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
1 cause of sepsis = ________
Poor handwashing
Factors in the development of MODS:
- Microaggregates (platelets, neutrophils, fibrin etc–clog microcirculation=dec. O2)
- ROM’s (reactive oxygen metabolites) out of control
- Endothelial Cell Injury
- Metabolic Derangement (mitochondrial dysfunction)
- Humoral Mediators (TNF-a, IL-1)
- Therapy induced dysfunction
When 3 or more systems are affected with MODS, the mortality rate climbs to ____; What systems are commonly affected?
80-100%; Renal, hepatic, GI, pulmonary, Cardiac, CNS, hematological
What happens to the kidneys with MODS? Treatment?
Oliguria/anuria
Acute tubular necrosis and/or need for hemodialysis
Inc. creatinine & BUN; Creatinine considered best indicator
Urinary sodium>20
Diuretics, Fluid Challenge, Low-dose Dopamine is controversial
What happens to the Liver with MODS? Treatment?
- Normally helps control systemic inflammation therefore, this is associated with higher mortality
- s/s usually 1-2 post injury
- Can spontaneously recover
- Inc. Bilirubin most sensitive marker related to mortality
- Also Inc. AST, ALT, LDH, Serum Ammonia
- Dec. serum Albumin
- LFT’s
- Jaundice, Hepatomegaly
- Complete failure not unusual
GI problems with MODS?
- GI normally contains 70-80% of immunologic tissue for the body, therefore GI involvement Increases morbidity significantly
- Hypoperfusion = submucosal damage
- Bacterial transference via “leaky gut” into systemic circulation
- Oropharynx becomes over-colonized with pathogens possibly leading to pulm. aspiration
- Failure
Pulmonary Injury with MODS?
Usually first organ involved (usually 24-72 hours after post initial injury process)
Dyspnea
hypoxemia
Usually ventilated
Common to find non-cardiogenic pulm edema secondary to intrapulmonary shunting & inc. cap permeability
Failure
Heart involvement with MODS?
Dec. RAP/SVR
Inc. venous capacity yet Inc. CO noted due to inc HR & dec. SVR
Dec SVR=mortality rates increase
Exacerbated by TNF-a release, acidosis
Failure: cardiogenic shock & biventricular failure
Brain involvement with MODS:
Hypoxia due to inflammation & vascular involvement=hypoperfusion
Immediate s/s unless sedation is used
What are the hallmark s/s of hematological involvement with MODS?
Anemia & Coagulation abnormalities are hallmark
DIC begins initially through hypercoagulation
Etiology & Risk Factors for MODS:
Etiology: -Prolonged shock states -Severe sepsis -Acute pancreatitis -Acute Renal Failure -Severe burns -ALI (Acute lung injury) -ARDS -Depleted immune system -Premature cell death (apoptosis) RF's -Advanced Age -Persistent infectious processes -All critically ill patients -Chronic dz -Compromised immune sys -Chemo/radiation -Corticosteroids/immunosuppressive agents -Invasive devices -Indiscriminate use of antimicrobial drugs
Treatment of MODS:
Antibiotics (long list)
Vasoactive drugs
Fluids: Crystalloids/colloids
Inotropes/Vasopressors (Dopamine, Dobutamine, Epinephrine, Norep)
Mech. Ventilation/O2
Prevention (hand-washing, frequent C&S tests in patients with fevers–sputum, blood, catheter tips, urine)
Disorder of the “clotting cascade”; results in depletion of clotting factors in the blood
DIC (Disseminated Intravascular Coagulation)
Etiology & Risk Factors for DIC:
Etiology: Infections Inflammatory Diseases Vascular dz Trauma Malignancy Venoms Obstetrical complications
RF's: Sepsis Injury/trauma Surgery/anesthesia Complications of labor/delivery Leukemia or disseminated cancer Blood transfusion Reaction Liver dz
Labs for DIC:
Acute DIC:
- Increased Prothrombin time/Thrombin time - Dec Fibrinogen level - Dec platelet count - Inc. D-dimer (denotes high levels of fibrin degradation products--over-clotting)
Chronic DIC:
- Inc. PTT - Partial thromboplastin time dec or inc - Thrombin time = normal - Fibrinogen dec, inc, or normal - Platelet count dec, inc., or normal - D-dimer increase
Treatment of DIC:
IV fluids PRBC (have clotting factors) Platelet transfusion FFP (have clotting factors) Anticoagulants (ie Heparin) Treatment depends on which stage they're in
4 rating scales for trauma:
GAP (GCS, age, & SBP)
MGAP (above plus mechanism)
RTS (revised trauma scoring)
T-RTS (Triage revised trauma scoring)
What do scores on the RTS (Revised Trauma Scoring) range from? A score of <__ identifies those needing admission/treatment at a trauma center. What are the factors of the RTS?
0-7.8; <4; GCS, SBP, & RR
Most common ages of trauma:
10-24
What’s a blast injury?
Combination of blunt & penetrating
Trauma where skin left intact
Damage to underlying tissue, structures, organs
Hemorrhage possible
Edema can cause problems distal to injury
Blunt force trauma
Trauma with hemorrhage highly likely
Instinct to remove object
Damage to underlying tissue, structures, organs may or may not be severe
Penetrating Trauma
What are the stages or peaks of trauma?
First peak:
Death occurs in minutes; from major neuro and/or vascular damage
Need to be recognized early in mass casualties
Rarely leads to positive outcome if transported
2nd Peak:
Occurs during “Golden Hour”, the 1st hour after initial trauma
Damage from intracranial hematoma, major thoracic, or abd. injuries are common
Immediate treatment can improve death rate
3rd:
Days to weeks following trauma
Usually the sequella of sepsis or MODS
Levels of Trauma Centers:
Level 1: Regional Trauma Center; capacity to provide all needed tertiary care
-UofL, Kosairs, UofK, Vanderbilt, Cincinnati, etc
Level 2: provides definitive, trauma based care, yet not at extent of Level 1
Level 3: Primary care is focus, patient is stabilized & transferred asap
Level 4: Community hospital or health/aid station, usually in remote areas, basic first aid, transfer ASAP
-none in KY
Primary Assessment pieces of Trauma :
Primary: Airway: ET tube placement; CO2 detection Breathing: Bilateral breath sounds ; Chest x-ray Circulation Disability (neurovascular status)
Secondary: Exposure/environment Full set of vital signs Giving comfort measures Head to toe assessment Inspection of posterior surfaces (ie penetrating object--assess exit wound)
Primary and secondary assessed by multiple people simultaneously
Patients with the following problems are highly likely to have problems with airway:
Apnea
GCS <9
Sustained seizure activity
Unstable mid-face injury (Le Fort injuries)
Large Flail Chest
Resp. Failure
High Aspiration risk (TBI can lead to n/v)
Transverse fracture involving detachment of the entire maxilla above the teeth =
Mid-facial trauma: Le Fort 1
Pyramidal fracture involving triangular segment of the mid-face and nasal bones; impact or fracture above the nasal bone forming a triangle that detaches the segment
Le Fort 2
A separation and detachment of the maxilla, nasal, and both zygomatic bones =
Le Fort 3
S/s with Le Forte Injuries:
Epistaxis Pain Facial swelling Face asymmetry/distortion Periorbital edema/ecchymosis CSF rhinorrhea (le fort 2/3) Intracranial or spinal injury s/s
Treatment: Correct positioning to enhance airway
What is Flail Chest?
A segment of rib cage is not attached to any other ribs; minimum of 2 adjoining rib fractures; movement is opposite of normal breathing (inward retraction upon inspiration; outward retraction upon expiration)
S/s of Tension Pneumothorax:
Dyspnea
Pain
Tracheal shift toward unaffected side
Tachycardia/Tachypnea
Treatment for Tension Pneumothorax:
Immediate chest tube
Needle decompression if chest tube is unavailable
14 gauge needle or bigger
2nd ICS, mid-clavicular on injured side
Should see immediate relief from dyspnea
Leave needle in place until chest tube is in place
Occurs when an injury to the chest causes air to enter the pleural cavity without a means of a escape =
Tension Pneumothorax
Collection of blood in the pleural space resulting from injuries to the heart, great vessels, or pulmonary parenchyma =
Hemothorax
Loss of negative intra-thoracic pressure due to entrance wound through the chest =
Open Pneumothorax (“sucking chest wound”)
S/s of Pneumothorax and Hemothorax:
Resonance upon percussion is considered classic finding ***
Loss of or diminished breath sounds on affected side
Crepitus on injured side
Dyspnea
Treatment of Pneumothorax and Hemothorax:
Immediate chest tube
With open pneumo (sucking chest wound)
-occlusive dressing taped on 3 sides; if nothing available, use plastic bag
-applied during Exhalation
-Make sure dressing is 2-3 inches larger than the wound or it may be sucked into the wound
What is Beck’s Triad?
Present in Cardiac Tamponade:
hypotension
muffled/distant heart sounds
elevated venous pressure
Also with cardiac tamponade: increase in CVP (JVD), Paradoxical pulse
Treatment of Cardiac Tamponade?
pericardiocentesis with V-lead attached; may only temporarily relieve problem, cause must be fixed if possible.
When do s/s of Compartment Syndrome usually show?
2 hours post-injury
Treatment for Compartment Syndrome?
Fasciotomy in most cases
What is a normal ICP? What is the equation for it?
5-15; Brain volume, Blood volume, CSF volume, plus Lesion volume (if present) = Intracranial volume/pressure
What is the Monroe-Kellie Doctrine?
The cranial vault contains 3 types of non-compressible contents: Brain tissue, Blood, and CSF. The pressure exerted by these three things is ICP. If the volume of any one of these increases, then the volume of one or both the other must decrease proportionally, or an increase in ICP occurs.
Brain’s auto-regulation compensation system that occurs in descending order if ICP is at 15-30:
1) Displacing cerebral blood flow
- blood can be moved/displaced into non-involved tissues in an attempt to alleviate the inc. ICP
2) Autoregulation: Altering CSF production and/or re-absorption
3) Movement of brain parenchyma (last ditch effort you don’t really want)
- partial collapse of cisterns, ventricles, vascular systems
What happens with an ICP greater than 30?
Auto-regulation mechanisms begin to fail
Small change=significant inc. pressure
Levels can change quickly
Brain herniation imminent if pressure continues to rise
How do you calculate CPP (Cerebral perfusion Pressure)? What is it?
It’s the pressure required to perfuse the brain; Normal = 60-100
CPP=MAP-ICP
MAP= (2DBP + SBP) divided by 3
What is a normal CPP?
60-100
Normal MAP?
70-105; should be kept above 60
A MAP greater than ___ is not acceptable even with normal CPP. An ICP greater than ___ is not acceptable even with normal CPP.
160; 30
A CPP of <____ usually means loss of auto-regulation and cerebral hypoxia
<40-50
Where is CSF produced?
Mainly in the choroid plexus in the lateral 3rd and 4th ventricles; reabsorbed mainly in the arachnoid villi in the subarachnoid space in superior sagittal sinus
CSF drains should be:
Leveled frequently (especially with position change)
Checked minimum of q hour
Turned off (clamped) temporarily to assess ICP level
Continuously assessed for drainage amount, color, consistency, etc
Should NOT leave room when you have a drain draining the CSF
What does CSF normally look like?
Looks like water. Clear. If not, send down sample.
A change in volume resulting from a change in presssure =
Compliance (ie stiff lungs); Low compliance=things get stiff
A change in pressure resulting from a change in volume =
Elastance (ie hypo/ervolemic)
Things that Increase ICP:
Hypercarbia/Hypercapnia (CO2 dilates BV’s normally)
Hypoxia
REM Sleep (can stop this with a barbiturate coma)
Pyrexia (Fever/hyperthermia)
Certain Anesthesia Meds
Volume-Pressure Curve measures what?
Compliance, Elastance
With LOW compliance, small volume INCREASES result in large INCREASES in ICP
An increased ICP greater than ___ for ____ minutes is considered potentially dangerous. An ICP greater than ___ for ___ minutes or longer are strongly associated with poor outcomes.
> 20 for 5-10 min; > 20 for 10 mins +
3 levels of GCS:
Mild: 13-15; brief periods of change of LOC possible and rare hospitalization
Mod: 9-12: injury severity related to duration of LOC and post-traumatic amnesia
Severe: 3-8 with motor score <5
3 almost always = death
What does the GCS measure?
Eye opening 1-4
Motor Response 1-6
Verbal: 1-5
Possible 3-15 total
If a pupil is blown on the right side=___ sided injury.
right
Dilated/”blown” pupil=? Nonreactive (fixed) dilated pupil indicates?
possible brainstem compression; CN 3 damage and possible brain herniation
Cranial nerve assessment for CN 2?
Check pupils
CNerve 3 assessment?
Pupils with consensual response
CNerve 5 assessment:
corneal reflex
CNerve 7 assessment =
Corneal reflex
CNerve 8 assessment =
Hearing; plus dizziness or tinnitus
CNerve 9 assessment =
Gag reflex
CNerve 10 assessment =
Gag reflex
What do decorticate and decerebrate postures mean?
Mean brain stem involvement; Decerebrate is worse, but they are both really bad.
What is Doll’s Eyes (OCulocephalic Reflex)?
When head is turned, eyes move with head=doll’s eyes absent and possible brainstem involvement= Bad
Make sure you rule out spinal injury before doing this!
What is the Oculovestibular Reflex (Cold Caloric Testing)?
Instill water into ear canal and you want reflex; patient will look toward involved ear with intact brainstem
What is Cushing’ s Triad?
Systolic HTN (with widened pulse pressure) Bradycardia Respiratory abnormalities (Cheyne-Stokes)
Most common cause of Increased ICP =
TBI
What type of TBI involves human body moving at high speed and suddenly stopped by impact “sloshing around effect” (ie MVA, fall,etc)
Coup-Contre Coup (Accleration-deceleration)
Common s/s of Primary TBI:
H/a, dizziness, blurred vision, confusion, lethargy, change in LOC, dec. HR/RR, dilated pupils and respiratory arrest
What is the most common type of skull fracture?
Linear/basilar fractures; child abuse cases
Raccoon eyes and Battle’s Sign may be indicative of ____
Linear/Basilar fracture
What is Halo Sign?
When blood encircled by a yellowish stain is seen on dressing; can indicate presence of CSF
What do you do if CSF leakage from the nose or ear is occuring?
Allow CSF to flow freely. Nothing should be placed in nose or ear. Bandages can be placed around or under it to collect drainage. Don’t have patient blow nose and also don’t suction them.
Treatment for Concussion?
rest or not treated; change in memory can last up to one year=educate patient
Type of Hematoma with blood located between the dura and inner table of the skull =
Epidural
Hematoma with blood below dura and above arachnoid covering of brain =
Subdural Hematoma
Hematoma where blood is within the brain tissue =
Intracerebral
Which type of Hematoma is usually caused by laceration of an extradural ARTERY? Can go from walkie-talkie to unconscious in minutes.
Epidural Hematoma
S/s of Subdural Hematoma:
s/s within 24-48 hours H/a focal neuro defect Unilateral pupil involvement Dec. LOC Herniation if Inc ICP
Treatment for Subdural Hematoma:
Craniotomy to remove clot and place drain
HOB may be flat to reduce tension
Treatment of Epidural Hematoma:
Immediate evacuation of clot
S/s of Epidural Hematoma:
Loose consciousness, regain it, deteriorate rapidly
Posturing & Unilateral dilation are late signs of cerebral herniation
Primary cause of Intracerebral Hematoma:
Penetrating brain injury (ie stab, gunshot)
Treatment for Intracerebral Hematoma:
Surgery only if lesion continues to expand and location is close to surface
manage edema and cerebral perfusion are key
What is a Secondary TBI?
Biochemical and cellular response to the primary injury beginning within mins to hours of initial injury.
Key difference is that secondary injury is global and harms tissue that may not have been involved in the primary injury.
MAIN FACTOR in secondary brain injury = cellular excitation
Diffuse Axonal Injury is what?
A rotational injury; often from kick to head by animal; looks black all around on the x-ray
Most common reason for Increased ICP =
Vasogenic Edema: disruption in the BBB with an inability of the cell walls to control movement of water in and out of cells; Common causes: brain tumors, cerebral abscesses, strokes
What is the most accurate but the most dangerous site for ICP monitoring? What is the least accurate?
Intraventricular catheter. Least accurate is Epidural probe.
