CC Test 4: Shock, MODS, Trauma, Neuro Flashcards
What is the most common shock state?
Hypovolemic (ie from blood loss)
Shock is defined as :
Inadequate tissue perfusion (hypoperfusion)
Impaired cellular metabolism (which leads to lactic acid buildup)
All body systems can be involved.
4 systems work together to maintain homeostasis:
Blood volume
Myocardial contractility
Blood flow
Vascular resistance
4 classifications of shock:
Hypovolemic (inadequate intravascular blood/fluid volume)
Cardiogenic (inadequate myocardial contractility)
Obstructive (blood flow–clots, damage to BV’s, etc)
Distributive (vascular resistance/inadequate vascular tone)
4 stages of shock:
1) Initiation
2) Early/compensatory (reversible)
3) Progressive (intermediate)
4) Irreversible (refractory)
Stage of shock:
Lack of tissue oxygenation; leads to production of lactic acid, which can lead to met. acidosis
Lack of intravascular volume leads to hypovolemia = decreased BP= hypoxia, etc.
Lack of myocardial contractility (same outcomes as above)
Vascular tone decrease = BP problems
*No obvious clinical indications of hypoperfusion are noted in this stage, although hemodynamic alterations (ie dec. CO) may be noted if invasive hemodynamic monitoring is used.
Stage One: Initiation
Stage of Shock:
Neural reaction by the SNS (increased BP, HR, bronchodilation)
Endocrine involvement (RAAS, ADH, re-absorption of Na/H2O, glycogenolysis/gluconeogenesis (producing BS via the liver)
Stage 2: Compensatory
Stage of Shock: Anaerobic metabolism (lactic acidosis) Progressive tissue hypoperfusion Failure of Na/K pump Cellular edema May have long-term deficits
Stage 3: Progressive
Stage of Shock:
Severe tissue hypoxia with end-organ ischemia
Worsening acidosis
SIRS
MODS
Outcome is usually death/organ failure; can survive, but usually bad
Stage 4: Refractory
Cause of hypovolemic shock :
Fluid and/or blood volume loss (generally 15-30% or more)
Severe vomiting and/or diarrhea
Burns (vascular network destroyed)
Loss from within internal cavities
DI (deficiency in ADH release from pos. pituitary gland –tumor, trauma, surgery, etc): significant loss of fluid/U.O
Trauma, GI bleed ruptured arterial aneurysm, surgery, etc
S/s of Internal bleeding:
Rigid abdomen, N/V, hypoxia s/s, back pain, Abdominal pain & Guarding, etc
Treatment modalities for hypovolemic shock:
- Fluid resuscitation (agressive): unless have bad TBI or heart problem); often use LR or NS; multiple large bore IV’s required
- Blood/blood products: PRBC often
- Other colloid solutions (especially if blood loss is primary problem): Albumin, Synthetic volume expanders (controversial)
- Stop loss of volume
Hypovolemic shock will do what to the Preload, Cardiac Output, & BP?
decrease them all
Class of Hypovolemic/Hemorrhagic Shock: 15% fluid loss Patients usually compensate themselves Increased heart rate or tachycardia May require some fluid resuscitation
Class one; usually in ER or med-surg
Class of Hypovolemic/Hemorrhagic Shock:
15-30% fluid loss
Tachycardia, Decreased pulse pressure, Anxiety, Decreased MAP by 10-15 mmHg
Requires crystalloid fluid resuscitation (NS, LR)
Class 2
Class of Hypovolemic/Hemorrhagic Shock:
30-40% fluid loss
HR greater than 120, Change in LOC, Dec. MAP by 20 with Dec. SBP due to non-compensatory mechanism by the body
Usually requires fluid and blood replacement (usually whole blood)
Class 3
Class of Hypovolemic/Hemorrhagic Shock:
>40% blood loss
HR >140
Tachypnea
Significant change in LOC (usually unconscious)
MAP <60 (=decreased perfusion)
Pale, cold skin
Cap refill >3
Crystalloid and blood replacement required (agressive; have to worry about hypervolemia)
Immediate treatment needed to preserve end-organ perfusion
*Worst class
*often Increased BUN, Increased LFT’s, May lose spleen, GI shut down
Class 4
Physical findings of Hypovolemic Shock:
Decreased LOC Rapid/shallow RR (will become labored as conditions worsen) Cool & clammy skin Weak & thready pulse Dec. MAP, RAP, PAWP = Dec. SV & CO/CI Inc. HR (in response to SNS activation) Dec. UO
Lab findings with Hypovolemic Shock:
- Serum Lactate: gives idea of what class of hypo. shock we are in; want less than 1; close to 4=bad
- Electrolyte studies: evaluate what type of solution and/or the effectiveness of fluid resuscitation
- Hgb & Hct: determine need for blood product replacement (may show hemoconcentration or hemodilution due to IV therapy); 8 tends to be the number they use when determining aggressive treatment )
- Decreased SvO2 <60%
Name some colloids:
5% Albumin
20% Albumin
Name some Crystalloid solutions:
Hydroxyethylstarch LR NS 3% Saline Hypertonic Solution *Stuff with different amounts of NS and/or Dextrose
Some s/s of Pulmonary Congestion:
Crackles, Resp. distress, cough, anxiety, want to sit up to expand lungs
What do you need to monitor for when giving volume replacement?
Pulmonary Congestion
Common causes of Cardiogenic shock:
AMI HF Cardiac dysrhythmias Cardiomyopathy Usually found with >40% of myocardial involvement
Clinical findings of Cardiogenic Shock :
Initial hypotension/hypovolemia brings about defense mechanisms (increases SNS as defense mech)
This worsens the shock state
Reflex tachycardia/HTN=Increased Myocardial O2 demand
Physical findings with Cardiogenic Shock:
SPB <90 ** MAP <70 ** CI <2.0 ** PAWP >18 ** Thready, rapid pulse Narrow pulse pressure Distended neck veins Dysrhythmias (usually tachydysrhythmias) CP Oliguria Change in LOC Inc. RR with dyspnea Inspiratory crackles with possible wheezing ABG showing Dec. PaO2
Lab findings of Cardiogenic Shock:
Cardiac Markers possible myocardial injury
CPK-MB
Troponin
Markers showing increased myocardial pressures
BNP–shows distress the heart is in
Treatment for Cardiogenic shock :
Goals of Tx: Dec. Myocardial workload, Inc. myo. O2 delivery, Maximize CO
O2 or possibly ventilation
*ACEI’s, ARB’s, Digoxin: Dobutamine (Dobutrex), Milrinone (Primacor), Inamrinone (Amrinone)
*May get Balloon Pump (#1 reason for B. Pump is Cardio. Shock)
Antidysrhythmics, cardioversion, or pacing
Determine Acidosis and treat accordingly (look at serum lactate & ABG’s)
Diuretics for fluid overload
Electrolyte replacement if needed (esp. K, Ca, and Mg)
What will Dobutamine do for the CO and PAWP?
Increased CO & Dec. PAWP ; It’s a Beta 1& 2 agonist
What med is often referred to as an inodilator due to its positive inotropic & vasodilatory properties?
Milrinone (Primacor)
What drug has a similar action to Milrinone (Primacor)?
Inamrinone (Amrinone)
Which two drugs are recommended only for short-term therapy (2-3 days) with Cardiogenic shock if diuretics and digoxin have failed to produce wanted responses?
Milrinone (Primacor) & Inamrinone (Amrinone)
Usually in men ages 20-40’s; prognosis of less than 5 years; don’t know cause; kinda mimics R. side HR; Tx with 24/7 IV
Primary Pulmonary HTN (PPH)
Causes of Obstructive (Extracardiac Obstructive) Shock:
- (Decreased CO)
- Impaired Diastolic Filling: (Tension pneumo, Cardiac Tamponade, Constrictive pericarditis, Compression of Great Vessel (ie Vena Cava during pregnancy))
- Increased RV Afterload: (PVR) (Pulm.Emboli–most common, PPH, Interstitial Fibrosis (Lung dz), PEEP (higher PEEP=Dec CO))
- Increased LV Afterload: (SVR) (Aortic stenosis, Aortic Dissection (usually from aneurysm))
Clinical Findings of Obstructive (Extracardiac Obstructive) Shock? Treatment?
Decreased CO = Dec. perfusion/cellular metabolism; Treatment depends on disease causing it
How does Cardiac Tamponade affect the Preload and CO?
Inc. Preload
Dec. CO
Causes of Distributive (Vasogenic) Shock :
Neurogenic (affects the ANS, specifically the SNS)
-Upper spinal cord injury
-Spinal Anesthesia
-Neuromuscular blocking agents
Anaphylactic (Histamine is potent vasodilator): most common cause***
Septic
S/S of Neurogenic Shock (Spinal Shock):
*S/s caused by lack of sympathetic input to the systemic vasculature = Dec. peripheral vascular resistance
- S/s=hypotension, severe bradycardia, loss of ability to sweat below the level of injury
- Dec. Preload/SVR/HR/CO/Temp
*Complete severing of the spinal cord=loss of sympathetic tone=massive Vasodilation
S/s of Anaphylactic Shock:
1st exposure=may not know/IgE specific antibody formation; 2nd=Get s/s; Antigen binds with circulating IgE activating mast cells and basophilss triggering release of Histamine, prostaglandins, leukotrienes, & other mediators
S/S:
Systemic Hypotension through massive vasodilation
Inc. capillary permeability
severe bronchoconstriction
coronary vasoconstriction
Urticaria (hives)
Severe cases will also show: Myocardial depression, systemic inflammation, excessive mucous secretions, and Increased peripheral vasodilation (can lead to death)
Treatment for Neurogenic Shock (Spinal Shock):
- Dependent upon level of injury (airway management may be needed temporarily or permanently)
- Stabilization of Spinal column
- Iced Lavage is currently used in most cases replacing high dose steroids (methylprednisolone) following the initial injury (circulate lavage through spinal column; Gold Standard, but not every hospital has it)
- Due to disruption of SNS outflow, bradycardia & hypotension usually follow so you need to manage these for survival
Treatment of Anaphylactic Shock:
Remove stimulus
Airway management–short-acting B2 agonist is essential (ie Epinephrine = DOC)
Assess cardiac & vascular stabilization following airway meds
Education important
How often should you change out your Epi Pen?
q 6 months
S/s of Sepsis:
must have 2 or more of the following; initially looks like an infection:
temp > 100.4 or <96.8
HR >90
RR >20 or PaCO2 <32
WBC >12,000 or <4,000
Can also have: Thrombocytopenia (platelets < 100,000) Hyperglycemia (BS >120) Plasma C Reactive Protein >2 SD above normal INR >1.5 or aPTT >60 Hyperbilirubinemia >4 Serum lactate levels >1; >4 = really bad
S/s of Severe Sepsis:
Organ dysfunction (s/s of hypoxia from vasodilation)
Hypoperfusion
Hypotension
What is the diagnosis of Septic Shock?
** Hypotension despite fluid resuscitation **
Poor perfusion to organs
Treatment for Sepsis:
Preserving organ perfusion and subsequent function is goal
Diagnosis should be made within first 4-6 hours or severe hypoperfusion can result
1st: Sepsis Resuscitation Bundles must be completed within first 6 hours
2nd: Sepsis Management Bundles must be completed within first 24 hours
Bundles to be completed within first 6 hours for Sepsis Resuscitation :
1) Obtain serum lactate measurement
2) Obtain blood cultures prior to antibiotic administration
3) Administer Broad-spectrum antibiotics (within 3 hours of ED admit and within 1 hour of non-ED admit)
4) Apply vasopressors if needed and fluid if elevated lactate levels
5) Obtain CVP levels if needed (b/c of preload problem)
Sepsis Resuscitation Bundle (6 hours) #1:
Serum lactate level
- if greater than 4, denotes movement into septic shock - helps determine if organ degeneration is beginning due to levels of anaerobic metabolism secondary to hypoxia
Sepsis Resuscitation Bundle (6 hours) #2:
Blood cultures prior to antibiotic administration
* ~30-50 with severe sepsis or shock have a positive blood culture * ASAP following onset of fever * Studies recommend cultures of sputum, urine, other drainage
Sepsis Resuscitation Bundle (6 hours) #3:
Broad-spectrum Antibiotic Usage
- within 3 hours of ED admit or 1 hour of non-ED admit - Review specific antibiotic 48-72 hours after initial start; eventually go to narrow-spectrum if available/warranted - Use priming/loading dose with every antibiotic change - Assess hepatic/renal function closely
Sepsis Resuscitation Bundle (6 hours) #4:
Vasopressors and/or Fluid
- If hypotension and/or serum lactate >4 - At least 20mL/kg or crystalloid/colloid equivalent; often 500-100 mL in ~30 mins. - Adequate response = MAP >70 with HR <110; need to get the CVP up; want SBP >70 - Give Vasopressors to maintain MAP >80 (Norep, Dopamine, or Neosynephrine); need Art-line - Continuously assess for pulm. edema/congestion/systemic edema
Sepsis Resuscitation Bundle (6 hours) #5:
CVP levels/Preload problem
- if hypotension despite fluid resuscitation (Septic Shock) and/or serum lactate >4 - aim for CVP greater than or equal to 8, unless ventilated can have CVP 12-15 - Fluid challenge of 20mL/kg - if Hct <30%, warrants PRBC transfusion - SVO2 greater > or equal to 65%; give PRBC and/or increase CO through inotropes (dobutamine gtt is popular) assuming adequate fluid levels/resuscitation and CVP > or equal to 8
Sepsis Management Bundles (24 hours):
*We aren’t sure if these management bundles decrease mortality like the resuscitation bundles do
Bundle 1: Low-dose steroid use
Bundle 2: BS maintain 80-150
Bundle 3: Median inspiratory plateau pressure <30 cm H2O if ventilated
Sepsis Management Bundle (24 hours) #1:
Low-dose Steroid
- Helps control inflammatory response with SIRS - Hydrocortisone 200-300 mg/day x 7 days TID or 4 times/day or continuous IV gtt (preferred due to difficulty with controlling BS with bolus)
Concerns:
BS control
Immune stress response (nosocomial infection rate increased)
Recurrent septic shock (inc. risk with steroid use)
Sepsis Management Bundle (24 hours) #2:
BS maintenance 80-150
Sepsis Management Bundle (24 hours) #3:
Median Inspiratory Plateau Pressure (IPP) <30 cm H2O for ventilated patients
- High Tidal Volumes can increase risk of ARDS with septic patients - Septic patients have inc. risk of ARDS - Decreasing volume stress on ventilated lungs can decrease risk of ARDS
Some nursing interventions for Sepsis :
- Comfort: be aggressive with this: pain killers; discomfort from multiple areas (infection, ventilation, bed rest, fever, possible trauma)
- Skin Integrity
- Nutrition: they are in hypermetabolic state
- Support: spiritually, family, etc.
One of the most common reasons for development of MODS (multiple organ dysfunction syndrome) is ______
Septic Shock
Prolonged exaggerated intravascular inflammation that results from an uncontrolled response to various stimuli that eventually activates a series of cascades =? Continuous stimulation or severe infection results in sustained inflammation; There’s an imbalance and deficit of cellular O2 extraction
SIRS (Systemic Inflammatory Response Syndrome)
Systemic Inflammatory response to a clinical insult including infection, pancreatitis, ischemia, trauma, or hemorrhagic shock =
SIRS
SIRS is a systemic reaction to infection as evidenced by 2 or more of the following symptoms (and must not be related to another know cause in order to be indicative or SIRS):
Temp >100.4 or less than 96.8
HR >90
RR >20 or PaCO2 <32
WBC >12,000 or <4,000 or >10% immature forms (bands)
Common findings of SIRS:
Chills Dec. UO Dec. Skin Perfusion Poor Cap Refill Skin Mottling Dec. Platelets Petechiae Hypoglycemia Unexplained change in mental status
_____ is the systemic reaction to an infection.
_____ results unless this process is reversed; characterized by hypotension, hypoperfusion, & the beginning of organ dysfunction.
______ is defined as hypotension <90 or >40 reduction from baseline that is refractory (resistant) to fluid resuscitation.
____ is the final stage with organ dysfunction so significantly altered that homeostasis cannot be maintained without interventions.
Sepsis; Severe Sepsis; Septic Shock; MODS
