Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
151 Cards in this Set
- Front
- Back
- 3rd side (hint)
Define SvO2
Normal SvO2? |
Measuring SvO2 provides information about the oxygen saturation of venous blood.
The venous blood from all body systems is considered “mixed” when it has reached the pulmonary artery. The saturation of this mixed venous blood (SvO2) represents an average of the venous saturation of blood from all parts of the body. Normal mixed venous oxygen saturation (SvO2) is 60-80%. |
|
|
What are the two main causes of DECREASE in SvO2?
|
1. Decreased O2 supply
2. Increased O2 consumption |
|
|
List the reasons for DECREASED O2 supply, which causes an overall decrease in SvO2
|
Decreased CO
Heart failure Hypovolemia Dysrhythmias Cardiac depressants (i.e., beta blockers) Decreased O2 sat Respiratory failure Pulmonary infiltrates Suctioning Ventilator disconnection Decreased Hb Anemia Hemorrhage |
|
|
List the reasons for Increased O2 consumption, which causes an overall decrease in SvO2
|
Hyperthermia
Seizures Shivering Pain Increased work of breathing Increased metabolic rate Exercise Agitation |
|
|
What are two main causes of INCREASE in Sv02?
|
1. Increased O2 supply
2. Decreased O2 demand |
|
|
List the reasons for INCREASED O2 supply, which causes an overall increase in SvO2
|
Increased CO
Inotropic drugs Intraaortic balloon pump Afterload reduction **Early septic shock Increased O2 sat Increase FiO2 (inspired O2) Improvement in lung problem Increased Hb Blood transfusion |
|
|
List the reasons for DECREASED O2 demand, which causes an overall increase in SvO2
|
Hypothermia
Fever reduction **Sepsis (late stages) Paralysis Pain relief Anesthesia |
|
|
What is the priority intervention for sepsis?
|
Give Abx!!!
-Key to successful therapy in managing sepsis is early initiation of abx. |
|
|
Situation: Your patient is a 52-year-old man who was admitted to the hospital with severe wound infection in his leg. He was malnourished and in poor health before his arrival. His condition has continued to deteriorate, and septic shock has been diagnosed. His laboratory values reveal decreasing fibrinogen and platelet levels. You are unable to maintain an acceptable mean arterial pressure with IV fluids. The physician prescribes an infusion of dopamine (Intropin). What is the action of this medication?
A) To decrease myocardial oxygen consumption B) To increase cardiac output and mean arterial pressure C) To decrease preload D) To decrease afterload |
B) To increase cardiac output and mean arterial pressure
|
|
|
Situation: Your patient is a 52-year-old man who was admitted to the hospital with severe wound infection in his leg. He was malnourished and in poor health before his arrival. His condition has continued to deteriorate, and septic shock has been diagnosed. His laboratory values reveal decreasing fibrinogen and platelet levels. Your directions are to start the dopamine (Intropin) at 5 mcg/kg/min. Your patient is also placed on a nitroprusside drip to increase cardiac perfusion. What should concern you about the addition of nitroprusside to this patient's regimen?
A) It will cause excessive increase in blood pressure. B) It will potentiate the actions of dopamine. C) It will cause vasodilation of peripheral vessels, possibly increasing symptoms of shock. D) It will increase potential for chest pain and myocardial necrosis. |
C) It will cause vasodilation of peripheral vessels, possibly increasing symptoms of shock
|
|
|
Situation: Your patient is a 52-year-old man who was admitted to the hospital with severe wound infection in his leg. He was malnourished and in poor health before his arrival. His condition has continued to deteriorate, and septic shock has been diagnosed. His laboratory values reveal decreasing fibrinogen and platelet levels. Your directions are to start the dopamine (Intropin) at 5 mcg/kg/min. What should you monitor to determine the medication is working? Select all that apply.
A) Hourly urine output B) Blood pressure every 15 minutes C) Blood glucose D) Serum creatinine |
A) Hourly urine output
B) Blood pressure every 15 minutes Dopamine improves blood flow by increasing peripheral resistance, increasing venous return to the heart, and increasing myocardial contractility. Nursing interventions include assessing the patient for chest pain, measuring urine output hourly, assessing blood pressure every 15 minutes, and assessing the patient for a headache. |
|
|
Situation: Your patient is a 52-year-old man who was admitted to the hospital with severe wound infection in his leg. He was malnourished and in poor health before his arrival. His condition has continued to deteriorate, and septic shock has been diagnosed. His laboratory values reveal decreasing fibrinogen and platelet levels. Your directions are to start the dopamine (Intropin) at 5 mcg/kg/min. Your patient is also placed on a nitroprusside drip to increase cardiac perfusion. What should be monitored in a patient on a nitroprusside drip? Select all that apply.
A) Blood pressure B) Urine output C) Heart rate D) Serum glucose |
A) Blood pressure
B) Urine output C) Heart rate Monitoring vital signs and level of consciousness is a major nursing action to determine the patient's condition and the effectiveness of therapy. Monitor pulse, blood pressure, pulse pressure, central venous pressure (CVP), respiratory rate, skin and mucosal color, oxygen saturation, mental status, and urine output. |
|
|
When caring for a patient admitted with shock of unknown etiology, which action should the nurse take first?
A) Obtain IV access, and hang prescribed fluid infusions. B) Take pulse rate and blood pressure. C) Assess level of consciousness and pupil reaction to light. D) Check the airway and breathing status. |
D) Check the airway and breathing status.
|
|
|
Which action should the emergency department nurse take first when caring for a 75-year-old patient who is complaining of faintness after working in the yard for 6 hours?
A) Auscultate the patient’s breath sounds. B) Obtain a list of the patient’s home medications. C) Check the patient’s blood pressure and heart rate. D) Assess the patient’s skin turgor and mucous membranes. |
C) Check the patient’s blood pressure and heart rate.
The patient's history and complaints of faintness indicate possible early hypovolemic shock; the nurse should first assess circulatory status by determining heart rate and blood pressure. The other assessments should be done after assessing the circulatory status. |
|
|
A patient who had recent oral surgery is admitted with a temperature of 102.4° F (39.1° C), heart rate 118, blood pressure 152/44, and respiratory rate 30. Which of these physician prescriptions should the nurse implement first?
A) Give vancomycin (Vancocin) 1 g IV. B) Infuse normal saline at 250 mL/hr. C) Administer acetaminophen (Tylenol) 650 mg. D) Give hydrocortisone (Solu-Cortef) 500 mg IV. |
A) Give vancomycin (Vancocin) 1 g IV.
This patient's history and clinical presentation are consistent with early septic shock. Administration of antibiotic therapy should occur as quickly as possible to prevent progression to the later stages of septic shock. The other prescriptions should also be implemented quickly, but antibiotic administration is the highest priority for this patient. |
|
|
The nurse assistant is concerned about the postoperative client with a blood pressure (BP) of 90/60, heart rate of 80, and respirations of 12. What does the supervising nurse do?
A) Asks about when vital signs were last taken and their readings B) Calls the surgeon C) Pushes IV fluids D) Reassesses vital signs using different equipment |
A) Asks about when vital signs were last taken and their readings
Vital sign trends must be taken into consideration; a BP of 90/60 may be normal for this client. |
|
|
Which clinical symptoms in the postoperative client indicate early sepsis with an excellent recovery rate if treated?
A) Localized erythema and edema B) Low-grade fever and mild hypotension C) Low oxygen saturation rate and decreased cognition D) Reduced urinary output and increased respiratory rate |
B) Low-grade fever and mild hypotension
Low-grade fever and mild hypotension indicates very early sepsis but, with treatment, there is a high probability of recovery. |
|
|
The nurse is providing discharge teaching to the postoperative client. Which statement by the client indicates the need for further education?
A) ''I must call my doctor if I develop a fever.'' B) ''I will call my provider if I have any pain.'' C) ''If the incision site begins to bleed, I must immediately notify my doctor.'' D) ''If the site becomes red and swollen, I will call my health care provider.'' |
B) ''I will call my provider if I have any pain.''
Some pain is normal for the postoperative client. |
|
|
The client recovering from an open reduction of the femur suddenly feels lightheaded, with increased anxiety and agitation. Which key vital sign differentiates a thrombus from early sepsis?
A) Temperature B) Pulse C) Respiration D) Blood pressure |
A) Temperature
A sign of early sepsis is low-grade fever. |
|
|
The client comes to the emergency department with a history of vomiting for 12 hours. The mucous membranes are dry and the client looks a little dazed and is pale. While starting the IV, what condition is the nurse careful to watch for?
A) Anaphylactic shock. B) Bulimia C) Progressive shock D) Sepsis |
C) Progressive shock
The nurse must vigilantly observe for progressive shock in this client, a stage of hypovolemic shock. |
|
|
Which clinical manifestation is a compensatory mechanism in the initial stage of hypovolemic shock?
A) Decreased urine output B) Elevated body temperature C) Increased heart rate D) Vascular vasodilation |
C) Increased heart rate
Increased heart rate is a compensatory mechanism in the initial stage of hypovolemic shock. |
|
|
Which complete blood count result is most indicative of effective therapy for sepsis?
A) Decreased hemoglobin B) Decreased segmented neutrophil count C) Increased numbers of monocytes D) Increased platelet count |
B) Decreased segmented neutrophil count
A decreased segmented neutrophil count indicates that the body is responding to the sepsis. |
|
|
The client is in the early stage of septic shock. Which drug does the nurse anticipate being prescribed?
A) Antibiotic B) Diuretic C) Cryoprecipitate D) Vasodilator |
A) Antibiotic
The underlying cause of the client's septic shock must be corrected with antibiotics. |
|
|
In anticipation of the need for oxygen, the nurse watches the client's pulse oximetry. In the nonprogressive stage of hypovolemic shock, what does the nurse expect the oxygen saturation to be?
A) Higher than 96% B) 90% to 95% C) 75% to 80% D) Less than 70% |
B) 90% to 95%
A pulse oximetry of 90% to 95% occurs in the nonprogressive stage of hypovolemic shock. |
|
|
The client is admitted with septic shock. The antibiotic dose has arrived at the unit and the client has an IV. What does the nurse do next?
A) Administers the antibiotic immediately B) Ensures that blood cultures were drawn C) Obtains a signed consent D) Takes the client's vital signs |
B) Ensures that blood cultures were drawn
Blood cultures must be drawn from the client with septic shock to identify the organism for more targeted antibiotic treatment. |
|
|
What is shock?
|
Acute circulatory failure leading to inadequate tissue perfusion and end organ injury.
Shock is hypotension with end organ injury. The book defines shock as a sequence of changes that occur when tissue oxygen supply does not meet oxygen demand. |
|
|
What are the main 3 or 4 categories of shock?
|
Book: Hypovolemic, Obstructive, Transport and Cardiogenic
Slides: 3 categories: The pump (heart), the tubing (vasculature), & the fluid (blood). Shock is classified as being due to malfunction of: 1. Cardiogenic & Obstructive = the Pump (heart) 2. Distributive = the “Tubing” (vasculature) 3. Hypovolemic = the Fluid (blood volume) |
|
|
What is hypovolemic shock?
|
Def: Impaired oxygenation because of inadequate cardiac output as a result of decreased intravascular volume. Begins to develop when intravascular volume has decreased by 15%. This is the most common cause of shock.
|
|
|
What is/are the causes/etiology of hypovolemic shock?
|
Etiology: Can result from two conditions:
1. Decreased fluid volume in circulation (fluid volume loss), OR 2. The size of the intravascular compartment has increased in proportion to fluid volume (vasodilation). |
|
|
Hypovolemic shock:
Decreased fluid volume in circulation (fluid volume loss) is caused by: |
• Hemorrhage: loss of blood volume
• Dehydration (inadequate intake, excessive output): loss of intravascular fluid from skin • Burns-results in plasma loss: loss of intravascular fluid from skin • Persistent vomiting or diarrhea: persistent loss of fluid • GI bleed • Abdominal aneurysm rupture |
|
|
Hypovolemic shock:
Condition of... decreased fluid volume in circulation (fluid volume loss) d/t decreased venous return to the right atrium can cause? |
• Reduced ventricular filling pressure
• Decreased stroke volume • Decreased cardiac output • Decreased blood pressure |
|
|
Hypovolemic shock:
Condition of... Increased size of intravascular compartment (vasodilation) in proportion to fluid volume causes? |
– Body in a state of hypovolemia.
– Blood volume may be normal but intravascular space has increased (vasodilation) • Reduced ventricular filling pressure • Decreased stroke volume • Decreased cardiac output • Decreased blood pressure |
|
|
Hypovolemic shock:
Vasodilation occurs with what types of states? |
Vasodilation occurs with neurogenic shock, anaphylactic shock and septic shock
|
|
|
Distributive shock can be divided into what subtypes?
|
Neurogenic shock
Anaphylactic shock Septic shock |
|
|
Describe (subtype) neurogenic shock.
Pathophysiology? Causes? |
Neurogenic shock: loss of sympathetic tone (vasoconstriction) usually from spinal cord injury, causing massive vasodilation (parasympathetic NS dominate) & prohibiting vasoconstriction. Blood pools in dilated peripheral venous system. Rt <3 receives an inadequate venous return & CO decreases.
Trauma, spinal shock, and epidural anesthesia are among the causes. |
|
|
What are the s/s (manifestations) of neurogenic shock?
|
s/s are related to the loss of sympathetic innervation:
Decreased SVR (d/t persistent vasodilation) Lower RAP, PAP, PAWP, CO (from pooling of blood in dilated vessels) Decreased heart rate , < 60 bpm (resulting from decreased parasympathetic innervation) Warm skin (d/t peripheral vasodilation) Hypothermia Absence of sweating below level of spinal cord injury |
|
|
Describe (subtype) anaphylactic shock:
Pathophysiology? Causes? |
- Subtype under distributive (tubing/vasculature) shock
- occurs with severe allergic reactions to foods (peanuts, fish, eggs, milk), drugs (aspirin, Abx, anesthetic agents, blood products), insect venoms, latex. - Massive amts of vasoactive substances (e.g. histamine and kinins) are released from mast cells --> Vasodilation --> increases capillary permeability & increases size of intravascular compartment --> fluid allowed to move from intravascular to interstitial spaces --> hypovolemia Net consequence of combined massive vasodilation & increased cap permerability = decrease in venous return, decrease in CO, and decrease in O2 delivery |
|
|
What are the s/s (manifestations) of anaphylactic shock (subtype)?
|
=> Normal pattern
- Generalized itching - Cutaneous flushing - Urticaria - Fullness in throat - Tightness in chest - Faintness - Loss of consciousness - Anxiety - Severe upper airway obstruction by edema can lead to asphyxia - Lower airway obstruction with wheezing and chest tightness is caused by bronchospasm |
|
|
Describe septic shock (subtype).
Pathophysiology? Causes? |
- Septic shock is a systemic response to invading microorganisms of all types: gram (+/-) bacteria, fungi, or viruses.
-Characterized by: Altered fluid volume r/t vasodilation, increased cap permiability, & maldistribution of circulating volume - Systemic response triggers a complex series of ceelular & humoral events (see Fig. 18-2) - These organisms release endotoxins that invade the bloodstream & stimulate the release of cytokines (i.e. tumor necrosis factor & interleukins) --> produce vasodilation & increased cap permeability --> reduces venous return, & cardiac output decreases. |
|
|
What are the s/s (manifestations) of septic shock (subtype)?
|
=> Normal pattern
- Generalized itching - Cutaneous flushing - Urticaria - Fullness in throat - Tightness in chest - Faintness - Loss of consciousness - Anxiety - Severe upper airway obstruction by edema can lead to asphyxia - Lower airway obstruction with wheezing and chest tightness is caused by bronchospasm |
|
|
Most authorities consider ____ w/n the body, a type of ____ shock
|
fluid shifts; distributive
|
|
|
What characterizes septic shock?
|
Altered fluid volume related to vasodilation increases capillary permeability, and misdistribution of circulating volume
|
|
|
Clinical S/s (manifestations) of ALL shock states are a result of ____ & ______?
|
inadequate O2 delivery; the activation of compensatory mechanisms
|
|
|
Clinical S/s (manifestations) of ALL shock states to be aware of include:
|
REFER TO FIG. 18-5 Multi-system effects of shock p. 483
- Cool skin (d/t volume depletion) - Poor Capillary refill (d/t volume depletion) - Hypotension (d/t fluid volume lost) - Orthostatic changes - Tachycardia - Decrease urine output - Low Right Atrial Pressure (RAP) & Cardiac output (d/t less volume return to rt. Atrium) - Low pulmonary artery wedge pressure - Low pulmonary artery pressure - Elevated SVR |
|
|
What is cardiogenic shock?
Causes/Etiology? |
Def: Impaired oxygenation because the heart fails to function as the pump to circulate the oxygenated blood.
Etiology: Heart fails to function as a pump (d/t MI or dysrhythmias). Cardiogenic shock occur as a result of impaired oxygen delivery d/t cardiac dysfunction. Most common cardiac dysfunction is MI |
|
|
What are some of the problems cardiogenic shock cause?
|
- Right-sided heart failure
- Left-sided heart failure - Acute myocardial infarction - Severe dysrhythmias - Valvular disease - End-stage Cardiomyopathy |
|
|
Clinical S/s of (manifestations) of cardiogenic shock is divided into what two categories?
|
Left-sided heart failure
& Right-sided heart failure |
|
|
Clinical S/s of (manifestations) of cardiogenic shock include:
1. Left-sided heart failure 2. Right-sided heart failure (answer on 3rd side) |
Left-sided heart failure:
- Hypoperfusion - Pulmonary congestion Dyspnea Bilateral crackles Distant heart sounds Third or fourth heart sounds are present - Hemodynamics Elevated PAWP Low cardiac index Sustained hypotension (systolic under 90mm Hg OR mean BP 30 mmHg lower than baseline) |
Right-sided heart failure"
- Systemic venous congestion Peripheral edema Clear lung sounds Split second heart sound d/t delayed closure of tricuspid valve - Hemodynamics Elevated RAP Normal or low PAWP |
|
What is obstructive shock?
Causes/Etiology? |
- Can be considered a subtype of cardiogenic shock
Definition: Form of indirect pump failure. Impaired oxygenation because of mechanical barrier to blood flow in or out of the heart Etiology: Mechanical barrier to blood flow. Occurs as a result of a mechanical barrier to blood flow that blocks oxygen delivery to tissues |
|
|
What are some problems that obstructive shock causes?
|
Pulmonary embolism
Tension pneumothorax Cardiac tamponade |
|
|
Clinical S/s of obstructive shock fall under which primary types of mechanical problems?
|
Cardiac tamponade
Tension pneumothorax Pulmonary embolism |
|
|
Clinical S/s of obstructive shock:
seen w/ Cardiac tamponade are... |
• Pulsus paradoxus-exaggerated decrease > 10 mmHg of the systolic BP during inspiration. Normally during inspiration, systolic blood pressure decreases ≤10 mmHg, and pulse rate goes up slightly.
• Muffled heart sounds • Some pts may have s/s of dysphoria • Pericardial friction rub • Elevated RAP equal to PAWP • Decreased blood pressure* |
|
|
Clinical S/s of obstructive shock:
seen w/ Tension pneumothorax are... |
• Tracheal deviation
• Poor ventilation • Increases pleural pressure • Decreased breath sounds • Decreased venous return • Decreased CO • Bradycardia |
|
|
Clinical S/s of obstructive shock:
seen w/ Pulmonary embolism are... |
• Dyspnea – most frequent SYMPTOM*
• Tachypnea – most frequent SIGN* • Pleuritic pain • Cough • Hemoptysis • T wave inversion • Cyanosis indicates massive pulmonary emboli |
|
|
What is distributive shock?
Causes/Etiology? |
Def.: widespread vosodilation & increased cap permeability
- Leak of Fluid to interstitium-3rd spacing - Increased Intravascular Compartment - Vasodilation causes blood to pool in venous compartment Neurogenic shock-loss of vasomotor tone after spinal cord injury Anaphylactic shock-inflammatory mediators vasodilate Sepsis |
|
|
What is transport shock?
Causes/Etiology? List causes. |
Def: Impaired oxygenation related to a diminished supply of hemoglobin, thereby reducing oxygen getting to the tissues
Etiology: Diminished supply of Hgb to carry oxygen. Anemia Carbon monoxide poisoning Hemorrhage Low hematocrit & hemoglobin |
|
|
Clinical S/s of transport shock include:
|
carbon monoxide poisoning symptoms
- headache - malaise - nausea - difficulty with memory - personality changes - elevated carboxyhemoglobin levels |
|
|
Tradition/hallmark signs of shock state (what to look out for on the unit) include:
|
- Decreased blood pressure (hypotension)
- Tachycardia - Reduced mentation - Inadequate urine output |
|
|
Define sepsis (how to suspect)
|
The systemic response to infection is manifested by two or more of the following conditions:
1. Temp > 38C or < 36C 2. HR > 90 bpm 3. RR > 20 breaths/min or PaCO2 > 32 mmHg 4. WBC count > 12,000/mL or < 4,000/mL OR > 10% immature (band) forms |
|
|
Define severe sepsis (how to suspect)
|
Sepsis associated w/ organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion & perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status.
|
|
|
Define septic shock
|
Sepsis associated w/ hypotenion despite adequate fluid resuscitation along w/ the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status.
|
|
|
Pharm managment of shock states (tx of shock) involve (3 ways):
|
1. treat underlying cause: varies by shock state
2. optimize oxygen delivery: inotropic agents, vasopressors drugs, vasodilators, combination tx 3. decrease oxygen consumption: decrease total body work, decrease pain, decrease anxety, decreased temperature |
|
|
Pharm managment of shock states (tx of shock):
Optimizing Oxygen Delivery involves: |
Crystalloid solutions (e.g. lactated ringers) restore interstitial and intravascular fluid volumes, increase preload and cardiac output. P.485
Colloid solutions: enhance the blood’s oxygen-carrying capacity Positive inotropic drugs: to increase contractility, which increases stroke volume and cardiac output Dopamine, dobutamine, & milrinone Dopamine: non selective. Increases Cardiac Output. Large doses can increase BP. Dobutamine: selective beta 1. Increases contractility, cardiac output, SVR Milrinone: increases contractility, reduces SVR, and improves CO Inotropic drugs increase myocardial oxygen consumption Vasoactive drugs: act on smooth muscle layer of blood vessels and affect preload and afterload Vasopressors or vasodilators Vasopressors: mimic SNS and increase blood flow to vital organs by increasing BP and CO - Epinephrine, norepinephrine, dopamine, vasopressors Vasodilators: reduce afterload, improve CO and O2 delivery. - Nitroprusside, Nitroglycerine - Afterload drugs should be given to pts w/ adequate fluid volume |
|
|
Pharm managment of shock states:
Tx of sepsis involve... |
Antibiotics!!!! First line tx.
Key to successful therapy in managing sepsis is early initiation of antibiotics Broad spectrum antibiotics and antifungals Duration of therapy usually 7-10 days but will take longer in immunocompromised patients Choice of antibiotic depends on most likely organisms involved & origin Most likely origin can be estimated to choose drug - After chemotherapy GI flora organisms (gram negative flora). Use: aminoglycoside and cephalosporins - Indwelling Catheter infection Staphylococcus. Use: Vancomycin - Oral infection (i.e. after chemo) Streptococcus or Candida (fungal). Use: Nystatin - Aspiration pneumonia. Use: Clindamycin Vasopressors: Levarternol (for sepsis) |
- Vasopressors: the primary problem in sepsis is inappropriate vasodilation with resultant distributive shock – 3 main choices
- Primary Vasopressor: Levarterenol (Levophed; 0.05 - 1.0 mcg/kg/min) is an alpha adrenergic vasopressor with some limited beta adrenergic properties and is the first line drug for most patients Other Vasopressors used: Dopamine & Phenylephrine - dopamine (2.5 - 20 mcg/kg/min) is a beta adrenergic vasopressor with some alpha adrenergic properties that is an alternative to levarterenol in some patients, particularly those who have accompanying myocardial dysfunction - phenylephrine (Neosynephrine; 0.5 - 10 mcg/kg/min) is a pure alpha adrenergic vasopressor with no beta adrenergic properties that is particularly useful when it is necessary to avoid tachycardia (eg, sepsis in the setting of atrial fibrillation) Inotropes for Sepsis: Doubutamine - Patho: Depressed myocardial contractility can occur with metabolic acidosis or if cardiogenic shock is involved - Dobutamine is drug of choice Insulin: - Hyperglycemia is common in severe sepsis. Blood glucose is frequently monitored and a continuous infusion of insulin and glucose may be used to maintain target blood glucose levels |
|
What is SIRS?
|
= severe inflammatory response to an initiating event; usually a complication of an infection
e.g. sepsis is a type of SIRS (think septic shock!) but it can also be initated by noninfectious disorders such as: acute trauma; pancreatitis; major surgery; burns |
|
|
SIRS is characterized by two or more of the following....
|
Criteria:
- temp > 38 or < 36 - HR > 90 bpmin. - RR > 30 breaths/min or PaCO2 < 32 mmHg - WBC count > 12,000 OR < 4,000 OR > 10% immature (band) forms |
|
|
Pathophysiology of uncontrolled systemic inflammation that characeterizes SIRS....
|
Proinflammatory mediators release nitric oxide --> vasodilations (IL, TNF, Histamine + others)
-Neutrophils cause increased vascular permeability -Mediators effect the function of the endothelium allowing hyper coagulation in the microcirculation--clotting factors get used up in microclots -This unregulated release of inflammatory mediators or cytokines may elicit toxic rxns --> potentially fatal sepsis syndrome. |
|
|
SIRS is basically....
|
hypercoagulability leading to multiple clots forming
|
|
|
Define MODS
|
Multiple Organ Dysfunction Syndrome:
altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis; usually involves at least two or more organ systems |
|
|
What contributes to the development of MODS?
|
- Microvascular thrombosis* - important factor
- Tissue factor released in response to presence of endotoxin or inflammatory cytokines --> activates factor VII of extrinsic pathway of the coagulation cascade --> formation of fibrin clots Fibrin clots play critical role in hemostasis & localizing microorganisms but these microvascular clots impede blood flow & oxygen delivery to cells --> leading to further release of inflammatory mediators. - Anticoag mechs such as activated protein C are impaired. |
|
|
What is the most common hematologic dysfunction in MODS?
Most severe? |
Thrombocytopenia s/t increased consumption, sequestration of platelets in the vasculature, & impaired thrombopoesis as a result of bone marrow suppression.
Disseminated Intravascular Coagulation (DIC) |
|
|
Define DIC
|
Disseminated Intravascular Coagulation (DIC): widespread intravascular clotting that uses up clotting factors in microclots. As a result, patient has no reserves for making clots when needed.
|
|
|
What S/s should you look out for in identifying DIC?
|
spontaneous hemorrhage into body cavities, bleeding from body orifices, IV sites may ooze, surgical wound leak fluids/blood, prolong bleeding, renal failure, ecchymosis, cool& mottled skin,cyanosis
|
|
|
What lab data should you see in DIC?
|
low platelet count, prolonged INR, high levels of D-Dimer and Fibrin Split Products (FSP) (D-Dimer and FSP are released when fibrin and/or fibrinogen are broken down.
|
|
|
Explain microvascular coagulopathy and how it develops into MODS
|
- It is important factor in development of MODS.
Important factor in the development of MODS Initiated through tissue factor on the endothelial cell membrane Formation of fibrin clots Impairment of activated Protein C |
|
|
What is an indirect measure of impaired oxygenation and shock?
|
Measure serum lactate levels
Normal levels: < 2 mMol/L. Lactate is a by-product of shock states in which there is impaired O2 delivery to meet cellular O2 demands leading to production by anaerobic metabolism |
|
|
What do lactate levels indicate?
How can you determine a pt's likelihood of survival and chance of organ dysfunction? |
Indicates a degree of hypoperfusion. Hyperlactemia can produce metabolic acidosis
Pt. whose lactate levels return to normal w/n 24 hrs have increased survival rates & decreased occurrence of organ dysfunction |
|
|
Define the "normal" or usual function of activated protein C in the body
|
Activated protein C mediates anticoagulation mechanisms.
-Protein C is activated in the presence of thrombin that is bound to thrombomodulin. Activated protein C acts as a feedback messenger to inhibit further thrombin generation. -In addition to its antithrombotic properties, activated protein C has anti-inflammatory and profibrinolytic properties. |
|
|
How is activated protein C (APC) altered in sepsis?
|
Under normal circumstances, microscopic clots, formed as a result of the coagulation cascade, are degraded by the body's fibrinolytic system.
-In sepsis: APC, a key component of fibrinolysis, is consumed at such a rate that clot dissolution is impeded. APC also plays a role in anti-inflammatory properties |
|
|
How can APC be given therapuetically if given as an IV replacement to tx sepsis?
|
- Studies indicate that administration of activated protein C improves outcomes of patients with sepsis.
Activated protein C (drotregin alfa; Xigris) effects in septic shock: reduces intravascular coagulation, reduces adherence of monocytes and neutrophils to endothelium, reduces IL-1, TNF, and IL-6 production Exerts antithrombotic and anticoagulation effects by inhibiting clotting factors Va and VIIIa. Exerts anti-inflammatory effects by inhibiting mediators and the thrombin-induced inflammatory responses of the endothelium. |
|
|
What is/are contraindications to giving Xigris (an APC)?
|
Increases the risk of bleeding. Xigris is contraindicated in patients with the following clinical situations:
• Active internal bleeding • Recent (within 3 months) hemorrhagic stroke • Recent (within 2 months) intracranial or intraspinal surgery, or severe head trauma • Trauma with an increased risk of life-threatening bleeding • Presence of an epidural catheter • Intracranial neoplasm or mass lesion or evidence of cerebral herniation |
|
|
What are important nursing implications for Drotrecogin alpha (Xigris) (recombinant form of APC)?
|
- Monitor closely for s/s of hemorrhage, stop infusion immediately for s/s of clinically important bleeding.
- D/c two hours before invasive procedure. Monitor prothrombin time |
|
|
Patients at risk for sepsis and septic shock include:
|
- Malnutrition
- Immunosuppression - Large, open wounds - Mucuous membrane fissures in prolonged contact w/ bloody or drainage-soaked packing - GI ischemia -Exposure to invasive procedures - Malignancy - Older than 80 years - Infection w/ resistant microorganisms - Receiving CA chemo - Alcoholism - DM - Chronic kidney disease - Transplantation recipient - Hepatitis - HIV/AIDS |
|
|
What are the hallmark signs of sepsis to look out for (Iggy)?
|
- An increasing serum lactate level
- A normal or low total WBC count - A decreasing segmented neutrophil level w/ a rising band neutrophil level --> Left shift |
|
|
Identity s/s associated w/ sepsis
|
Sepsis: the systemic response to infection is manifested by two or more of the following
conditions: 1. Temperature >38 C (100.4 F) or <36 C (96.8 F) 2. HR > 90bpm 3. RR >20 or PaCO2 < 32mm Hg 4. WBC count >12,000/mL or <4,000/mL or >10% immature (band) forms |
|
|
Discuss antibiotic (abx) management guidelines for tx sepsis
|
– Key to successful therapy in managing sepsis is early initiation of abx (w/n 1 HOUR after a HCP initiates the order!!!)
– Broad spectrum abx and antifungals – Duration of therapy usually 7-10 days but will take longer in immunocompromised patients – Choice of antibiotic depends on most likely organisms involved. – Most likely origin can be estimated to choose drug **Antibiotic Therapy—For diff causative sources of sepsis |
|
|
Drug management of tx sepsis:
What do you give for a pt post-chemo w/ GI flora organisms (gram negative flora)? |
Use aminoglycoside and cephalosporins
|
|
|
Drug management of tx sepsis:
What do you give for a pt w/ an indwelling catheter infection? |
For Staphylococcus infection --> Use Vancomycin
|
|
|
Drug management of tx sepsis:
What do you give for a pt w/ an oral infection (i.e. after chemo)? |
Streptococcus or Candida (fungal) ---> Use Nystatin
|
|
|
Drug management of tx sepsis:
What do you give for a pt w/ aspiration pneumonia? |
Use Clindamycin
|
|
|
Patients at risk for developing Disseminated Intravascular Coagulation (DIC) include:
|
• over the age of 45
• advancing ager of all organ systems • pts with cirrhosis, ischemic heart dz, COPD, DM • Impaired stress response |
|
|
What is/are the rationale(s) for using heparin therapy with DIC?
|
- With DIC, make sure to treat the underlying cause. Etiology determines exact therapy needed
- Most of the drugs used same as sepsis therapy since the two usually part of a continuum of illness - Heparin use: o Controversy over effectiveness o Irony of therapy: using anticoagulant that promotes bleeding to treat bleeding disorder o Rationale for therapy: In DIC, clotting factors are used up in microcirculation. Heparin blocks fibrin formation and can prevent further progression of clotting cascade. |
|
|
Identify the components of cerebral tissue perfusion.
What is the formula for CPP? |
Involves the following:
Arterial circulation Venous circulation Cerbral oxygenation CPP formula: It is the difference between the mean arterial pressure (MAP) and ICP CPP = MAP – ICP |
|
|
Cerebral tissue perfusion components:
Arterial circulation involves... |
• Cerebral arteries
• Thinner • More delicate • 2 major pairs right and left internal carotid arteries right and left vertebral arteries join to form Circle of Willis |
|
|
Cerebral tissue perfusion components:
Venous circulation involves.... |
• Craniospinal veins
Valveless Drain by gravity • Venous pressure reflect intracranial pressure (ICP) |
|
|
Cerebral tissue perfusion components:
Cerebral oxygenation involves... |
- Since brain requires continuous supply of glucose, oxygen, and substrates for energy b/c it cannot store oxygen, and its glucose reserves last for only a few minutes, the brain attempts to regulate by increasing or decreasing CBF as needed. --> localized matching of CBF with cerebral metabolism through the use of autoregulation
- When CBF is inadequate to meet the brain’s metabolic needs, a state of mismatching occurs, and ischemia results --> Anaerobic metabolism --> produce lactate build-up. |
|
|
What is autoregulation? How does it promote cerebral oxygenation?
|
Autoregulation: a protective capacity of cerebral arterioles to alter their blood flow within an average systemic arterial pressure limit of 60-130 mm Hg in adults, thereby promoting a constant blood supply to the brain irrespective of systemic blood pressure fluctuations
• When systemic blood pressure increases, cerebral arterioles constrict • When systemic blood pressure decreases, cerebral arterioles dilate, ensuring adequate cerebral perfusion |
|
|
Autoregulation maintains an average systemic arterial pressure limit of _____ in adults
|
60-130 mmHg
|
|
|
What is the normal range for CPP?
Ischemia occurs when? What should you watch out for regarding CPP in order for a pt to receive adequate cerebral oxygenation? |
- Normal range: 80-100 mm Hg
- Ischemia occurs with 40-70 mm Hg - Must be >70 mm Hg to ensure adequate cerebral oxygenation. In managing patients with elevated ICP, target goal is to keep CCP around 80 mm to avoid ischemia. - If ICP RISES to level of MAP, brain perfusion ceases and brain death occurs. |
|
|
What is your first check/assessment indicator of a pt's adequate cerebral tissue perfusion?
|
Change in Level of Consciousness (LOC) Is the First Sign of Neurologic Deterioration
Neuro checks are done q2hrs on a critical unit Call physicians ASAP. Pt going back to CT. Changes in neuro of 2pt decrease call physician! |
|
|
Etiology for impaired consciousness is _____
|
VOWEL & TIPPS:
Vowel Alcohol Epilepsy Insulin Opiates Urates (renal failure) TIPPS Trauma Infection Psych Poisons Shock |
|
|
How do changes (elevations or decreases) in blood pressure and ICP alter CPP?
|
BP:
- If increased, will cause MAP [ MAP = SBP + 2(DBP)/3 ] to increase, therefore CPP [CPP = MAP - ICP] will increase proportionally assuming ICP remains low. - If decreased, the opposite is true. ICP: If elevated due to factors that increase ICP such as in cranial surgery, increased CBF, increased intrathoracic pressure, or decreased cerebral venous drainage (Table 20-2), will decrease the CPP. |
|
|
What are the main components of the intracranial vault?
|
Brain (volume), cerebral blood volume, and cerebrospinal fluid (volume)
|
|
|
How do changes (elevations or decreases) in blood pressure and ICP alter CPP?
|
BP:
- If increased, will cause MAP [ MAP = SBP + 2(DBP)/3 ] to increase, therefore CPP [CPP = MAP - ICP] will increase proportionally assuming ICP remains low. - If decreased, the opposite is true. ICP: If elevated due to factors that increase ICP such as in cranial surgery, increased CBF, increased intrathoracic pressure, or decreased cerebral venous drainage (Table 20-2), will decrease the CPP. |
|
|
What are the main components of the intracranial vault?
|
Brain (volume), cerebral blood volume, and cerebrospinal fluid (volume)
|
|
|
CPP depends on all of the following (choose all that apply)
a. cerebral blood volume b. brain volume c. CSF volume d. cerebral medullary regulation |
a. cerebral blood volume
b. brain volume c. CSF volume |
|
|
CPP must be greater than ____ mmHg to ensure adequate cerebral oxygenation.
|
70 mmHg
|
|
|
Your patient's MAP is 80 mmHg and the ICP is 15 mm Hg. What is the cerebra perfusion pressure?
|
65 mm Hg
|
|
|
Interventions for patients w/ decreased CPP include mechanisms to (choose all that apply)
a. increase MAP b. increase ICP c. decrease ICP d. decrease MAP |
a. increase MAP
c. decrease ICP |
|
|
According to the Monro-Kellie hypothesis, an increase in one intracranial compartment must be accompanied by a reciprocal
a. decrease in another compartment b. increase in the blood-brain barrier c. decrease int he blood-brain barrier d. increase in another compartment |
a. decrease in another compartment
|
|
|
ICP remains relatively stable and, under normal conditions, it is usually less than _____.
|
15 mm Hg
|
|
|
Normal adult CSF pressure in the supine position is
a. 1-5 mmHg b. 5-13 mmHg c. 13-20 mmHg d. 50-200 mmHg |
b. 5-13 mmHg
|
|
|
Which of the following is a cause of increased ICP?
a. decreased CBF b. decreased CSF production c. increased cerebral venous drainage d. increased intrathoracic pressure |
d. increased intrathoracic pressure
|
|
|
Conditions that INCREASE cerebral blood flow (CBF) and cerebral blood volume (CBV) include:
|
-Systemic hypotension
-Increase in body metabolic rate (fever, pain) -Systemic acidosis (hypercapnia, ischemia) -Cerebral vasodilation |
|
|
Conditions that DECREASE cerebral blood flow (CBF) and cerebral blood volume (CBV) include:
|
-Systemic hypertension
-Decrease in body metabolic rate (sedation, pralysis, hypothermia) -Systemic alkalosis (hypocapnia) -Cerebral edema -Low cardiac output -Cerebral vasoconstriction |
|
|
Blood-brain barrier is permeable to _______
|
Water
Oxygen Lipid-soluble compounds CO2 Electrolytes (slightly) Most drugs DO NOT cross BBB. General anesthetics are designed to be highly lipid soluble & small m.w. to cross BBB. |
|
|
The Monro-Kellie hypothesis state s that increases in the adult intracranial vault
a. are initially well tolerated through compensatory mechanisms b. are tolerated well b/c of flexibility of the cranial vault c. can be compensated for only by CSF buffering techniques d. usually result in death because the vault is unable to accomodate increases in volume |
a. are initially well tolerated through compensatory mechanisms
|
|
|
Causes of increased ICP include:
|
Cranial surgery
-Blood clot/hematomas -Pneumocephalus (air) -Cerebral edema Increased CBF -Increased BP -Increased PaCO2 -Decreased PaO2 -Vasodilator drugs (nitroprusside, nitroglycerine) Increased intrathoracic pressure -Coughing -Straining (valsalva) -Suctioning -PEEP Decreased cerebral venous drainage -Supine position w/ head of bed flat -Neck flexion/rotation |
|
|
Which mechanism controls brain volume?
a. cerebral blood flow b. displaement of CSF c. blood-brain barrier d. vasoconstriction |
c. blood-brain barrier
|
|
|
Which of the following components of intracranial volume is displaced most easily and rapidly?
a. brain volume b. cerebral blood volume c. CSF d. cranium |
c. CSF
|
|
|
Cerebral blood vessels dilate in response to
a. increased serum oxygen b. increased serum CO2 c. systemic HTN d. decreased serum CO2 |
b. increased serum CO2
|
|
|
Generally, what causes an increase in CSF?
|
- Increased production (hydrocephalus)
- Obstructed circulation (mass, lesions, infections) - Decreased absorption (subarachnoid hemorrhage, meningitis) |
|
|
Cerebral vasodilation and increased blood volume occurs with conditions that produce ____ and _______?
Examples of these include: |
hypercapnia; hypoxemia
E.g.: Chronic respiratory insufficiency Inadequate ventilation Hypoventilation Sedation by drugs Insufficient supplemental oxygen |
|
|
Flexion of the neck may cause elevation in intracranial volume (ICP) by
a. causing a decrease in venous outflow b. causing an increase in venous return c. causing cerebral vasodilation d. increasing venous outflow |
a. causing a decrease in venous outflow
|
|
|
What are the functions of CSF?
|
Cushion and support the brain and spinal cord
Maintain stable chemical milieu for CNS Excrete toxic waste: CO2, lactate, H+ ions |
|
|
What interventions can you perform to lower a pt w/ high ICP?
|
Place pt w/ high ICP in a LOW STIMULATION ROOM (i.e. low light, closed blinds, no touch, no talking, etc.)
This is b/c ICP tends to have constant fluctuations in response to changes in respiratory rate, body position, coughing, and sneezing |
|
|
An increase in brain volume can result in
a. herniation b. cerebral vasodilation c. cerebral edema d. intracranial hypertension |
a. herniation
|
|
|
List the four possible herniation syndromes
|
-Cingulate herniation
-Central or transtentorial herniation -Uncal or lateral transtentorial herniation -Tonsillar herniation |
|
|
A downward shift of brain tissue through the foramen magnum which results in compression of the medulla and upper cervical spinal cord is called a(n)
a. cingulate herniation b. uncal transtentorial herniation c. lateral transtentorial herniation d. tonsillar herniation |
d. tonsillar herniation
Really bad prognosis if happens. No tx available for this! |
|
|
Lateral shift of brain tissue, usually as the result of a lesion in one of the cerebral hemispheres is called a(n)
a. cingulate herniation b. uncal transtentorial herniation c. transtentorial herniation d. tonsillar herniation |
a. cingulate herniation
Occurs when the cingulated gyrus is compressed under the falx cerebri |
|
|
Lateral and downard shift of brain tissue, usually the temporal lobe, as a result of lesions located most laterally, such as the middle fossa in the temporaral lobe; this type of herniation causes compression of the oculo nerve, or CN III, AEB classic sign of a unilaterally dilated pupil is called a(n)
a. cingulate herniation b. uncal transtentorial herniation c. central herniation d. tonsillar herniation |
b. uncal (or lateral) transtentorial herniation
Very serious. Try to intervene! |
|
|
Downward shift of one or both cerebral hemispheres, usually b/c of lesions in the frontal or parietal lobes is called a(n)
a. cingulate herniation b. uncal transtentorial herniation c. central herniation d. tonsillar herniation |
c. central (or transtentorial) herniation
|
|
|
Suppose a pt is admitted w/ a BP of 90/50, MAP of 49. The ICP is 15. What is the CPP? Should further interventions be needed for this pt to ensure adequate perfusion?
|
CPP = MAP - ICP
CPP = 49 -15 = 34 You need to have a CPP > 70 to perfuse the brain. |
|
|
Suppose a pt is admitted w/ a BP of 149/72, MAP is 84. The ICP is 12. What is the CPP? Should further interventions be needed for this pt to ensure adequate perfusion?
|
If the BP is 149/72 MAP is 84, ICP is 12,
84-12=72. CPP is 72 which is > 70 brain is being perfused. No further interventions needed at this time. |
|
|
What are clinical s/s of increased ICP?
|
• Severe headache
• Decreased level of consciousness (LOC), restlessness, irritability • Dilated or pinpoint pupils that react sluggishly or are nonreactive • Altered breathing pattern (central neurogenic hyperventilation, Cheyne-Stokes respirations, apnea) • Decreased motor function sometimes accompanied with abnormal posturing (decorticate, decerebrate, or flaccidity) • Cushing reflex (--> triad) is a late neurological response resulting in severe hypertension with widening pulse pressure and bradycardia |
|
|
Differentiate between decorticate VS decerebrate posturing
Which indicates a more condition? |
Decorticate Posturing
Abnormal flexion=upper arms move upward to the chest; elbows, wrists, and fingers flex Indicates cerebral hemisphere dysfunction Decerebrate Posturing = an ominous sign!!!!!! Abnormal extension= neck is extended with jaw clenched; arms pronate and extended straight out; feet are plantar flexed Indicates brainstem dysfunction More ominous sign |
|
|
Explain the categories of Glascow Coma Scale assessment.
What is normal? What does low scores mean? |
The Glascow Come Scale (GCS) is the most frequently used assessment tool to identify changes in arousal. The scale assesses eye opening, verbal response, and best motor response to stimuli
• The best possible score is 15 and the lowest score is 3. A score less than 7 in consistent with a significant alteration in level of consciousness (coma state). • Any deterioration in the GCS score is significant and requires immediate physician notification to allow for early intervention and prevention of further neurologic compromise. |
|
|
In what patient conditions is the Glascow Coma Scale use contraindicated?
|
- Patients with periorbital edema who are unable to open their eyes receive an eye opening score of 1, which may or may not be valid.
- Motor deficits, such as hemiparesis or paraplegia, may be overlooked because the motor response scored is the best response elicited. - Finally, it is impossible to evaluate a verbal response for patients who are intubated or have a tracheostomy; they also receive a score of 1, which may not be valid. There may also be some limitations in the pediatric population. |
|
|
Differentiate between primary and secondary brain injury patterns.
|
- Primary injury: occurs when neurons sustain direct injury from the offending event (e.g., a person’s head striking the dashboard resulting in DAI [diffuse axonal injury] during a motor vehicle crash). The primary injury in this case is the shearing of the axons.
- Primary injury is immediate and often irreversible damage. - Secondary injury: occurs in response to the primary injury. Four causes of secondary injury: 1. Ischemia 2. Neuronal death 3. Cerebral swelling 4. Inflammation - Collaborative interventions are directed at preventing these causes of secondary injury in order to maximize positive patient outcomes. Many of the traditional methods to prevent secondary injury target the reduction of intracranial pressure (ICP) and the improvement of cerebral perfusion pressure (CPP), thus minimizing ischemic injury to the brain. |
|
|
What is ICP monitoring?
|
- Classified by the anatomic placement of the device, uses a device, placed inside the head, which senses the pressure inside the skull and sends its measurements to a recording device.
- Can be used for both diagnostic and therapeutic purposes. |
|
|
Which of the following ICP monitoring systems is the most accurate and reliable, and allows for drainage of CSF?
a. intraventricular catheters b. intraparenchymal catheters c. subarachnoid bolt d. epidural catheters |
a. intraventricular catheters
• Gold Standard-used for both diagnostic and therapeutic purposes • Diagnostically most reliable provides precise and consistent wave forms • Therapeutically CSF can be drained from intraventricular cavity, thereby decreasing CSF compartment and reducing ICP • Drainage can be continuous or intermittent • Continuous drainage is open system whereby CSF automatically drains when ICP exceeds a certain point which is determined by how high or low drainage bag is placed above the foraman of Munro-anatomic landmark-top of outer ear • At risk for infection and bleeding because it is the most invasive of the monitoring devices • Wagner says not to use this one in pts with severe cerebral edema or small collapsed ventricles |
|
|
What kinds of ICP monitoring placements are there?
|
intraventricular catheters
intraparenchymal catheters subarachnoid bolt epidural catheters |
|
|
What is the goal of managing CPP?
|
Control blood pressure-IV fluids to maintain euvolemia, vasoactive agents
Temperature-important to control to avoid hyperthermia which raises cerebral metabolism Venous return-body position, HOB 30-45 degrees |
|
|
Pharmacologic ways to manage DECREASED cerebral perfusion include:
|
Opioid narcotics-fentanyl, morphine
Benzodiazepines-midazolam (Versed), or lorazepam (Ativan) Sedative—Hypnotics-propofol Chemical paralysis-vecuronium |
|
|
Pharmacologic ways to manage INCREASED cerebral perfusion:
|
Osmotic diuretics
o Mannitol (0.5 – 1.5 Gm/kg) given to reduce cerebral edema. o Monitor Serum osmolality, electrolytes o Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma Loop diuretics: o Lasix (40 mg) given to reduce cerebral edema. Corticosteroids : o Decadron - for treatment of edema post tumor resection. Barbiturates-no longer a first line therapy for elevated ICP o Phenobarbital – CNS depression and reduce seizures. o Pentobarbital – Treatment for uncontrolled ICP > 20 mm Hg o Uses: head injury or intracranial hypertension management that hasn’t responded to first line therapies Anticonvulsants: o Dilantin – Infuse in Normal Saline solution “only!!!” o Cardiac Monitor o Serum levels; therapeutic range 10 – 20 cg/ml. Calcium Channel Blockers: o Nimotop – Used to decrease cerebral vasospasm. |
|
|
What is a called when there's a sustained elevation in ICP and is potentially life threatening?
|
Intracarnial hypertension
|
|
|
When administering mannitol to a patient, the nurse should monitor which of the following lab tests?
a. serum osmolality b. urine sodium c. serum calcium d. serum potassium |
a. serum osmalality
|
|
|
What are the first goals in treating traumatic brain injury?
|
Limit the primary ischemic tissue injury by aggressive prevention & tx of hypoxia & hypotension
--> Use supplemental oxygen & mech ventilation to maintain PaO2 > 60 mmHg & PaCO2 between 35-40 mmHg. |
|
|
Leveled approach for tx of elevated ICP involves:
|
Level 1: Pain & sedation medications
Maintain normothermia Pt. positioning w/ head-of-bed elevation & midline neck alignment Lvl 2: Consideration of external ventricular drainage Hyperosmolar therapy Mech. vent maintaining PaO2 > 60 mmHg & PaCO2 35-60 mmHg Lvl 3: NM blockade; Mild hyperventilation; mild hypothermia Lvl 4: Barbiturate coma; decompression craniotomy |
|
|
Secondary injury is caused by
a. hypoxia & ischemia b. cerebral swelling c. inflammation of cerebral tissue d. all of the above |
d. all of the above
|
|
|
What do you give for autonomic hyperreflexia?
|
Give Nifedine, Hydralizine, Nitro for Spinal cord autonomic hyperreflexia
|
|