-Bradycardia
-Temperature dysregulation
SHOCK NEUROGENIC PHYSICAL EXAM
-Heat loss
-Potential for hypothermia
-Skin is warm and dry
SHOCK DISTRIBUTIVE (ANAPHYLACTIC SHOCK)
-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
SHOCK ANAPHYLACTIC MANIFESTATIONS
-Angioedema
-Swelling of lips and tongue
-Wheezing and stridor
-Flushing
-Pruritus and urticaria
-Sense of impending doom
SHOCK DISTRIBUTIVE (SEPSIS)
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
SHOCK SEPTIC
-The clinical presentation of sepsis is complex, and no single specific symptom
-↑CO: stresses myocardium
-Tachycardia
-Tachypnea
SHOCK SEPTIC MANIFESTATION
-Fever
-Hyperglycemia
-Edema
-Hypotension
-Oliguria
-Decreased capillary refill
Respiratory failure is common (85%)
A.) Patient hyperventilates to compensate
B.) Respiratory alkalosis
C.) Respiratory acidosis
Stages of Shock
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
Stages: Compensatory
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
Stages: Compensatory
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
Stages: Progressive
-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
STAGES PROGRESSIVE (PULMONARY SYSTEM)
-Blood flow is already reduced
-Arterioles constrict
-Edema
-Bronchoconstriction
-Impaired gas exchange
STAGES PROGRESSIVE (CARDIOVASCULAR SYSTEM)
-CO falls
-Hypotension
-↓ perfusion to coronary, cerebral & peripheral arteries
-Weakening of peripheral pulses
-Ischemia of distal extremities
-MI, dysrhythmias
-Acute tubular necrosis: AKI
STAGES PROGRESSIVE (GI SYSTEM)
-↓ 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.
Stages- Refractory
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
Shock Diagnostics
-Lactate levels are elevated >4 mmol/L
-12 lead ECG
-Continuous cardiac monitoring
-Continuous pulse oximetry (EAR)
-Arterial pressure
Shock Goals of Care
-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
Shock Collaborative Care
-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
Collaborative Care- Cardiogenic Shock
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
Collaborative Care- Hypovolemic Shock
-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
Collaborative Care: Septic Shock
-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
Collaborative Care: Neurogenic Shock
-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
Collaborative Care: Anaphylactic Shock
-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
Nursing Assessment
-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
Nurse Implementation
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)
Nurse Implementation (Neuro Status)
-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
Nursing Implementation (Cardiovascular Status)
-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
Nurse Implementation (Respiratory Status)
-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
Nursing Implementation
RENAL STATUS: urine output q1h
BODY TEMP: q1h
SKIN:
pallor, flushing, cyanosis diaphoresis, capillary refill
GI: bowel sounds q4h (decreased motility)
SIRS & MODS
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
Organ & Metabolic Dysfunction
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
Organ and Metabolic Dysfunction (Respiratory)
-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
Organ & Metabolic Dysfunction (Cardiovascular)
-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
Organ & Metabolic Dysfunction (Neuro)
-Mental status changes can be an early sign of MODS
Pt can become:
-Confused & agitated
-Combative
-Disoriented
-Lethargic
-Comatose
Organ & Metabolic Dysfunction (Renal)
↓ perfusion to kidneys
AKI
Organ & Metabolic Dysfunction (GI Tract)
↓ motility: abdominal distension & paralytic ileus
Blood is shunted away from GI mucosa: ischemic injury (Ulceration & GI bleeding)
Metabolic Changes
-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
SIRS & MODS
-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
Nursing & Collaborative Care
(Prevention & Treatment of Infection)
-Aggressive IPAC strategies to ↓ risk for HAIs
-Host dysfunction may lead to infection
Nursing & Collaborative Care
(Maintenance of Tissue Oxygenation)
-Hypoxemia frequently occurs in patients with SIRS & MODS
-Interventions aim to ↓ O2 demand and ↑ O2 delivery
Nursing & Collaborative Care
(Nutritional & Metabolic Support)
-Hypermetabolism: profound weight loss, cachexia & more organ failure
-Enteral or parenteral nutrition
-Tight glycemic control is important
(blood glucose <10 mmol/L)
Nursing & Collaborative Care
(Appropriate Support of Individual Failing Organs)
-ARDS requires aggressive O2 therapy & ventilator
-Treat DIC
-Dialysis for renal failure
Blood Components & Products
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
After A Blood Donation…
each unit is centrifuged to create:
-Plasma
-Buffy coat (contains platelets)
-Red blood cells
Each layer is then separated and processed into blood components
Blood- Types & Antigens
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
Blood- Rhesus (Rh) Factor
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)
Blood- Putting It Altogether
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
Blood- Putting it Together
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
Blood Component Therapy (Blood Transfusions)
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
Blood Component Therapy
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
Blood Transfusions- Nursing Management
-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
Blood Transfusions- Reactions
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
