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Shock
Decrease in blood flow and O2 to organs (no tissue perfusion)
Builds up waste and acid
Distributive shock
Excessive vasodilation
Impaired blood flow distribution
Kinds of Distributive Shock
Neurogenic
Septic
Anaphylactic
Neurogenic Shock
Can occur within 30 minutes of a spinal cord injury or in response to spinal anesthesia
Bradycardia
Warm, dry
Injury at T5 or higher
Unable to regulate
Meds for Neurogenic Shock
Phenylephrine
Atropine
Neurogenic Shock Impact on Hemodynamics
Decreased CVP & SVR
Anaphylactic Shock
System wide histamine releases which leads to leaky capillaries causing massive edema
Anaphylactic Tx
Low dose epi
Anaphylactic Shock Impact on Hemodynamics
Decreased CVP & PAWP
Kinds of Hypovolemic Shock
Absolute: Fluid loss to outside (ex: bleeding out)
Relative: Fluid shift, loss to another area (ex: edema, ascites)
Direct: Blood
Indirect: Any other bodily fluid
Causes of Hypovolemic Shock
Hemorrhage
Extensive burns
Diabetes Insipidus
Hypovolemic Shock Impact on Hemodynamics
Decreased PAWP & CVP
Cardiogenic Shock
Problem with the heart, not pumping effectively
Causes of Cardiogenic Shock
Cardiac dysrhythmias
MI (#1 Cause)
Valvular stenosis/regurgitation
Cardiogenic Shock s/s
EKG change
Crackles
Drugs for Cardiogenic Shock
inotropes
Dopamine (gold standard)
Dobutamine
If SVR is high, give vasodilator (sodium nitro)
Cardiogenic Shock Impact on Hemodynamics
May see increase in CVP, PVR, PAWP, & SVR because blood is backing up
Obstructive Shock
Physical blockage
Causes of Obstructive Shock
PE
Tension Pneumothorax
Cardiac Tamponade
CAD
Obstructive Impact on Hemodynamics if cause is Pneumo/Cardiac Tamponade
Increased CVP, PAWP, PVR, and SVR
Obstructive Impact on Hemodynamics if cause is PE
Increased PVR & CVP
Decreased PAWP
Shock Process
1. Decreased tissue and cellular perfusion
2. Hypoxia
3. If uncorrected: tissue and cellular death
4. Organ dysfunction
5. Organ failure
6. Organ death
7. Death
Shock Stages
1. Early signs
2. Compensatory Signs
3. Progressive Signs
4. Refractory Signs
Early signs of shock
MAP 10 below baseline
Effective compensation
O2 going to vital organs
Slight tachycardia
Compensatory Signs of Shock
MAP 10-15 below baseline
RAAS (Renin) compensation
ADH Compensation
Vasoconstriction
Decreased pulse pressure
Tachycardia
Decreased pH
Restless
Apprehensiveness
Increased K+
Progressive Signs of Shock
MAP > 20 below baseline
Tissue organ/hypoxia
Oliguria
Weak rapid pulse
Decreased pH
Sensorineural changes
Refractory Signs of Shock
Excessive cell/organ damage
Multisystem organ failure
Decreased pH
*at this point, death is expected
Shock Progressive NC
Progresses quickly, must catch while still able to compensate
Tx Shock in this order:
1. ABCs
2. Fluids
3. pressors
4. Tx cause
Sepsis Steps
1. SIRS
2. Sepsis
3. Severe Sepsis
4. Septic Shock
SIRS
Systemic Inflammatory Response Syndrome
Step 1: SIRS Criteria (must have 2 or more of the following)
T: >100.4 or <96.8
RR: >20
HR: >90
WBC: >12000 or <4000 or >10% BANDS (leukocytosis)
PCO2: <32
Step 2: Sepsis Criteria
SIRS + confirmed or suspected infection
Step 3: Severe Sepsis
Sepsis + Signs of end organ damage, or Hypotension (SBP < 90), or lactate >4
Step 4: Septic Shock
Severe Sepsis + persistent signs of end organ damage, or Hypotension (SBP < 90), or Lactate >4
Septic Shock
Life threatening syndrome in response to an infection
Sepsis is body's overwhelming immune response to severe infection that can result in damaged tissues and organs
Septic Shock s/s
Hypotension despite adequate fluid resuscitation
Increased capillary permeability
If Sepsis is suspected
1. Call MET code
2. Draw STAT lactate
- If >2, start protocol
- Get 2 cultures from 2 places
3. Notify HCP & get abx order
4. CBC & another lactate
- Low prealbumin, high procalcitonin (indicates inflammation & bacterial infection), high C reactive protein (indicates inflammation)
Septic Shock Risk Factors
S: Suppressed Immune System
E: Extreme age
P: Post-Op
T: Transplant recipients
I: Indwelling devices
C: Chronic Disease
Septic Shock NI
S: Start abx (w/in 1st hr)
E: Enteral nutrition
P: Pressors (keep MAP>65)
T: Trend VS, labs, Is&Os
I: Inotropes (dobutamine)
C: Crystalloids or Colloid solutions
S: Steroids
H: Hemodynamic monitoring
O: O2 (Keep >95%)
C: Cultures (b4 abx)
K: Keep glucose <180
DIC
Clotting & hemorrhage simultaneously
Always due to underlying cause
Organ ischemia due to bleeding
Steps of how Septic Shock leads to DIC
1. Recruiting WBCs which causes vasodilation
2. Decreased SVR & BP
3. Increased vascular permeability
4. Deceased O2 to tissues
5. Damage to blood vessels
6. Clotting to fix damage
7. Decreased clotting factors
8. Hemorrhaging & clotting simultaneously = DIC
Intrinsic Causes of DIC
Damage to Blood
Transfusion reaction
Sepsis
Sickle Cell disease
ARDS
Malignant hyperthermia
Extrinsic Causes of DIC
Damage to physical tissue
Endotoxins
Crush injuries
Malignancies
Neurologic damage
Extensive surgery
Obstetrical conditions
What lab values would you expect to see in a patient with DIC?
a. increased fibrinogen, increases plts
b. decreased fibrinogen, no change in plts
c. decreased fibrinogen, decrease plts
d. no change in fibrinogen, decrease plts
c. decreased fibrinogen, decrease plts
DIC expected lab values
Decreased plts & fibrinogen
Prolonged PT, PTT
Increased D-Dimer
Decreased Hgb & Hct
DIC Clinical manifestation of decreased plts
Petechiae
Ecchymosis
DIC Clinical manifestation of Hemorrhage
Tachycardia/pnea
Hypotension
Blood in all mucosal surfaces (RR, vaginal bleeding, hematuria, hematemesis, melena)
DIC Tx
1. Eliminate underlying disorder
2. Correct hypovolemia, hypotension, hypoxia, and acidosis
3. Stop microclotting to maintain perfusion & protect vital organs with heparin
4. Stop the bleeding:
- direct pressure
- replace with blood products
Blood products
1. FFP
2. Cryoprecipitate
3. Plts
4. PRBCs
Plt tranfusion NC
Only give if px has 20,000 or less, or is symptomatic
#1 Drug for septic shock
Norepi
Neurogenic shock s/s
Warm, pink & dry skin
Septic Shock Body Temp NC
Temp initially increases, but after prolonged time, it deceases - this is ominous sign
Vitamin K
Need for prothrombin formation in the liver
Helps form clotting factors in liver
How quickly does transfusion need to begin after receiving PRBCs?
within 30 mins
How splenomegaly affects blood cell counts
normal filtering capacity increases, thus decreasing amount of filtering blood
Autonomic dysreflexia S/S
HTN
Pounding HA
Profuse sweating
Nasal congestion
Bradycardia
Flushed & clammy skin
Goosebumps
The nurses recognizes that which patient would be most likely to develop hypovolemic shock? A patient with:
a. decreased CO secondary to EKG changes
b. severe constipation causing watery diarrhea
c. ascites
d. Syndrome of Inappropriate ADH
c. ascites
Third spacing shift fluids
3rd Spacing
Fluid shifts, drop in circulating blood volume
Commonly caused by burns and ascites
Often leads to hypovolemic shock
Position tx for hypovolemic shock
Lay down, feet elevated above head
Trendelenburg positioning
Hypovolemic shock s/s
restlessness
orthostatic hypoTN
decreased skin perfusion
Life-threatening complications of hypovolemic shock
Renal insufficiency
Cerebral ischemia
The nurse is concerned that a patient is at risk for developing obstructive shock because of which assessment findings? SATA
a. Age 80
b. Hx of a fib
c. bacteremia
d. T3 spinal cord injury
e. latex allergy
a. Age 80 (increased risk of PE development)
b. Hx of a fib (increased risk of PE development)
Anaphylactic Shock Steps
1. Release of histamine
2. vasodilation
3. plasma leakage
4. profound HypoTN, hypovolemia, reduced preload, and reduced CO
A px with cardiomyopathy is demonstrating signs of cardiogenic shock. The nurse realizes that this type of shock is d/t:
a. reduced CO
b. increased SV
c. reduced blood flow
d. blood flow blacked in the pulmonary circulation
a. reduced CO
Rationale: in cardiogenic shock, stroke volume and CO are reduced leading to poor tissue perfusion
A px being treated for cardiogenic shock is being hemodynamically monitored. Which findings are consistent with the patient's dx? SATA
a. abnormal PAWP
b. abnormal SVR
c. elevated MAP
d. elevated SV
a. abnormal PAWP
b. abnormal SVR