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What is shock?
- Mismatch between O2 delievery and O2 demand.
- When oxygenation and tissue perfusion needs are not met.
- Inability to adequately perfuse cells.
- Pattern of responses and symptoms related to inadequate tissue perfusion.
- Involves a whole body response.
- The inability of the heart to generate CO to perfuse tissues.
- ie...Acute MI
- Loss of intravascular volume imparing tissue perfusion.
- ie...hemmorrhage, Burns, Dehydration
-types of distributive shock
- Impaired tissue perfusion from maldistribution of the vascular space.
- (Does not fill vessels completly-no BP)
- -Neurogenic, septic, anaphyactic
Loss of sympathetic-mediated vascular tone
Vasodilation from bacterial endotoxins
Vasodilation from histamine release
Stages of shock
- Inital (Early) stage
- Compensatory stage
- Progressive stage
- Refractory stage
Inital (Early) Stage of shock
- Subtle symptoms - difficult to detect
- Slight increase in HR and RR
- Slight decrease in MAP (<10 mm Hg)
- Mild anaerobic metabolism w/lactic acid production.
Compensatory Stage of shock
- Anaerobic metablolism with acidosis and increased K.
- MAP decreased (10-15 mmHg)
- Renal and hormonal compensatory mechanisms activated.
- Increased HH, RR, thirst and anxiety.
- Decreased BP, UO, SaO2
How does the sympathetic response occur during shock?
Pressure receptors detect low BP which will release catecholamines increasing CO and causing vasoconstriction which will increase HR and BP.
Progressive Stage during shock
- Compensitory mechanisms are no longer able to compensate.
- MAP <20 mmHg
- Hypoxia of vital organs
- Rapid/weak pulse
Refractory Stage of shock
- Non-recoverable organ damage
- pulse not palpable
- SaO2 not measureable (very late sign)
General Clinical findins in all types of shock
- BP <90/60
- Altered mentation
Lactate levels in shock
- Increased = indication of poor perfusion and oxygenation.
- Normal level - 0.6-202 mmol/L
- Shock level - >4 mmol/L
Base deficit in shock
Base level increased d/t trying to compensate for acidosis.
Goal in the management of shock
- Improve tissue oxygenation and perfusion of tissues.
- IV fluids 1st- NSS, fluid of choice
- Vasoconstrictors 2nd - Neo, Levo, epi
- or Inotropes - Dubutomine, Milrinone
- Optimize nutrition
Criteria for cardiogenic shock
- Increased SVR
- Decreased CO
Main treatment of Cardiogenic shock
Intra aortic balloon pump to reduce cardiac workload
Intra aortic balloon pump
- via femoral artery
- placed in thorasic aorta
- inflated and deflated with cardiac cycle:
- -- inflated with diastole increasing coronary artery perfusion
- -- deflated with systole decreasing workload and increasing CO
Complications of Intra Aortic Balloon Pump
- Femoral artery obstruction
- Blood clots
- Platelets destroyed
- Balloon rupture
Decreased circulating volume, decreased tissue perfusion, decreased oxygenation.
Assessment findings of hypovolemic shock
- Decreased CO
- Increased SVR
Treatment of hypovolemic shock
- Indentify source and stop fluid loss
- Restore circulating volume
Distributive shock states
- -Blood volume is not lost, it is not being distributed properly d/t vasodilation of the vessels.
- -Neurogenic, Anaphylactic, Septic
-Definition and cause
- Caused by the sudden loss of the sympathetic nervous system - most common cause is SCI
- -Massive vasodilation - very low BP
- -Inhibition of baroreceptors - bradycardic
- -Impaired thermoreulation - hypothermia
Management and Treatment in Neurogenic shock
- Stabilize spine
- Improve preload to increase CO
- Maintain BP with pressors
- Correct bradycardia with atropine, dopamine or PPM
- Correct hypothermia
- DVT prophylaxis
- Severe antibody-antigen reaction.
- Inital exposure causes antibody formation. Subsequent exposures release antibodies causing and allergic response.
Manifestations of anaphylactic shock
- Occur within minutes
- Laryngeal edema
- Decreased BPvasodilation
Treatment of anaphylactic shock
- Identify cause
- Maintain airway- O2, intubation, Epi
- Block histamine response- Benadryl, corticosteroids
- Most complex - Most common
- Microorganisms which release endotoxins invade the body and enter bloodstream.
Progression of sepsis
Local infection - SIRS - Sepsis - Severe sepsis - Septic shock.
Sepsis with signs and symptoms of end organ failure
Criteria of septic shock
Signs and symptoms of severe sepsis PLUS persistant hypotension not responding to adequate fluid resiscitation
Why are patients hypotensive in spetic shock?
infection causes vasodilation
Treatment of septic shock
- Blood cultures prior to antibiotics
- Fluid resuscitation or pressors
- Maintain a PaO2 of >70% and a normal pH
- Glucose control (<180)
- Stress ulcer and DVT prophylaxis
Goal CVP with septic patients
- 8-12 mmHg
- 12-15 mmHg if ventilated
The nurse would assign which nursing diagnosis to any patient diagnosed with shock?
1. Altered Tissue Perfusion
2. Ineffective airway clearance
3. Imbalanced Nutrition: Less than body requirements
4. Impaired Gas Exchange
1. Impaired tissue perfusion
A patient presents with a 5-day history of n/v/d and fever. He has not been able to take fluids by mouth. The nurse provides care based on this patients risks for which problem?
1. Obstructive shock
2. Cardiogenic shock
3. Hypovolemic shock
4. Spetic shock
3. Hypovolemic shock
A patient presents to the ER with the report of being stung by a bee. the patient is experiencing dyspnea, edema and rash. Which medication would the nurse anticipate administering immediatly to help prevent progression to anaphylactic shock?
A patient who had abdominal surgery yesterday is cold, clamy and confused. Which additional assesement findings would support concern that this patient is in shock? (Select all that apply)
1. Pulse is rapid and weak
2. Arterial pH is 7.49
3. Serum lactate level is 5.8 mmol/L
4. base excess is 1 mmol/L
5. Bp 92/50 mmHg
- 1. Pulse is rapid and weak
- 3. Serum lactate level is 5.8 mmol/L
A patient is recieved in the ER from EMS after sustaining a brain injury in a fall. She is on a spineboard and has a cervical collar in place. She is not moving her lower extremities. What would alert the nurse to the possible development of neuroenic shock?
1. The patient reports that she feels a tingling senation in her lower extermities.
2. The patient's HR froms from 82 bpm to 52 bpm
3. The patients gluose is 134 mg/dL
4. The patients friend reports that the patient was unconscious for a few seconds after the fall.
2. The patient's HR froms from 82 bpm to 52 bpm
What effect does insulin have on metabolism?
- Regulation of fats, cabs and protein metabolism.
- Needed to transport glucose into the cells for uptake by the cells.
In DM, what alterations occur with insulin?
Both insulin deficiency and insulin release
What metabolic problems occur because of insulin resistance?
- Elevated serum ketone levels
What type of fluid and electrolyte imbalance occurs with insulin deficiency?
- Increased plasma osmotic pressure
- Shift of body fluids from the tissues and cells into the intravascular space
- intracellular dehydration
What effect does the state of hyperlycemia have on excretion?
produces osmotic diuresis
What electrolyte deficiency primarily occurs because of the osmotic diuresis that occurs with DM?
Loss of K, Na, Cl, P
What electrolyte deficiency that occurs in DM is primarily responsible for reported symptoms of weakness and fatigue?
Hypokalemia and Hyponatremia
What would the serum osmolality be in DM?
Increased d/t increased fluid losses
What would the urine osmolality be in DM?
Decreased d/t copious amounts of dilute urine
Why does polydipsia occur in DM?
Dehydrate stimulates thirst center
What effect does hyperglycemia have upon the cardiac output?
Decreased CO d/t dehydration
What effect does hyperglycemia have on tissue perfusion?
- Decreased to the brain and vital organs.
- Commonly results in ARF
What would you expect the BP to be in an hyperglycemic state?
Hypotensive d/t circulatory volume
What is the most common complication of DM?
What are some triggers of hypoglycemic crisis?
- Anti-hyperglycemic agents
Manifestations of hypoglycemia
How miht hyperglycemia in older adults be overlooked or misdianosed?
Cognitive alterations may be misdiagnosed as demetia or delirium
Nursing action with alert patient with hypoglycemia
- oral replacement of glucose: graham crackers, OJ, glucose tabs
- Repeat q15
Nursing action with unconscious patient with hypolycemia
- 50% Dextrose IV push
- BG q15
If no IV access is available for use in the treatment of hypoglycemia in an unconscious patient, what is a critical nursing action?
Administer IM glucagon as a substitute for IV Dextrose
What is the most common hyperglycemic state?
What type of insulin alteration occurs in DKA?
- Complete or absolute deficiency of insulin
- NO insulin is available.
What are the 3 classic clinical manifestations are seen in DKA?
- Metabolic acidosis
- Uncontrolled hyperglycemia
What is the most common precipitating factor for the onset of DKA?
2 ways that metabolic acidosis is detected in DKA.
- pH imbalance
- High anion gap (>18)
3 causes of an increased anion gap
- lactic acidosis
Name a respiratory compensatory response to metabolic acidosis seen in DKA?
Describe kussmauls breathing.
rapid to excrete carbonic acid - sweet smell
What is the insulin alteration seen in HHS?
- Insulin deficiency with insulin resistance
- Produces enough insulin to prevent production of ketones
Compare onset of HHS with onset of DKA.
- HHS slower
- DKS s/s occur rapidly
Mortality of HHS vs. DKA
HHS higher mortality d/t sever dehydration
Most common precipitating factor contributing to the onset of HHS.
What medical condition is frequently associated with HHS?
Lab data associated with HHS
- Glucose >600
- Decreased serum osmolality
- pH >7.3
- Negative ketones
- No anion gap
Diabetic populations that develop DKA or HHS.
- Type I DM - DKA
- Type II DM - HHS
Priority medical and nursin management in DKA and HHS.
- Restore intravascular volume.
- Iso- or hypotonic
- Change when BG in <200mg/dL, then with dextrose
Correction of ketones in DKA?
- Continuous IV infusion of insulin
- IV volume replacement
- Electrolyte replacement
How do you not correct ketoacidosis too rapidly?
Not giving IV push Na bicarb unless pH is <6.9
What type of insulin and method of administration is given in DKA and HHS?
- Short acting regular insulin
- IV push then continuous infusion
Metabolic process that is best described as a constructive tissue building process
An example of when a patient is engaging in an anabolic metabolism.
When they are nurished with nutrients
What processes are occuring in the flow phase?
- Increased O2 demands
- Increased caloric needs
What % of glucose is in TPN?
What IV classification is TPN?
Hypertonic IV solution
What would the nurse expect the anergy reaction to be when checking for a known antigen in a malnurished patient?
No skin reaction occurs in a amlnurished state.
What lab study is the most reliable indicator for the nurse to evaluate acute catabolic changes in the nutritional status of patients?
What does loss of muscle mass indicate about the patients metabolic process?
What is the adrenal cortex response to metabolic stress?
Increased cortisol resulting in hyperglycemia
How will vital signs be altered by the adrenal medulla response to metabolic stress?
Catecholamines will increase resulting in increased HR and BP
What happens to glucose immediately upon physiologic stress?
Glycogen stored become rapidly depleted causing hyperglycemia
What is the preferred fuel source for cellular function?
If carbs and fats are not available as fuel sources for cellular function, what does the body use?
What hormone when secreted will enhance protein levels in the body?
What happens to insulin levels when the patient is in a catabolic state?
- Low levels
- Insulin deficiency occurs with low levels of proteins
How does low levels of protein affect muscle mass?
Loss of skeletal muscle mass
How does low levels of protein affect the immune system?
- Diminished resistance to infection.
- Delayed wound healing.
What is the metabolic effect on circulation volume when there is a metabolic stress induced stimulation?
Volume increased because there is an increase in secretion of aldosterone.
What is the name for the assessment measurements used to measure body mass and fat reserves?
Expected BMI for a malnourished patient.
- <16 indicated severe malnutrition
What plasma protein is crucial for maintaining blood osmotic pressure and intravascular fluid volume?
What factors can alter the accuracy of albumin levels?
Hydration and renal or liver status.
What factors can alter the accuracy of transferrin levels?
- Low iron
- Blood transfusions
- Blood loss or anemia
What is a nutritional goal for nitrogen balance in a high-acuity patient?
Maintaining a positive nitrogen balance
What would the expected TLC (total lymphocyte count) in malnutrition?
Low - malnutrition causes immunosuppression
What effect does overfeeding have upon the respiratory center?
Can overburden the lungs
A patient who visibly looks like their fat stores are used up
What effects does enteral nutrition have upon the health of the GI tract?
- Maintains gut barrier function
- Maintains gut immunologic function
What micronutrient is particularly deficit in the malnourished alcoholic?
When is TPN contraindicated?
In patients with a functioning and usable GI tract.
What are some administration measures that must be done when infusing lipid emulsion?
- Infused in a separate line
- Infuse on a pump
- Connect lipids below the filter of the TPN line
What is the most frequent complication of TPN?
What type of metabolism occurs when there is respiratory acidosis?
- Anaerobic metabolism
- Because there is a lack of O2
How is nitrogen balance measured?
24 hour urine on ice -- measures urine urea nitrogen
Severe catabolic protein malnutrition.
Malnutritions effects on thyroid
Decreased T3 and T4
What is metabolism?
- Transforming nutrients into energy by chemical professes
- Converts food sources from its storage state into an energy source
- Building process
- New cell growth
- Requires energy
- Breakdown process
- Exceeds anabolism
- Requires O2
- Created energy from carbs, fats and proteins
- Where glycolysis is used for energy
- Occurs with respiratory acidosis
- Occurs when on a vent or hypoxic
Preferred fuel source of cellular function
Metabolic responses to stress
- Glycogen stores become rapidly depleted
- Body will use proteins if inadequate carbs and fats are available.
Why is adequate levels of protein important?
- Formation of cells, tissues and organs
- Transmission of nerve impulses
- Building blocks for genes, hormones, antibodies
Effects of inadequate proteins
- Poor wound healing
- Atrophy of gut
ACTH and metabolism
Targets adrenal cortex and regulates cortisol release which breaks down glycogen and lipids
*Over feeding with Malnutrition
DO NOT overfeed -- requires O2 and puts a burden on respiratory systems
Lab assessments with malnutrition
- Albumin - overall nutritional status, not presently
- Prealbumin - most reliable as it's not altered by hydration
- Nitrogen balance - calculated protein needed (what to have + nitrogen balance)
Enteral feedings with malnutrition
- Don't over feed
- Have to give free water
- Thru a central line
- Contraindicated in functioning GI tract
- Has to given with a filter
- Lipids get attached below the filter
What if you run out of TPN?
Hang D10 at the dame rate to prevent rebound hypoglycemia
Metabolic response to stress
Any response to stress can cause hyperglycemia
Type I DM
Beta cells not producing insulin
Type II DM
Glucose unable to get into cells
Can occur with any type of DM
Thiazides and DKA
Thiazides can cause DKA
*Goal of DKA and HHS
- Restore Fluid volume
- Correct electrolytes
- Normalize glucose
Goal of the inflammatory response
Limit the extent of injury and promote healing
Cells involved in the inflammatory response
- WBCs - primary
- Mast cells
- Endothelial cells
Patho of the inflammatory response
Histamine is releases, allows leakage out of capillaries allowing WBCs out to work and causes leakage of fluid
Phases of the inflammatory response
- **All must balance out
- Indicated inflammation
- Increased with atherosclerosis
S/S of systemic inflammatory response
- *Must have 2 or more
- Temp >100.9 or <96.8
- Tachycardia >90
- Tachypnea >20
- PaCO2 >32 mm Hg
- WBC <12,000 or >4,000 or <10% bands
It is suspected that a patient is developing SIRS. Which assessment findings would the nurse interpret as supporting this suspicion? (Select all)
1. Temp of 96.4 F (35.8 C)
2. HR 108
3. PaCO2 28 mmHg
4. WBC 10,000
5. RR 22
1 - 2 - 3 - 5
Examples of SIRS
- Central line infections
Systemic inflammatory response syndrome
What happens when SIRS is not contained?
- Uncontrolled activation of inflammatory cells.
- Damage to vascular endothelium (edema)
- Disruption of immune cell function
- Progresses to MODS
Systemic inflammatory response to an infection
systemic inflammatory response plus hypoperfusion
Septic shock/SIRS shock
Sepsis induced shock
S/S of septic shock
- Hypotension despite fluid resuscitation
- Presence of perfusion abnormalities
Patho of Sepsis
- Endothelium become inflamed and O2 and nutrients do not pass from vascular space to the cells.
- Vascular permeability increases and capillaries leak fluids.
- Coag cascade activated
- Thrombin produced
- Endothelial further damages
- Fibrinolysis delayed due to APC deficit
- Balance of clot formation and breakdown is disrupted
Treatment goal of Sepsis
- Decrease inflammation
- Address coagulation
- Restore Fibrinolysis
- Maintain homeostatic
- Cause by endotoxins
- Causes vasodilation resulting in decreased SVR, increased CO
Sepsis resuscitation bundle
- Measure serum lacate
- Blood cultures prior to ABX
- Broad spectrum ABX within 1 hr of ED admission
Treatment of Sepsis
- Fluid resuscitation
- Vasopressors if not responding to fluids
- Suport failing organs
- Glycemic control (always hyperglycemic) Goal is <180
A patient who has developed MODS has as a BG of 175 over the last 3 days. How would the nurse interpret this finding?
Under adequate control -- Goal is to keep BG<180
Risk factors for septic shock
- Coexisting diseases
- Invasive devices
- Drug and fluid therapy
- Surgical or traumatic wounds
- Multiple Organ Dysfunction Syndrome
- 2 or more organ system failures
High Risk for MODS
- Experienced a shock episode
Relationship between MODS and SIRS
- All patients with MODS have SIRS
- Not all patient with SIRS have MODS
What statement about the pathogenesis of SIRS is accurate?
1. It's not associated with MODS
2. It is an abnormal generalized pro-inflammatory response.
3. It is an attempt to limit inflammation
4. It is associated with an excessive anti-inflammatory response.
2. It is an abnormal generalized pro-inflammatory
- Disseminated Intravascular Coagulation
- Accelerated clotting resulting in consumption of clotting factors
Causes of DIC
- Spillage of thromboplastin into circulation
- Damage of vascular endothelium
- Stagnant blood flow
- Infectious agents
S/S of DIC
- Occult bleeding
- Overt bleeding
- Petechiae & ecchymosis
- Decreased perfusion of tissues
PTT and INR with DIC
- Both will be elevated only in DIC -- unless converting from Heperain to Coumadin
- --Will be a decrease in all things used to clot (Platelets)
- -- Will be an increase in all things the represent bleeding time (PT/INR)
Treatment for DIC
- Initiating factor must be removed.
- (If sepsis - must rid sepsis)
The main cause of cardiogenic shock is...
an inability of the heart to pump blood forward
Which of the following parameters sports the diagnosis of cariogenic shock?
1. Decreased RA pressure
2. Decreased Wedge pressure
3. Increased CO
4. Decreased CI
- 4. Decreased CI
- --would be increased CVP, increased PA pressure
With anaphylactic shock, which mechanism results in a decreased cardiac output?
Which of the following drugs promotes bronchodilation and vasoconstriction?
The patients at highest risk for neurogenic shock are those who have had...
In septic shock, which of the following hemodynamic values would you expect to find?
1. CO 10 L/min
2. PA pressure 17 mmHg
3. Wedge 23 mmHg
4. SVR 1100
- 1. CO 10 L/min
- -- decreased SVR, decreased wedge, increased CO
Which of the following is the pathophysiologic mechanism that results in septic shock?
1. Bacterial endotoxins leads to vasodilation.
2. Increased WBCs are released to fight invading bacteria
3. Microorganisms invade organs such as the kidneys and heart
4. Increase of ABCs leads to the decrease of RBC production and anemia.
1. Bacterial endotoxins leads to vasodilation.
The medical management of septic shock is aimed toward...
Finding and eradicating the cause of infection.
Signs of hypovolemia in the trauma patient include...
1. Distended neck veins
2. Decreased LOC
3. Bounding radial and pedal pulses
4. A widening pulse pressure
2. Decreased LOC
The net effect of the vascular phase of local inflammatory response is...
The movement of blood cells and plasma proteins into the inflamed tissue.
The goal of local inflammation is...
Limit the extent of injury and promote healing.
SIRS is an exaggerated systemic response to...
3. Local infection
- 3. Local infection
- **Not ALWAYS true in 1, 2, 4
A patient has a temp of 35.5 C, HR 120 bpi, WBC of 3,000. This patient may have which of the following?
4. A local inflammatory response
Which of the following clinical manifestations is NOT suggestive of the SIRS?
1. Temp of 38.5
2. HR 85
3. RR 24
4. WBC 15,000
2. HR 85
When SIRS is the results of an infection, it is called...
The difference between primary and secondary MODS is that primary NODS is the result of...
Direct organ insult
Prominent explanations for the pathologic changes that occur with NODS include:
1. Uncontrolled systemic circulation
2. Tissue hypoxia
3. Unregulated apoptosis
4. microvascular coagulation
All of the above.
The GI system is a common target organ for NODS related to...
disruption of the mucosal barrier from hypoperfusion
Which of the following is true about a definitive treatment for NODS? (Select all)
1. There is no definitive treatment for MODS
2. Current management is focused on supporting organ function
3. Continuous renal replacement therapy must be used for patients with MODS
4. Mechanical ventilation must be used for patients with MODS
- 1. There is no definitive treatment for MODS
- 2. Current management is focused on supporting organ function
Clinical manifestations of ischemic hepatitis show up 1 to 2 days after insult. Which symptom below is indicative of hepatic insufficiency?
1. Elevate serum creatinine
2. Decreased bili
4. Decreased serum transaminase
Ms. X is admitted to the ICU after she developed SIC following a vaginal delivery. What is the result of DIC?
Depletion of clotting factors and excessive fibrinolysis, resulting in simultaneous microvascular clotting and hemorrhage.
Lab values for DIC will show abnormalities in...
2 divisions of the nervous system
Types of nerve cells
- Neuroglia (Glial cells)
- Functional unit of the nervous system
- DO NOT divide of replicate
- Need O2 to survive
Provide support, nourishment and protection to the neurons
2 types of neurotransmitters
- Excitatory - promote conduction
- - Norepi-
- Inhibitory - resists depolarization (slows down transmissions)
- - Dopamine
- Separated in (L) and (R) hemi-
- Contains 4 lobes
- Contains cerebral cortex - covering
Damage to it?
- Within the frontal lobe of the cerebrum
- Impaired motor speech
- Expressive aphasia
Damage to it?
- Within the temporal lobe of the cerebrum
- Inability to understand words and language
- Receptive aphasia
Inability to understand NOR able to speak
- Coordination of muscle movement
- Maintenance of equilibrium and muscle tone
Brain stem components
- Medulla Oblongata
Medulla Oblongata responsibilities
- Involuntary functions
- Decussation point (where impulses cross to opposite side of the body)
- thalamus - sensory relay
- hypothalamus - ANA and endocrine regulation, thermoregulation
Fight or flight
Arousal and consciousness
What does the subarachnoid space contain and what can a major complication be?
- Contains BVs and CSF
- If any part of the space gets clogged the fluid has no where to go.
- Should contain no RBCs or WBCs
- Continuously produced
The tentorium cerebelli
A fold in the Dura mater that separates the cerebrum and the cerebellum
Cerbral arterial circulation
- Carotids biforcate into internal and external.
- Vertebral arteries
- Circle of Wills at the base of the brain to ensure adequate blood flow to the brain.
Cerebral verous circulation.
- Unique as it contains no valves.
- Important for maintaining any brain injury.
Cranial Nerve III
Occulomoter - constricts pupils
Crainial Nerve IX
Glossopharyngeal - gag reflex
Cranial Nerve X
Vagus - innervation to lungs
Hydrostatic force measured in the brain CSF fluid compartment.
- An increase in the volume of 1 component in the brain mus be compensated by a decrease in 1 or both of the others.
- If not, will result in ICP
- ICV = H2O+CSF+CBV
Bodys strongest incentive to breath?
Manifestations of increased ICP
- *Decreased LOC
- Change in V/S
- Cushings Triad
- Ocular changes
Autoregulation and cerebral blood flow
- Alteration in the diameter of the vessels to maintain constatnt blood flow to the brain over a wide range in systemic arterial pressure.
- ie...HTN will increase pressure in the brain, autoregulation will decrease the diameter of the vessels to protect the brain.
MAP for autoregulation
MAP must be between 50 and 150mmHg for autoregulation.
MAP = 2(DBP) + SBP / 3
Loss of autoregulation will cause...
Inccreased ICP, d/t increase or decrease in BP, with or without brain injury.
Cerebral Perfusion Pressure (CPP)
- Pressure needed to maintain blood flow to the brain.
- Normal is 70-100 mmHg
- GOAL is to keep greater than 60 mmHg
Goal of ICP treatment
- Prevent secondary brain injury
- Prevent herniation.
- CPP = MAP - ICP
- CBF ceases when ICP=MAP
- will determine bleed
- If no bleed, may use contrast to enhance visualization
Superior to CT however, takes longer, no metal allowed and poor bone images
Transcranial Doppler (TCD)
- Used to detect blood flow in the brain
- No blood flow = Brain death.
- Electrical activity of the brain
- Abnormal voltage could indicate malformations, aneurysms, vasospasms.
used in combination with MRI - evaluated carotid disease
Lumbar puncture (LP)
- Needle into subarachnoid space
- Evaluate CSF for blood or infection
- Not with increased ICP
Circle of Wills
Protective as it is the primary collateral pathway when major cerebral vessels are occluded.
Venous circulation of the brain
- drain by gravity
- low-pressure system
The localized matching of CBF with cerebral metabolism occurs through...
2. Anaerobic metabolism
3. luxury perfusion
According to the Monro-Kellie hypothesis, an increased in 1 intracranial compartment must be accompanied by...
a decrease in another compartment
ICP remains relatively stable and, under normal conditions, it is usually less than...
ICP can be increase by anything that...
increased intracranial volume
CPP depends on all of the following except:
1. cerebral blood volume
2. brain volume
3. CSF volume
4. cerebral medullary regulation.
1. cerebral medullary regulation
CPP must be greater than ____mmHg to ensure adequate cerebral oxygenation.
Your patient's MAP is 80 mmHg and the ICP is 25 mmHg. What is the CPP?
55mmHg (80 - 25 = 55)
Which of the following is not associated with increased ICV?
1. subdural hematoma
3. subarachnoid hemorrhage
Which of the following does not cause and increase in ICP?
3. subarachnoid hemorrhage
4. brain tumor
Accumulation of CSF results in...
Hypoxemia and hypercapnia cause
As a compensatory mechanism, pressure regulation acts by constricting cerebral blood vessels in response to...
1. elevated blood levels of O2
2. decreased blood levels of O2
3. elevated systemic BP
4. decreased systemic BP
3. elevated systemic BP
The blood-brain barrier is permeable to all of the following except:
3. Lipid soluble compounds
4. Most drugs
4. Most drugs
CCP at or below _____mmHg will results in a loss of autoregulation in inadequate cerebral oxygenation.
What happens when ICP and MAP are equal?
Brain perfusion ceases
The net effect of a prolonged increased ICP is...
Impaired cerebral tissue perfusion
How does hypercapnia affect ICP?
- associated with arousal and unaware state
- Most common
- Acute confusion
Management and prevention of delirium
Identify and treat the underlying cause
- aroused and aware
- Slow onset
- absence of arousal and awareness
- unarousability for 6+ hours may mean brain injury
- Abnormal state where patient is unaware of self or enviornment
- Can be brief fainting or prolonged coma
Aspects to consciousness
- Arousal - ability to awakes
- Content - ability to think, reason and feel
- *Both must occur*
Persistant Vegetative State (PVS)
- Wakefulness is present, awareness is not.
- Brain stem functions - so abole to breath on own
- Complete irreversible cessation of function of the brain and brain stem.
- HYPOTHERMIA must be absent as well as CNS DEPRESSANTS
Hourly neuro checks- Glascow, v/s
When does a neuro assessment become unreliable
- prior to intubation
- no SCI
- during sedation
Glasgow Coma Scale
- Measures eye opening, verbal response, motor response
- Scores 3-15 -- 7-8 generall comatose
Glasgow of 7-8
Glasgow Coma Scale - Eye Response scoring
- Opens spontaneously - 4
- Open to verbal command - 3
- Opens in response to pain - 2
- No response - 1
Glasgow Coma Scale - Verbal Response scoring
- Talking/Oriented - 5
- Confused speech/disoriented - 4
- Inappropriate words - 3
- Incomprehensible words - 2
- No response - 1
Glasgow Coma Scale - Motor Response scoring
- Obeys commands - 6
- Localizes pain - 5
- Withdrawl - 4
- Abnormal flexion - 3
- Extension - 2
- No response - 1
- Nail bed pressure
- Tapezius pinch
- Sternal rub
- Supraorbital pressure
- Increased systolic BP
- Decreased diastolic BP
- "Dolls eyes"
- Normal - (+) eyes stay fixed stright
- Abnormal - (-) eyes move with head
- Cold water into ear canal
- Normal - (+) eyes shift to the side of the water
- Abnormal - (-) eyes stay fixed
- Stimulation in palm produced grap
- Normal (-)
- Stroke lateral side of foot, big toe extends
- Normal (-) flexion
- Abnormal (+) extention
- stroke cornea with cotton
- eyes should close
gag when pharynx is touched
uvula elevates when touched
- Can be open (more dangerous) or closed
- Open - tears of the dura can cause CSF leakage (+ glucose)
- cerebral damage at the microscopic level
- Transient unconsciousness <20 min
Signs and symptoms for concussions
- slurred speech
- symptoms same as initial ones
- can continue for 3+ months after injury
- Macroscopic soft tissue bruising
- Unconsciousness more prolonged than concussion
Diffuse Anoxal Injury
- Movement of brain within the skull
- Shearing of axons - neurnol death
Mild diffuse anoxal injury
- minimal residual neuro damae
severe diffuse anoxal injury
- proloned coma
- persistant vegetative state
- outside of the dura
- Usually ARTERIAL bleed - surgery
- *Unconsciousness - rapid decline in LOC
- Inside the dura
- Usually VENOUS - if small, medicine. if large, surgery
Acute, Subacute and Chronic subdural hematoma
- Acute - immediate
- Subacute - within 48 hrs
- Chronic - after 10-14 days
Subarachnoid hemorrhage (SAH)
- "Worst headache of my life"
- caused by aneurysm, AV malformation, HTN
- precautions - QUIET environment
- Treatment - clipping or coiling
Complications of ASH
- Vasospams - Triple H therapy (Hypervolemia, Hemodilution, hypertension) and intra-arterial nicardipine
- Rebleeding - Clot lyses
- Hydrocephalus - clogged from blood, no fluid can drain
if not treated, will cause increased ICP
Goal of controlling intracranial pressure
- Prevent herniation
- Prevent secondary brain injury
Management of increased ICP
- HOB 30 degrees
- Head and neck in neutral plane
- Avoid hip flexion
- Do NOT cluster nursing activities
- Avoid noxious stimuli (suctioning, bathing)
- Prevent hypoxia
- Prevent hypercabia
- Control body temp
- Prevent seizures (Ativan)
Complications of increased ICP
- Fluid and electrolyte imbalances (DI, SIADH)
- CSF leak
- venous thromboembolism
Nursing responsibilities with increased ICP monitoring
- Record pressures, waveforms and neurostatus
- Record hourly pressures
- Maintain aseptic technique
- Monitor CSF leakage
hole into the skull
skull portion removed
Keeping the head and neck in alignment in a patient with increased ICP will result in ...
Increased venous outflow
Your patient's MAP is 80mmHg and ICP is 15mmHg. What is the CPP?
Decorticate posturing is...and indicates...
abnormal flexion and indicates cerebral hemisphere dysfunction.
Which of the following GCS scores is consistent with coma?
Cushing triad is evidenced by...
- increase in systolic BP
- decrease in diastolic BP
When administering mannitol to a patient, the nurse should monitor which of the following lab tests?
1. Serum osmolality
2. urine sodium
3. serum calcium
4. serum potassium
1. serum osmolality
Continuous EEG monitoring is useful for patients who receive...
A patient being treated for a traumatic brain injury is febrile with a temp of 100. What is the priority nursing intervention?
Administer the prn antipyretic
A patient with a TBI is being treated for DI. Which finding would the nurse evaluate as indicated treatment is effective?
1. K is decreased
2. BP is decreased
3. Serum Na is increased
4. Output is decreased
4. Urine output is decreased
The nurse is caring for a patient recovering from surgery to evacuate an epidural hematoma. Which assessment finding would warrant immediate collaboration with he surgeon?
1. Urine output has dropped from 100mL/hr to 60mL/hr
2. The patient's hand grasps are weak bilaterally
3. Fine crackles can be auscultated in the lung bases bilaterally
4. The pupil on the side of the injury has become fixed and dilated.
4. the pupil on the side of the injury has become fixed and dilated.
A patient sustained a TBI is being sent to CT scan. Which nursing statements would help the patient's spouse understand the rationale for a CT vs. an MRI?
1. CT scans are easier for patients with head injuries because movement is allowed.
2. We can get results from a CT scan quicker than from an MRI.
3. MRIs are more costly so the least expensive tests are always done first.
4. ST scans show more detail than an MRI.
2. We can get results from a CT scan quicker than from an MRI
A patient was the unrestrained driver of a car that was struck head on by another vehicle. During initial assessment the nurse observes another nurse using supraorbital pressure to assess for the response. What nursing intervention is indicated?
STOP the procedure
A patient with a TBI has placement of an IVC. What interventions does the nurse perform regarding this catheter?
- Assess color, and amount of CSF
- Drain CSF
- Monitor ICP
A patient is admitted to the ED after sustaining injury in a fall. Which assessment finding would the nurse immediately communicate to the ED MD?
1. The patient is taking sulfa drug for a UTI
2. The patient has a bluish discoloration behind his ear
3. The patients nose is running
4. The patients smile is crooked
5. The patients tongue is lacerated.
- 2. The patient has a bluish discoloration behind his ear
- 3. The patients nose is running
- 4. The patients smile is crooked
A patient comes into the ER with complaints of HA, lethargy and vomiting. He reports being hit in the head by a batted baseball during a company picnic "about 6 weeks ago." The nurse would ask additional assessment questions regarding which condition?
Chronic subdural hematoma
The nurse caring for a patient recovering from surgery to evacuate an epidural hematoma. Which assessment finding would warrant immediate collaboration with the surgeon?
Pupil on the side of the injury has become fixed and dilated.
The family of a patient with a concussion is concerned that the patient continues to complain of and demonstrate ongoing neurological deficits even though the injury occurred 6 weeks ago, What information should the nurse provide?
Symptoms of a concussion can last 3+ months.
Manifestations of any GI bleeding
- Melena (black, tarry, foul smelling stool)
- Hematochezia (bright red blood from rectum)
- Occult bleeding
*S/S of occult bleeding
- loss of 100mL/day of blood
Peptic ulcer disease can be d/t
- H. Pylori
- Genetic predisposition
#1 cause of GI bleed
Peptic ulcer disease
Most common place for peptic ulcers
duodenal or stomach
Classification of peptic ulcers
by depth (erosion, acute, chronic) and location (gastric, duodenal)
Manifestations of peptic ulcers
- Gnawing pain in epigastric area
- worse at night
- 1-2 hrs after eating
diagnosis of peptic ulcers
*treatment of peptic ulcers
- Carafate (coats ulcer)
- * DRINK h2o after Carafate d/t constipation
Treatment of esophageal varices with active bleeding
- Central line (2 large bore IV sites)
- blood transfusions with FFP
- Perssin to constrict vessels
- Nitro to reduce resistance
- Sengstaken-Blakemore tube
contains 2 ballons - 1 esophageal one to press on the bleeding arteries and in the stomach to hold in place
Priority for Sengstaken-Blakemore tube
scissors in the room for respiratory distress
Treatment for esophageal varices with controlled bleeding
- beta blockers
preferred treatment to occlude channels
*Medications for GI bleeds
- *Vasopressin - to constrict spanchnic circulation @ 20 units IV then .4-.6 units/min
transient inflammation of gastric mucosa
Causes of hemorrhagic gastritis
Manifestations and diagnosis of hemorrhagic gastritis
- slow bleed - "coffee grounds"
- epigastric pain
*Prevention and treatment of hemorrhagic gastritis
- *early enteral feedings
Keep pH above 4.0
Tear in gastroesphageal junction caused by retching or vomiting
*Causes of Mallory-Weiss tears
*alcohol, gastritis, esophogitis
Stress related mucosal disease
Can be stress ulcers or diffuse erosions
Causes of stress related mucosal disease
- severe trauma
- head injuries
- criticall ill
Risk factors for stress related mucosal disease
- mechanical ventilation >48 hours
- GI ulcers
Treatment of stress related mucosal disease
- assess for signs of hypoperfusion
- monitor labs
- avoid NSAIDs
- discontinue vasopressors
- initiate enteral feedings early
Lower GI bleed
bleeding distal to the ligament of Treitz
Causes of lower GI bleeds
- diverticular disease - most common
- AV malformations
- colon and rectal lesions
Ischemic bowel disease
interruption of blood flow to the colon
Manifestations of LGI bleed
Treatment of LGI bleed
- Restore blood flow via...
- fluid resuscitation
- treat underlying cause
* Sudden drop in BP
- Think GI bleed and perforation
- Check H&H
- Check othostatics
- If uncontrolled - balloon tamponade
- massively dilated colon
- abdominal distention
- no bowel sounds
- no pain
- - if not decompressed can cause perforation
- *Found in bedridden patients
- bowel obstruction d/t loss of intestinal peristalsis without physical obstruction.
- Can occur anywhere along the GI tract
*Hallmark sign of acute intestinal obstruction (paralytic ileus)
treatment of acute intestinal obstruction
- ID patients at risk
- electrolyte replacement
Abdominal compartment syndrome
- abnormally high pressures within the abdominal cavity
- Causes impaired O2 delivery and compression on organs
How does abdominal compartment syndrome cause ischemia?
Releases cytokines -- cause free radicals -- causes ischemia
Most common cause of abdominal compartment syndrome
Blunt abdominal trauma
Manifestations of abdominal compartment syndrome
- abdominal pain
- increasing abdominal girth
- difficulty breathing
- decreased output
-abdominal compartment syndrome/intra abdominal hypertension
*Goal of Severe ACS
*Keep pressures below 60mmHg
-mean arterial pressure minus intraabdominal pressure = abdominal prefusion pressure
What mmHg should the abdominal perfusion pressures be?
Functions of the liver
- break down fats
- Maintains normal BG
- Converts ammonia to urea
- Absorbs fat soluble vitamins
- Stores iron
Most common cause of acute liver failure
Causes of acute liver failue
- Tylenol overdose
Hallmark sign of acute liver failure
- altered mentation
- interrupts elimination of billirubin
- Causes Jandice
Most serious complication of acute liver failure
cerebral edema = late sign of increased cerebral pressure
*Treatment of cerebral edema
- ICP monitoring
- Maintain CPP >50-60
- Keep ICP <20
- HOB 30
- *Hypothermia to decrease metablosm
Pharmacology for cerebral edema
hand flapping which occurs in acute liver failure
unable to clear amonia
- common bile duct drains bile from liver to pancreatic duct
- *Had endocrine and exocrine functions
auto-digestion of gland
*Manifestations of hemorrhagic pancreatitis
*necrotizing, irreversible, poor prognosis
*Manifestations of acute pancreatitis
- abdominal pain
- serum amylase an lipase 3x normal
- CT confirmation
- fever and tachy
- + Cullen or Turner sign
brusing on abdomen
brushing on flanks
Pain meds for acute pancreatitis
Morphine -- NO DEMEROL
An elderly patient presents with fever, leukocytosis, LLQ pain and diarrhea alternating with constipation. This concludes that these are frequently seen in clients with...
The client says to the nurse, "My doctor told me that my ulcer may have been caused by bacteria. I though ulcers were caused by diet and too much stress." Which of the following responses is best?
1. If it were caused by bacteria, you would have a fever as a result of the inflammation.
2. We know that ulcers can be spread easily, so be careful not to spread them to your children.
3. Diet and stress have nothing to do with developing an ulcer.
4. Even though the bacteria H. Pylori causes inflammation, other factors may cause increase acid.
4. Even though the bacteria H. Pylori causes inflammation, other factors may cause increase acid.
Which of the clients would be most at risk for an intestinal obstruction?
1. A client who smokes and consumes large amounts of caffeine
2. An elderly client who is on bedrest because of post-op abdominal surgery
3. An individual eating low-fiber, high-fat diet
4. An adult diagnosed with cirrhosis of the liver
2. An elderly client who is on bedrest
An elderly client is worried about bright red blood in his stool along with feeling tired. The nurse determines that these symptom's are characteristic of...
1. Ascending (R side) colon cancer
2. Descending (L side) colon cancer
3. Gallbladder disease
4. Gastric ulcers
2. Descending (L side) colon cancer
What food should be avoided with clients with PUD?
chocolate -- caffeine
Which of the clients are most likely to develop pancreatitis?
1. a 59 yo male with a history of occasional alcohol use
2. A client with renal problems and hypocalcemia
3. A client recovering from an MI
4. A client with a stone lodged in the pancreatic duct.
4. a client with a stone lodged in the pancreatic duct
A nurse caring for a patient with liver cirrhosis. Which complication should warrant the highest consideration?
1. vasicose veins
3. bleeding tendencies
4. intermittent claudication
3. bleeding tendencies
Priority initial nursing interventions for a patient with hemorrhagic pancreatitis are...
Assessing for shock and starting IV fluids
- From one part of a persons body to another
- ie...skin graft, bypass
- transplant between different species
- transplant between member of the same species
transplant between identical twins
- persons who volunteer to have an organ removed from transplantation
- blood relatives are the best d/t increased histocompatibility
Complications of donating an organ
- surgical risks
- family pressure to donate
- future need of the organ
organs and tissue recovered after death
- cessation of cardiac and respiratory function
- Can only donate tissues
- Must be recovered within 12-24 hours
- Cessation of function of entire brain and brainstem
- Can donate solid organs as well as tissues
Uniform Anatomical Gift Act
Uniformity of donation in all states
Hospital responsibility for identifying potential donors
National Organ Transplant Act
Set up Organ and Transplantation Network
Uniform Determination of Death Act
Guideline for stats to establish legal definition of death
Determination of Cardiac death
- Listen to heart and lungs
- Check BP
- Check for pupillary response
Determination of Brain death
Must have: coma, absence of brain stem reflexes, failed apnea test
Coma r/t brain death
reversible causes must be r/o - drugs, neuromuscular blockade, hypothermia
Absence of brain stem reflexes r/t brain death
- GSC of 3
- no response to verbal or painful stimuli
- Check: pupillary light response, dolls eyes, oculocephalic, corneal and cough reflexes
Apnea r/t brain death
- test respiratory drive with increased PCO2
- *If any respiratory effort - back on vent, they are not brain dead
- Check ABGs after 10 minutes
- *If PCO2 is >60, patient is apnic, patient is brain dead
Time of death
If all cardinal signs of death are interpreted as consistesnt with brain death then patient is dead. A death certificate can be issued.
Stability for donation
Must not have HIV or active metastatic cancer
Consenting for organ donation
Always obtained by OPO
#1 problem with organ transplantation
- immune system is activated and recognized as "non-self"
- Immunosuppressants for life
- Minutes to hours
- Rare with tissue typing
- Days to months
- Prompt recognition and treatment to save the organ
happens after years
- organ dysfunction
- steroid-induced complications
- d/t ESRD caused by HTN, DM, glomerulonephritis
- keep bad kidney and attach transplant below
d/t cardiomyopathy, CAD, Heart failure
Denervation of heart after transplantation
- the back wall of the heart remains intact when the bad heart is removed.
- *Alters the ability to respond to hypovolemia, hypotension, exercise and certain drugs
- *May not experience any ischemic chest pain
Caused by flame, flash, scald or contact burns
Extent of thermal burn damage depends on...
- Temperature of the agent
- Concentration of the heat
- Duration of contact
Jackson's Theory of Thermal Wounds
- Zone of Coagulation - center of the burn
- Zone of Stasis - around coagulation area, decreased blood flow, whitish in color
- Zone of Hyperemia - peripheral area with increased blood flow, red and inflammed
Patho of thermal burns
- Capillary disrupted by secretion of histamine and serotonin
- Can cause burn edema
- Creates massive fluid shifts
- Can cause fluid loss by evaporation
Thermal burns at risk for...
Hypovolemic shock/Burn shock d/t fluid loss
From exposure to a corrosive agent (acids, alkalis)
Extent of chemical burns depends on...
- Amount and concentration
- length of exposure
- Mechanism of chemical action
Tissue destruction by acids
- Forms mass at area on contact causing necrosis and eschar
Tissue destruction from alkalis
- Destroys cell membrane through liquefaction necrosis.
- Deeper tissue penetration
Current travels from once point to another
Complication of electrical burns
- Outer skin may not appear too bad, but it burns from the inside out.
- Cardiac dysrhythmias
From the transfer of radiant energy to the body
Area at risk for radiation burns
- tissues that multiple at a continuous rate
- ie...skin, BVs, intestinal lining, bone marrow
Extreme cold burns
- Exposure to severe cold temps, mircovascular occlusion
- Reperfusion causes additional tissue damage
System-wide complications of burns
- Vascular permeability and edema
- Decreased renal blood flow
- Altered hemodynamics
- Increased gut mucosal permibility
Initial emergency management of burn wounds
- Stop the burning process - cold water, NOT ice.
- Protect the airway, breathing and circulation
- Top layer of skin
- May have blistering and peeling
- Heals 3-5 days
Superficial partial-thickness burns
- into the dermis
- Heals 10-14 days
- Do not break blisters, provide comfort, will be sore underneath
Deep partial-thickness burns
- deep into the dermis
- No blisters
- Heals 2-3 weeks
- May scar and may need skin graft
- Into the subcutaneous layer
- Yellow-leathery appearance
- *No pain
- Will need skin grafts
Deep full-thickness burns
- Deep into the subcutaneous layer
- Can involve muscle, bone, tendons
- May require amputation
Lund and Browder Chart
Percentage of body burned determined by Total BSA
Rule of Nines
- Body divide into areas of 9% and 18% to determine extent of body damage
- Hand and genitals = 1% each
- Head and arms = 9% each
- Legs, chest and back = 18% each
#1 cause of death from burns
- Begins at time of injury
- Lasts 48-72 hours
- Maintain CV and Pulm. stabilization
Cardiovascular effects of burns >40%
- *Decreased CO
- hypovolemic shock
- Increased capillary permeability
- Massive fluid and electrolyte shifts
- 4ml of Ringers x TBSA % burned x wt
- 1/2 given in 1st 8 hours - 1/2 in the next 16 hours
Patient weighing 68kg with 50% TBSA burn
How much fluid should he get?
- 4 x 50 x 68 = 13,600
- 6,800 during first 8 hours
- 6,800 during next 16 hours
Peripheral vascular effects of burns
blood flow is compromised by eschar and compartment syndrome
Signs of limb ischemia
- Reduced sensation
- stiff, non-elastic
- Tough, dead tissue
- Requires emergency escharotomy
opening of the eschar to relieve pressure
Carbon Monoxide poisoning
- Chemical inhalation
- CO attaches to Hbg and does not allow O2 to attach
Confirmation of CO exposure confirmed by...
serum carboxyhemoglobin level
S/S of CO poisoning
Treatment of CO poisoning
- 100% O2
- Aggressive hypobaric O2 therapy
SaO2 with CO poisoning
not accurate -- must use COH levels
lyisMetabolic effects of burns >40% TBSA
Nutritional needs of burn patients
increased calories and protein to maintain immune system and wound healing
Renal effects of burns
Risk for myoglobinuria d/t the release of myoglobin from muscle damage
Myoglobinuria s/s and treatment
- red to reddish brown urine -- signs of ARF d/t clogged tubules
- flush kidneys to maintain output of 75-100mL/hr
Inflammatory stage of wound healing
- lasts 2 weeks
- vasodilation - increased blood flow, increased O2 and increased nutrients
Proliferative phase of wound healing
- last up to a month
- collagen synthesis - skin repair
Maturation phase of wound healing
- Lasts 6-18 months
- Collage strengthens
- hypertrophic collage can become rigid and decrease mobility
Goal of acute rehabilitative phase of burns
- Prevent and control infection
- Preserve viable tissue
- Promote wound closure
- Minimize complications