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54 Cards in this Set

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Definition of Shock
Clinical definition of shock: a complex syndrome of decreased blood flow to body tissues resulting in cellular dysfunction and eventual organ failure.
A. Inadequate blood flow (HYPOTENSION) to peripheral tissues (HYPOXIA)
B. Homeostasis dependant on the balance of 3 variants:
Circulating Fluid Volume
Cardiac Function
Vascular Bed Size
Stages of Shock
1. Early, Reversible and Compensatory Shock (p.I50)
2. Intermediate or Progressive Shock (p. I 50)
3. Refractory or Irreversible Shock (p.151)
TYPES: Underlying cause
List types
1. Hypovolemic Shock
2. Cardiogenic Shock
3. Septic Shock
4. Neurogenic Shock
5. Anaphylactic Shock
1. Hypovolemic Shock
Hypovolemic Shock - caused by insufficient intravascular blood volume
Caused by loss of blood, plasma or extracellular fluid- hemorrhage OR, injuries, GI bleed, coagulation disorders, bums, severe dehydration, persistent vomiting or diarrhea, diuretics, diabetes insipidus, third spacing or fluid shifts as with ascites, pleural effusion or intestinal obstruction. (L&B, 2004, p.153)
2. Cardiogenic Shock
2. Cardiogenic Shock - caused by failure of the heart's pumping action
(Loss of adequate cardiac output due to pump failure)
Myocardial infarction, cardiac tamponade, restrictive pericarditis (myocardial or pericardial infection), cardiac arrest, valve changes, Left heart failure, pulmonary embolism, dysrhythmias
Most frequent with Left Anterior MI (L&B, 2004, p. I 55)
3. Septic Shock
3. Septic Shock - cased by infection-produced toxins Infection-bacteremia-septicemia (presence of pathogens and toxins in the blood) -endotoxins leak into plasma-disrupt coagulation and immune response-septic shock- multi organ failure-
Most common gm- organism (Pseudomonas, E. Coli, Klebsiella)-- can be gm+ (Staphylococcus & Streptococcus)
Early (warm) phase and Late (cold phase)
Disseminated intravascular coagulation (DIC)-simultaneous bleeding and clotting throughout the vasculature (L&B, 2004, p.952-954)
Definition: Multiple organ dysfunction as a result of pathogenic organisms in the blood resulting in vasodilation and changes in permeability of capillaries; often a precursor to ARDS and DIC
4. Neurogenic Shock
4. Neurogenic Shock - caused by alterations in vascular sympathetic tone (overstimulation of the parasympathetic or understimulation of the sympathetic nervous systems)
Head injury, trauma to spinal cord, insulin reactions, central nervous system depressants, spinal or general anesthesia, severe emotional stress or pain, prolonged exposure to heat Prevent--immobility after spinal & raise HOB 15-20 degrees post spinal anesthesia. (L&B,2004, p.156)
5. Anaphylactic Shock
5. Anaphylactic Shock - caused by immunologic reaction (precipitating vasodilitation). (Acute allergic reaction)
Sensitized person has contact with allergen (not on first exposure where body produces IgE antibodies) (L&B, 2004, p.I56)
Occurs within 20 minutes of contact.
EDUCATE on allergies
Allergens: Antibiotics(penicillin, sulfa) vaccines local anesthetics, iodine dyes, blood and blood products, narcotics, shellfish, legumes, nuts, seeds, egg white(albumen) milk chocolate, stings and bites of insects, snake venom
Treatment Priorities for Shock
ER CARE:--stabilized within first hour
1. Airway--Breathing
2. Circulation--Hemorrhage- Pressure at pressure points
3. Assess for -decreased-BP, rapid thready pulse, rapid shallow respirations, cold pale moist skin, thirst, restlessness, change in level of consciousness
4. Position with trunk and head flat(or up 10 degrees) and legs slightly elevated (200) if no head injury NOT in cardiogenic (L&B, 2004, p.161)
5. Maintain warmth
6. Communicate to decrease anxiety
H&H ABG Lytes
BUN, creatinine
Blood Cultures-aerobic vs. anaerobic, antibiotic removed, at time intervals not sooner than
30-45 min WBC and Differential
Cardiac enzymes & CPK total (BB, MB, MM) C-reactive protein-
Fibrin split products
Shock pts
1. 02-All in shock get O2 to keep Pa02 above 80
2. Fluid Replacement
A. Crystalloids-Dextrose and/or electrolytes in water-isotonic(NS & LR) -hypotonic (.45% NS & D5W)--NS & .45%NS can be run fastest---Potential for edema-25% remains intravascular & 75% moves to interstitial
B. Colloids-cannot diffuse through capillary walls- raised osmotic pressure - ex. Albumin, hetastarch, dextran, plasma protein fraction -expensive & lowered platelet adhesiveness and blood coagulation (L&B, 2004, p.159)
C. Blood- goal hematocrit 30-35% & hemoglobin 12.5-14.5 ex. Whole blood PRBC's, platelets, FFP, cryoprecipitate -expensive transfusion reactions-type & crossmatch
Drugs for shock
3. Drugs for shock- (L&B, 2004, p.158)
A. Adrenergics (Sympathomimetics)--Vasoconstrictors & inotropes ex. Norepinephrine (Ievophed), Metaraminol (Aramine)-Dopamine (Intropin), Dobutamine (Dobutrex)-only after fluid replacement
B. Epinephrine - only one given sub-q -Anaphylactic (NOT LISTED in L&B p. 158 column I under adrenergics but is only one given sub-q)-
C. Vasodilators-Nitroglycerin & Nitroprusside (Nipride)
D. Diuretics after fluid replacement
E. Sodium bicarb to treat acidosis-WATCH COMPATABILITY not even LR
F. Calcium to replace calcium lost with blood transfusions
G. Antiarrhythmic agents to stabilize heart rhythm
H. Antibiotics- Sepsis
I. Cardiotonic glycoside- ex. Digitalis
J. Benedryl- Anaphylactic
K. Steroids - Anaphylactic
L. Intra aortic balloon pump
Shock pts
A. Decreased Cardiac Output
Assess BP, HR, O2 Sat, Peripheral pulses, hemodynamic monitoring I & 0 hourly
Bowel sounds, abd distension, abdominal pain
Sudden sharp chest pain, dyspnea, cyanosis, anxiety, restlessness
Position- NO LONGER TRENDELENBERG (L&B, 2004, p. I 6 I) Now modified trendelenberg-(NOT USED in which type of shock-Neurogenic?)
B. Altered Tissue Perfusion
Skin pale, cool moist, with eventual cyanosis
Assess BP, HR, R, O2 Sat, Peripheral pulses (brachial, radial, dorsalis pedis and posterior tibial) doppler if necessary, JVD, CVP measurements
I&0 hourly
Mental status
C. Anxiety
Prescribed pain meds Explain and educate Support family
D. Risk for Infection
E. Risk for Fluid Volume Excess
F. Impaired Gas Exchange
G. Activity Intolerance
H. Altered Thought Processes
I. Altered Urinary Elimination
J. Fear
K. Risk for injury
Types of blood products
Whole Blood (Black, p. 589) Red Blood Cells (Black, p. 591) Platelet Concentrations
Fresh Frozen Plasma Cryoprecipitate
Granulocyte Concentrations
Plasma Derivatives - Albumin & Plasma protein fraction Coagulation Factor Concentrates
Infusion of Whole Blood
Rarely given component- "Fresh frozen plasma (FFP), packed RBCs, and crystalloid and colloids are preferred for treatment of massive hemorrhage over whole blood." (Phillips, p.589)
Approximately 500 ml-200ml RBCs and 300ml plasma and platelets Catheter 20 gauge or larger preferred
Rate- 2-4 hours
Requires type and crossmatching-ABO and Rh Requires 170-260 micron filter
Whole blood is indicated for the treatment of acute, massive blood loss (depletion of more than 30% of the total volume) when there is the need to replace plasma volume and supply red blood cells to increase the oxygen carrying capacity.
Whole blood can be separated into its specific constituents (red and white blood cells, platelets, plasma proteins, fresh frozen plasma, and globulins.
Red Blood Cells
Approximately 300ml- RBCs, 20-30% original plasma, leukocytes, and some
platelets(Phillips, p.591) Adv-decreased risk of circulatory overload
Less citrate, potassium, ammonia, and other metabolic byproducts are transfused. 1 unit raises hemoglobin 1g/dL & hematocrit 3 percent
Improves 02 carrying capacity in blood
Criteria- H&H, symptoms, amount & time frame of blood loss
Transfuse RBC Criteria
Hypovolemia- acute loss - tachycardia, decreased BP - not corrected with volume 30% blood loss in otherwise healthy patient
Hbg- 7 or 8-10 g/dL or less
Symptomatic anemia in a euvolemic patient ( angina, syncope, IrA, CHF, dyspnea, HR increased above 100
RBC Transfusion
Approximately 250-300ml
Catheter 18-20 gauge or larger preferred Usual rate: 1 ½ -2 hours; maximum 4 hours.
Requires 170-260 micron filter
Requires type and crossmatching-ABO and Rh
May be leukoreduced - decreased febrile, nonhemolytic reactions
May be deglycerolized- prolongs storage to 10 years
Transfusion Risks
Hemolytic transfusion reactions
Infectious diseases ie. HIV, Hepatitis B or C, graft-versus-host disease, Cytomegalovirus, Epstein-Barr virus, and West Nile Virus
Antibodies to complicate transplants
Transfusion Administration Procedure
Explain need, benefits, risks, and alternatives (After order written) Signed permit (Refusal at bottom of the page)
Pre-transfusion Testing- Infectious diseases, ABa, Rh (a-negative is universal donor)
antibody screens in crossmatching, labeling of specimen (Fenwall Band with name and number)
Obtain Venous Access--Peripheral IV 20-gauze or larger
Normal Saline ONLY dilutant to prevent hemolysis -Why not Ringers Lactate?
Central Venous catheter acceptable site. Rapid administration of cold blood causes cardiac dysrhythmias
Transfusion Administration
Transfusion Administration - Continued IV site flushed
Vital signs taken
Fever may delay transfusion
Premedicate if history of adverse reactions Tylenol or benadryl 30 minutes prior Set up NS and administration line with blood filter if needed
Request blood release- 30 minutes is maximal allowable time out of monitored storage
Confirm Blood Acceptability-
Confirm Blood Acceptability- 80% of reactions are labeling errors.
Correct component Expiration date
Blood types, and ID patient Verified by 2 qualified people
Blood Infusion
Blood Infusion
Standard filters- 4 units of blood- change every 4-6 hours
Blood warmers- dry or wet - used only when giving blood rapidly or multiple units Start PRBCs @ 5 mL/min (Phillips, p.617)
@ 2mL/min Phillips, (p.618)
@60- 75 mL/hr per Via Christi policy
< 180 mL/hr per Wesley policy
First 10-15 minutes and first 50 ml are most critical times for monitoring. Stay with
the patient.
After 15 minutes increase rate- client to report new symptoms
Vital signs- start, 15 minutes, and every hour -not to exceed 4 hours/unit
No Medications or solutions other than 0.9% NS should be added to blood
Reaction Symptoms- Acute hemolytic
Chills, fever, low back pain, flushing, tachycardia, tachypnea hypotension, shock, hemoglobinuria, bleeding, acute renal failure, cardiac arrest, death
Treatment for Acute Hemolytic
Treatment for Acute Hemolytic
Stop transfusion and keep IV line open with NS
Treat shock- IV colloids
Draw blood for repeat testing,
Send UA and blood bag & tubing to lab
Diuretics, Foley for hourly I & 0, Dialysis
Complete form & collect urine and blood samples (free Hb indicates hemolysis)
Reaction Symptoms- Febrile, nonhemolytic (most common)
Febrile, nonhemolytic (most common)
Sudden chills and fever (rise in temp of more than 2 degrees F
Flushing, headache, anxiety, muscle pain
Treatment for febrile nonhemolytic
Do Not Resume Transfusion
Allergic Symptoms
Allergic Treatment
No fever

Allergic Treatment
Administer antihistamines as ordered
If manifestations mild and transient, transfusion may be resumed.
Anaphylactic Symptoms
Anaphylactic Treatment
Wheezing progressing to cyanosis
Cardiac arrest

Anaphylactic Treatment
Stop Transfusion, Aspirate Line and discard, Flush with Saline Initiate CPR if indicated
Have epinephrine ready for injection (0.4 mL of a I: 1000 solution SC)
Congenital WBC dysfunction, severe infections unresponsive to antibiotics
High incidence of nonhemolytic febrile reactions-tx benadryl, steroids, Tylenol, & slowing
the transfusion rate
Don't stop unless severe respiratory distress occurs Prepared by leukapheresis
Catheter 18-20 gauge or larger preferred Usual rate: 1 1/2 -2 hours; maximum 4 hours. Requires 170-260 micron filter
Requires type and crossmatching-ABO and Rh
Platelets (Phillips, p. 598)
Usual dose is 6-10 units from random blood donors or 1 unit single donor pheresis Prevent bleeding from platelet deficiencies in thrombocytopenia (depends on condition) Approximately 30-50ml/Unit; usual dose 6-8 units
Catheter 18-20 gauge or larger preferred
Usual rate: 1 Unit in 5-10 minutes as tolerated; no longer than 4 hours after platelets pooled Filter-170 micron rubber free tubing to prevent platelet sticking
Crossmatching and Rh matching is preferred but not required.
1. The most effective method of monitoring fluid volume in the client with refractory hypovolemic shock is:

1. BP trends
2. HR comparisons
3. CVP trends
4. Arterial line comparisons
CVP trends
Rationale: CVP gives the best information about fluid volume changes in clients. If the CVP is low (less than 5 cm H20) the client has hypovolemia. If the CVP is high (over 12 cm H2O) the client has hypervolemia or right-sided heart failure.
2. The client with cardiogenic shock will show evidence of improved tissue perfusion by a(n):

1. change in level of consciousness
2. increased urine output
3. decreased pCO2
4. O2 saturation increase from 84% to 88%
increased urine output
Rationale: Increased urine output indicates an increase in renal function which indirectly reflects more fluid and oxygen to the kidney (improved tissue perfusion). If option 1 indicated an improved level of consciousness it would be correct, but it only indicates a change in LOC. LOC reflects changes in tissue perfusion in minutes while urine output takes an hour or longer. Systemic O2 saturation and pCO2 level do not reflect tissue perfusion.
3. The most appropriate position for a client in hypovolemic shock with compromised vital signs is:

1. positive tilt
2. reverse Trendelenburg
3. modified Trendelenburg
4. Trendelenburg
modified Trendelenburg
Rationale: A modified Trendelenburg position is the upper body in a supine position and the legs elevated above the level of heart. This increases blood flow to vital organs but does not induce cerebral congestion or breathing difficulties. Positive tilt is the same as reverse Trendelenburg (the head up and the feet down) and would not be appropriate for this client. Trendelenburg (head down and feet elevated) is preferred with pregnant women in the event of a prolapsed cord and for clients before and during central venous catheter insertion into the subclavian or jugular vein.
Signs and symptoms you would expect to see in a client in hypovolemic shock include:

1. Increased venous return
2. Increased cardiac output
3. Decreased tissue perfusion
4. Decreased pulse rate.
Decreased tissue perfusion
Rationale: 3. The ultimate problem associated with all forms of shock is a decrease in tissue perfusion. The cardiac output and venous return are decreased and the heart rate is increased.
5. Cardiogenic shock is caused by:

1. Decreased venous return
2. Decreased pumping ability of the heart
3. Increased blood pressure.
4. Massive vasodilation.
Decreased pumping ability of the heart
Rationale: 2. Cardiogenic shock is also known as pump failure. The heart fails to adequately pump the blood. Decreased venous return is a symptom of cardiogenic shock but not a cause.
6. The major pathophysiological mechanism causing distributive shock is:

1. Failure of the heart as a pump.
2. Massive blood loss.
3. Increased cardiac output.
4. Massive vasodilation.
Massive vasodilation.
Rationale: 4. The major pathophysiological mechanism in distributive shock is massive vasodilation.
7. Which clinical manifestations are a direct outcome of the altered tissue perfusion associated with shock?

1. Elevated body temperature
2. Tachypnea
3. Urine output greater than 30 ml/hr
4. Peripheral vasodilation
Rationale: 2. Decreased tissue perfusion results in hypoxia and the body attempts to compensate for the low oxygen by hyperventilating. The body temperature is usually low during shock and high fever would further increase hypoxia, as would vasodilation. Urine output would be low in shock (< 30 ml/hr).
8. When a client is suffering from cardiogenic shock, the CVP reading will be:

1. High, usually above 15 cm H2O
2. Low, usually below 5 cm H2O
3. Normal, between 5 - 10 cm H2O
4. Extremely low, less than 1 cm H2O
High, usually above 15 cm H2O
Rationale: 1. With cardiogenic shock, the venous pressure is often elevated because of the back-up of pressure into the venous system when the heart can't pump the blood through the heart effectively.
9. Inotropic drugs such as dobutamine are often used to treat shock. One of the negative effects of these drugs is:

1. Increased myocardial oxygen need
2. Increased cardiac output and tissue perfusion
3. Increased renal blood flow and output
4. Decreased coronary perfusion
Rationale: 1. Inotropic drugs increase the force of heart contraction thus increasing the amount of oxygen the heart needs, which can result in angina. Choice 2 & 3 are positive effects of inotropic drugs. These drugs do not cause decreased coronary perfusion.
10. Which clinical manifestation reflects an improvement in the client's shock?

1. Systolic pressure between 80 and 90
2. Respiratory rate greater than 24
3. Urine output greater than 30 ml/hr
4. CVP greater than 10 cm H2O
Urine output greater than 30 ml/hr
Rationale: 3. When the urine output is above 30 ml/hr, it means that the kidneys are being adequately perfused, which means that the shock has improved. Choices 1 & 2 are signs of continuing shock and choice 4 could indicate fluid overload or cardiogenic shock.
Plasma and Fresh Frozen Plasma FFP
Approximately 200-300 mL
No platelets or RBCs
To replace plasma proteins lost from injury
To provide replacement coagulation factors-PT increase above 19, INR above 5, or PTT above 53
Catheter size 20-22 gauge
Usual rate 1-2 hours
Filter: 170 micron
Identify recipient's ABO group
Concentrated source of fibrinogen and clotting factors
Fribrinogen below 100 mg/dl (DIC)
transfused as rapidly as patient tolerates
Approximately 10-15 ml diluent added to precipate (3-5 ml/unit); usual dose 6-10 units
Catheter 18-20 gauge
Usual rate: 1-2 mL/min
Filter 170 micron filter
80 % of plasma's osmotic activity
5-25% solution
25% solution used to draw fluids out of tissues and body cavities into intravascular spaces
Contraindicated in dehydration and those at risk for circulatory overload
Special tubing-Not blood tubing or filter
Amount 5% =250mL and 25% = 50-100 mL
Meds to stimulate Blood regeneration
Iron-Ferrous Sulfate
Folic Acid
Symptoms of a patient in Shock
1. Pale
2. Clammy
3. Cool

1. Rapid breathing
2. Shallow respirations

1. Low temperature
2. Thirst
3. Acidosis
4. Low urine output

1. Restlessness
2. Anxiety
3. Lethargy
4. Confusion

1. Tachycardia
2. Thready pulse
3. Low cardiac output
4. Low Blood pressure
Describe Colloids-why are they given
Colloids are proteins or other large molecules that stay suspended in the blood for a long period, because they are too large to cross membranes. while circulating, they draw water molecules from the cells and tissues into the blood vessels through their ability to increase oncotic pressure. Colloids include normal human serum albumin, plasma protein fraction, and serum globulins. The nonblood product colloids are dextran (40, 70, and high molecular weight) and hetastarch (Hespan)
Describe Crystalloids and what are they for
Crystalloids are IV solutions that contain electrolytes in concentrations resembling those of plasma. Unlike colloids, crystalloid solutions can readily leave the blood and enter cells. They are used to replace fluids that have been lost and to promote urine output. Common crystalloids include normal saline, lactated ringer's, Plasmalyte, hypertonic saline, and 5% dextrose in water
Role of the nurse in crystalloid and colloid therapy
Careful monitoring of a patient's condition and providing education as it relates to the prescribed drug regimen.
Monitoring for blood pressure changes is essential; presure may increase with a healthy heart, or decrease if the heart fails with fluid overload.
Lung sounds must also be monitored; crackles will be heard with pulmonary congestion. Pulse oximetry can be utilized to monitor for changes in oxygenation.
Monitor I&O and body weight will assist in assessing fluid retention or loss
Disseminated Intravascular Coagulation
What causes this
Disseminated intravascular coagulation is a disruption of hemostasis characterized by widespread intravascular clotting and bleeding. It may be acute to life threatening or relatively mild

Sepsis is the most common cause of DIC
What is the sequence of DIC
1. Endothelial Damage, tissue factors, or toxins stimulate the clotting cascade
2. Excess thrombin within the circulation overwhelms naturally occuring anticoagulants
3. Widespread clotting occurs within the microvasculature
4. thrombi and emboli impair tissue perfusion, leading to ischemia, infarction, and necrosis
5. Clotting factors (including platelets) are consumed faster than they can be replaced
6. Clotting activates fibrinolytic processes which begin to break down clots.
7. Fibrin degradation products (FDPs, potent anticoagulants) are released, contributing to bleeding
8. Clotting factors are depleted, the ability to form clots is lost and hemorrhage occurs.
Manifestations of DIC
Disseminated intravascular coagulation
-Frank hemorrhage from incisions
-Oozing of blood from punctures, intravenous catheter sites
-Purpura, petechiae, bruising
-Cyanosis of extremities
-Gastrointestinal bleeding or hemorrhage
-Dyspnea, Tachypnea, bloody sputum
-Tachycardia, hypotension
-Hematuria, oliguria, acute renal failure
-Manifestations of ICP: decreased LOC, papillary, motor and sensory changes,
-Mental status changes
Treatments for DIC
When bleeding is the major manifestation of DIC, fresh frozen plasma and platelet concentrates are given to restore clotting factors and platelets. Heparin, although controversial, may be administered. Heparin interferes with the clotting cascade and prevent further clotting factor consumption due to uncontrolable thrombosis.
nursing diagnoses for DIC
Ineffective Tissue Perfusion
Thrombi and emboli forming throughout the microcirculation affect the perfusion of other organs and tissues.

Impaired gas Exchange
Microclots in the pulmonary vasculature are likely to interfere with gas exchange in the client with DIC.