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NURS 425 > Exam #1: Shock, SIRS And MODS > Flashcards

Exam #1: Shock, SIRS And MODS Flashcards

1
Q

What is shock?

A
  • Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
  • Imbalance in supply/demand for O2 and nutrients
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2
Q

Add stuff that was on the board

A

*Listen to lecture for more clarification

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3
Q

Low dose of dopamine can cause (<2mcg/min)

A

Vasodilation

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4
Q

If we give dopamine at 5-10mcg/kg/min, what while happen

A

It will stimulate beta1 adrenergic receptors -> increases contractility of the heart -> increases CO

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5
Q

If you give dopamine at >10 mcg/kg/min, it will cause

A

Vasoconstriction

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6
Q

Dobutamine

A

Causes vasoconstriction.

*may need more info

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7
Q

Nitro/Nitroprusside

A

Vasodilators

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8
Q

Norepinephrine aka Levophed

A

Drug of choice.

Listen to lecture for more info.

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9
Q

What are the classifications of shock?

A
  1. Cardiogenic Shock
  2. Hypovolemic
  3. Distributive
  4. Obstructive
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10
Q

What is Cardiogenic Shock?

A
  • Systolic (hearts inability to pump the blood forward) or diastolic dysfunction
  • Compromised cardiac output (CO)
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11
Q

What can cause cardiogenic shock?

A
  • Myocardial infarction
  • Cardiomyopathy
  • Blunt cardiac injury
  • Severe systemic or pulmonary hypertension
  • Cardiac tamponade
  • Myocardial depression from metabolic problems
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12
Q

What is the pathophysiology of cardiogenic shock caused by systolic dysfunction?

A

Slide 6

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13
Q

What is the pathophysiology of cardiogenic shock caused by diastolic dysfunction?

A

Slide 6

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14
Q

What are early manifestations of cardiogenic shock?

A
  • Tachycardia
  • Hypotension (<90)
  • Narrowed pulse pressure (diastolic and systolic BP come closer together)
  • ↑ Myocardial O2 consumption
  • ↑ Pulmonary artery wedge pressure
  • Decreased renal perfusion and urinary output
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15
Q

What are physical assessment findings that you would find in a patient with cardiogenic shock?

A
  • Tachypnea, pulmonary congestion
  • Pallor and cool, clammy skin
  • Decreased capillary refill time
  • Anxiety, confusion, agitation (Ativan, morphine could be helpful)
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16
Q

Hypovolemic Shock

A
  • Loss of intravascular fluid volume

- Either absolute or relative hypovolemia

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17
Q

What can cause hypovolemic shock?

A
  1. Absolute Hypovolemia:
    - Hemorrhage
    - GI loss (e.g., vomiting, diarrhea)
    - Fistula drainage
    - Diabetes insipidus
    - Hyperglycemia
    - Diuresis
  2. Relative hypovolemia
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18
Q

What is relative hypovolemia?

A
  • Results when fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary space)
  • Termed third spacing
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19
Q

Describe the pathophysiology of hypovolemic shock.

A

Slide 11

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20
Q

Hypovolemic Shock: Response to acute volume loss depends on

A
  • Extent of injury
  • Age
  • General state of health
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21
Q

What are clinical manifestations of hypovolemic shock?

A
  • Anxiety
  • Tachypnea
  • *Increase in CO, heart rate
  • Decrease in stroke volume, Pulmonary Artery Wedge Pressure, urinary output
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22
Q

Hypovolemic Shock: What is done if loss is >30%?

A

Compensatory mechanisms may fail and immediate replacement of blood products should be started

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23
Q

What is neurogenic shock?

A
  • Hemodynamic phenomenon
  • Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
  • Can last up to 6 weeks
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24
Q

Neurogenic Shock can occur in response to

A

Spinal cord injury or spinal anesthesia

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25
Q

Neurogenic shock results in

A

massive vasodilation (d/t loss of SNS vasoconstrictor tone), leading to pooling of blood in vessels, tissue hypoperfusion, ultimately impaired cellular metabolism

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26
Q

What is the pathophysiology of neurogenic shock?

A

…

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27
Q

What are the types of distributive shocks?

A
  1. Neurogenic Shock
  2. Anaphylactic Shock
  3. Septic Shock
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28
Q

What are clinical manifestations of neurogenic shock?

A
  • Hypotension and bradycardia
  • Inability to regulate body temperature (resulting in heat loss)
  • Dry skin
  • Poikilothermia- taking on temperature of environment
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29
Q

What is anaphylactic shock?

A

Acute, life-threatening hypersensitivity (allergic) reaction

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30
Q

What do you give for a patient in anaphylactic shock?**

A

Epinephrine

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31
Q

Anaphylactic shock can lead to

A
  • Massive vasodilation (in the periphery, the feet, top of head, and in airway)
  • Release of vasoactive mediators
  • Increased capillary permeability
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32
Q

What are clinical manifestations of anaphylactic shock?

A
  • Anxiety, confusion, dizziness
  • Sense of impending doom
  • Chest pain
  • Incontinence
  • Swelling of lips and tongue, angioedema
  • Wheezing, stridor due to laryngeal edema
  • Flushing, pruritus, urticaria
  • Respiratory distress and circulatory failure
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33
Q

What is sepsis?

A

Systemic inflammatory response to documented or suspected infection

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34
Q

What is severe sepsis?

A

Sepsis complicated by organ dysfunction

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35
Q

What is septic shock?

A
  • Presence of sepsis with hypotension despite fluid resuscitation
  • Presence of inadequate tissue perfusion resulting in hypoxia
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36
Q

What is the pathophysiology of septic shock?

A

Slide 23

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37
Q

Volume Resuscitation Guidelines

A
  1. If you’re not aware of loss: 30-50 mL/kg

2. If you are aware of the loss: use 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss)

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38
Q

What are clinical manifestations of septic shock?

A
  • ↑ Coagulation and inflammation
  • ↓ Fibrinolysis: Formation of microthrombi; Obstruction of microvasculature
  • Hyperdynamic state: increased CO and decreased SVR

*Read notes!

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39
Q

What are three major pathophysiologic effects of septic shock?

A
  • Vasodilation
  • Maldistribution of blood flow
  • Myocardial dysfunction: Decreased ejection fraction and ventricular dilation

*Read notes!

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40
Q

What will findings will you find in a patient with septic shock?

A
  • Tachypnea/hyperventilation: Results in respiratory alkalosis and respiratory failure develops in 85% of patients
  • ↓ Urine output
  • Altered neurologic status
  • GI dysfunction, GI bleeding, paralytic ileus

*Read notes!

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41
Q

What are the stages of shock?

A
  1. Initial
  2. Compensatory
  3. Progressive
  4. Refractory
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42
Q

Stages of Shock: Initial

A
  • Usually not clinically apparent

- Metabolism changes at cellular level from aerobic to anaerobic

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43
Q

What happens as metabolism changes at the cellular level from aerobic to anaerobic during the initial stage of shock?

A
  • Lactic acid builds up and must be removed by liver

- Process requires O2, unavailable due to decreased tissue perfusion

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44
Q

Compensatory Stage of Shock: Compensatory Mechanisms include

A
  • Neural
  • Hormonal
  • Biochemical
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45
Q

Stages of Shock: Compensatory Stage

A

Attempt to overcome consequences of anaerobic metabolism and maintain homeostasis

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46
Q

What happens during the compensatory stage of shock?

A
  1. Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP (vasoconstriction while blood to vital organs (brain and heart) are maintained)
  2. SNS stimulation increases myocardial O2 demands
  3. Shunting blood from lungs increases physiologic dead space
  4. Impaired GI motility (risk for paralytic ileus)
  5. Cool, clammy skin (except in patients who is warm and flushed)
  6. ↓ Blood to kidneys activates renin–angiotensin system

*Read notes!

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47
Q

Compensatory Stage: What happens when blood is shunted from the lungs increasing physiologic dead space?

A
  • V/Q mismatch
  • ↓ Arterial O2 levels
  • Increase in rate/depth of respirations

*Read notes on slide 32

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48
Q

Compensatory Stage: What happens when there is a decrease in blood flow to kidneys?

A

Activates renin-angiotensin system where angiotensin I is converted to angiotensin II. This causes:

  • Vasoconstriction
  • Increased venous return to heart
  • Stimulates the release of aldosterone
  • Increased sodium reabsorption stimulates ADH

*Read Notes

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49
Q

Overall Compensatory Stage

A
  • Body is able to compensate for changes in tissue perfusion
  • If cause of shock is corrected, patient recovers with little or no residual effects
  • If cause of shock is not corrected, patient enters progressive stage
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50
Q

Progressive Stage begins when

A
  • Begins when compensatory mechanisms fail

- Patient moved to ICU for advanced monitoring and treatment

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51
Q

What is the progressive stage of shock?

A

-Distinguishing features of ↓ cellular perfusion and altered capillary permeability: This causes leakage of protein into interstitial space
and ↑ systemic interstitial edema

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52
Q

What can happen during the progressive stage?

A
  1. Anasarca
  2. Sustained hypoperfusion
  3. Myocardial dysfunction
  4. Movement of fluid from pulmonary vasculature to interstitium
  5. Mucosal barrier of the GI system becomes ischemic
  6. Fluid moves into the alveoli
  7. Hypoperfusion can lead to renal tubular ischemia
  8. Liver fails to metabolize drugs and waste
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53
Q

Progressive Stage: Anasarca

A
  • Diffuse profound edema.
  • This causes fluid leakage that affects solid organs and peripheral tissues
  • There will also be decreased BF to pulmonary capillaries
54
Q

Progressive Stage: Sustained Hypoperfusion can cause

A
  • Weak Peripheral pulses

- Ischemia of distal extremities

55
Q

Progressive Stage: Myocardial Dysfunction results in

A
  • Dysrhythmias
  • Myocardial ischemia
  • Possible myocardial infarction
  • End result: complete deterioration of cardiovascular system
56
Q

Progressive Stage: Movement of fluid from pulmonary vasculature to interstitium can lead to

A
  • Pulmonary edema
  • Bronchoconstriction
  • ↓ Functional residual capacity
57
Q

Progressive Stage: What happens when fluid moves into the alveoli?

A
  • Edema
  • Decreased surfactant
  • Worsening V/Q mismatch
  • Tachypnea
  • Crackles
  • Increased work of breathing
58
Q

Progressive Stage: What can occur as the mucosal barrier of GI system becomes ischemic?

A
  • Ulcers
  • GI bleeding
  • Risk of migration of bacteria
  • Decreased ability to absorb nutrients
59
Q

What can happen as hypoperfusion leads to renal tubular ischemia?

A
  • May result in acute kidney injury
    (Worsened by nephrotoxic drugs)
  • Decreased urine output
  • Elevated BUN and serum creatinine
  • Metabolic acidosis
60
Q

Progressive Stage: What can happen as the liver fails to metabolize drugs and waste?

A
  • Jaundice
  • Elevated enzymes
  • Loss of immune function
  • Risk for DIC and significant bleeding

*Read notes on slide 45!

61
Q

Stages of Shock: Characteristics of the refractory stage

A
  • Exacerbation of anaerobic metabolism
  • Accumulation of lactic acid
  • ↑ Capillary permeability
  • Profound hypotension and hypoxemia
  • Tachycardia worsens
  • Failure of one organ system affects others
  • Recovery unlikely

*Read notes on slides 46 and 48.

62
Q

Diagnostic Studies for Shock

A
  • Thorough history and physical examination

- No single study to determine shock

63
Q

What are some studies to evaluate shock?

A
  • Blood studies: Elevation of lactate and Base deficit
  • 12-lead ECG, continuous ECG monitoring
  • Chest x-ray
  • Hemodynamic monitoring
64
Q

Successful Management of Shock includes

A
  1. Identification of patients at risk for developing shock
  2. Integration of patient’s history, physical examination, and clinical findings to establish a diagnosis
  3. Interventions to control or eliminate cause of decreased perfusion
  4. Protection of target and distal organs from dysfunction
  5. Provision of multisystem supportive care
65
Q

Shock: General Management Strategies

A
  • Ensure patent is responsive
  • Ensure a patent airway
  • Maximize oxygen delivery
66
Q

Treatment for Shock includes

A
  1. Oxygen and ventilation
  2. Volume expansion (cornerstone of therapy for septic, hypovolemic and anaphylactic shock)
  3. Fluid resuscitation
67
Q

Shock Treatment: Oxygen and Ventilation

A

Increase supply:

  • Optimize CO with fluid replacement or drugs
  • Increase Hemoglobin by Transfusion
  • Increase arterial oxygen with supplemental oxygen and mechanical ventilation
68
Q

Shock Treatment: Volume Expansion

A
  • Insert one or two large-bore IV catheters, intraosseous access device, or central venous catheter
  • Isotonic crystalloids (i.e normal saline or lactated ringers) and colloids (albumin) play a role in fluid resuscitation.
69
Q

Shock Treatment - Volume Expansion: Fluid responsiveness is determined by what clinical assessments?

A
  • Vital signs
    -Cerebral and abdominal pressures
  • Capillary refill
  • Skin temperature
  • Urine output
70
Q

Lactated ringers should not be given to a patient who is

A

Acidodic

71
Q

Shock Treatment - Volume Expansion: What are two major complications of large volume infusions?

A
  • Hypothermia

- Coagulopathy

72
Q

Shock Treatment - Volume Expansion: If the patient has persistent hypotension after adequate fluids resuscitation, what can be added?

A

-Vasopressors (**norepinephrine, dopamine or an inotrope and/or dobutamine may be added

73
Q

Shock Treatment: Fluid Resuscitation

A
  • Administering warm crystalloid and colloid solutions

- Replacing clotting factors

74
Q

What is the primary goal of drug therapy for shock?

A

to correct decreased tissue perfusion

75
Q

Shock Treatment: Drug Therapy includes

A
  • Vasopressor Drugs

- Vasodilator Therapy

76
Q

Shock Drug Therapy: Vasopressor Drugs

A
  • i.e norepinephrine
  • Achieve/maintain MAP >60 to 65 mm Hg
  • Reserved for patients unresponsive to fluid resuscitation

*Read notes

77
Q

For patients taking vasopressor drugs, what should be continuously monitored?

A

Continuously monitor end-organ perfusion (i.e kidney perfusion)

78
Q

Shock Drug Therapy: VAsodilator Therapy

A
  • I.e nitroglycerin/nitroprusside
  • Decreases afterload
  • Achieve/maintain MAP >65 mmHg

*Read notes on slide 59!

79
Q

Shock Therapy: Nutrition Therapy

A
  • Start enteral nutrition within first 24 hours
  • Parenteral nutrition used only if enteral feedings contraindicated
  • Start trophic feeding- slow drip of small amounts of enteral nutrition

*Read notes on slides 60 and 61

80
Q

What should you monitor in relation to nutritional therapy?

A
  • Weigh patient daily

- Monitor serum protein, total albumin, prealbumin, BUN, glucose, electrolytes

81
Q

What is the overall goal of cardiogenic shock?

A

restore blood flow to myocardium by restoring balance between O2 supply and demand

82
Q

What are specific measures to restore blood flow in cardiogenic shock?

A
  • Angioplasty with stenting
  • Emergency revascularization
  • Valve replacement

*Until these interventions are performed, the heart must be supported to optimize stroke volume and CO to achieve optimal perfusion.

83
Q

Cardiogenic Shock: Drug Therapy includes

A
  • Nitrates to dilate coronary arteries
  • Diuretics to reduce preload)
  • Vasodilators to reduce afterload
  • β-adrenergic blockers to reduce HR
84
Q

Cardiogenic Shock: Interprofessional Care

A
  • Hemodynamic Monitoring
  • Drug Therapy
  • Circulatory assist devices
  • Heart transplantation
85
Q

What are you doing when using circulatory assist devices?

A
  • Decrease SVR and left ventricular workload
  • Intraaortic balloon pump
  • Ventricular assist device (VAD)

*Read notes

86
Q

Hypovolemic Shock management focuses on

A

stopping loss of fluid and restoring the circulating volume

87
Q

Septic Shock: Interprofessional Care Includes

A
  • Fluid replacement to restore perfusion (Hemodynamic monitoring)
  • Vasopressor drug therapy
  • Exogenous vasopressin for patients refractory to vasopressor therapy
  • IV corticosteroids
  • ABT
  • Keep glucose levels <180 mg/dL
  • Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole [Protonix])
  • Deep vein thrombosis prophylaxis (e.g., heparin, enoxaparin [Lovenox])

*Read notes on slide 66 and 69!

88
Q

Septic Shock Interprofessional Care: IV corticosteroids

A

For patients who cannot maintain an adequate BP with vasopressor therapy despite fluid resuscitation.

89
Q

When should antibiotics be started in patients with septic shock?

A

Started within the first few hours after cultures are obtained.

90
Q

Interprofessional Care for Septic Shock: Antibiotics

A
  • Broad-spectrum antibiotics are given first

- More specific antibiotics may be ordered once the organism identified

91
Q

Interprofessional Care for Neurogenic Shock includes

A
  • In a spinal cord injury: spinal stability*

- Treatment of hypotension and bradycardia with vasopressors and atropine*

92
Q

What should you watch closely for in treatment for neurogenic shock?

A
  • Fluids infused cautiously as hypotension generally is not related to fluid loss
  • Monitor for hypothermia
93
Q

Interprofessional care for anaphylactic shock includes

A
  • Epinephrine, diphenhydramine, ranitidine
  • Maintain a patent airway: i.e nebulized bronchodilators, aersolized epinephrine, or endotracheal intubation or cricothyroidotomy may be necessary.
  • Aggressive fluid replacement: usually crystalloids
  • IV corticosteroids if significant hypotension persists after 1–2 hours of aggressive therapy
94
Q

INursing Management: Shock Nursing Assessment

A

ABC’s

95
Q

Shock Nursing Assessment: Focused assessment of tissue perfusion include

A
  • Vital signs
  • Peripheral pulses (central pulses are more important) will diminish
  • Level of consciousness (neurologic status will decline
  • Capillary refill (will be delayed d/t vasoconstriction)
  • Skin (e.g., temperature, color, moisture) will become cooler and mottled**
  • Urine output (may decrease)
96
Q

If you are in septic shock and were warm but are now cold,

A

This is bad. You are no longer compensating.

97
Q

Shock Nursing Assessment: Brief History

A

Events leading to shock

Onset and duration of symptoms

98
Q

Shock Nursing Assessment: Health History includes

A
  • Medications
  • Allergies
  • Vaccinations, recent travel
99
Q

Nursing Management: Shock Planning Goals include

A
  • Evidence of adequate tissue perfusion
  • Restoration of normal or baseline BP
  • Recovery of organ function
  • Avoidance of complications from prolonged states of hypoperfusion
100
Q

Shock Nursing Implementation: Acute Care includes

A
  • Monitor patient’s ongoing physical and emotional status
  • Identify trends to detect changes in patient’s condition
  • Plan and implement nursing interventions and therapy
  • Evaluate patient’s response to therapy (i.e looking at the MAP, lactic acid level, etc.)
  • Provide emotional support to patient and caregiver
  • Collaborate with other members of interprofessional team to coordinate care
101
Q

Shock Nursing Implementation: Neurologic Status

A
  • Assess orientation and level of consciousness, clinical manifestations
  • Orient to person, place, time, events
  • Reduce noise and light levels in ICU**
  • Keep a day-night cycle
102
Q

Shock Nursing Implementation: Cardiovascular Status

A
  • Continuous ECG , BP, CVP, PA pressures:
    • CO, SVR, SVV
    • Monitor for dysrhythmias
    • Do not treat hypotension with Trendelenberg position
  • Heart sounds: murmurs, S3, S4
103
Q

Shock Nursing Implementation: Respiratory Status

A
  • Respiratory rate, depth, and rhythm
  • Breath sounds
  • Continuous pulse oximetry
  • Arterial blood gases
  • Many patients will be intubated and on mechanical ventilation
104
Q

Shock Nursing Implementation: Renal Status

A
  • UO (<0.5 mL/kg/hr may indicate inadequate perfusion to the kidneys)
  • Serum Creatinine
105
Q

Shock Nursing Implementation: Body temperature and skin changes

A
  • Core temperature

- Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection

106
Q

Shock Nursing Implementation: GI Status

A
  • Auscultate bowel sounds

- NG drainage/stools for occult blood

107
Q

Shock Nursing Implementation: Personal Hygiene

A
  • Perform bathing, nursing measures carefully
  • Turn every 1 to 2 hours
  • Passive/active range of motion
108
Q

Shock Nursing Implementation: Assess level of anxiety, fear and pain

A
  • Drugs PRN
  • Talk to patient
  • Give simple explanations of all procedures
  • Visit from clergy
  • Caregiver involvement
  • Privacy
  • Call light within reach
109
Q

Shock Evaluation includes

A
  • Adequate tissue perfusion with restoration of normal or baseline BP
  • Normal organ function with no complications from hypoperfusion
  • Decreased fear and anxiety and increased psychologic comfort
110
Q

SIRS

A
  • Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults
  • Generalized inflammation in organs remote from the initial insult
  • High mortality rate
111
Q

What can trigger SIRS?

A
  • Mechanical tissue trauma: burns, crush injuries, surgical procedures
  • Abscess formation: intraabdominal, extremities
  • Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
  • Microbial invasion
  • Endotoxins release: gram-negative bacteria
  • Global perfusion deficits: postcardiac resuscitation, shock states
  • Regional perfusion deficits: distal perfusion deficits
112
Q

What is MODS?

A
  • Multiple organ dysfunction syndrome (MODS) is failure of two or more organ systems
  • Homeostasis cannot be maintained without intervention
  • Results from SIRS
113
Q

What is the relationship between shock, SIRS and MODS?

A

Slide 91

114
Q

SIRS and MODS Pathophysiology: Consequences of inflammatory response

A
  • Release of mediators
  • Direct damage to endothelium
  • Hypermetabolism
  • Increase in vascular permeability
  • Activation of coagulation cascade
115
Q

SIRS and MODS Pathophysiology: Organ and metabolic dysfunction can be caused by

A
  • Hypotension
  • Decreased perfusion
  • Formation of microemboli
  • Redistribution or shunting of blood
116
Q

SIRS and MODS Pathophysiology: Respiratory System

A
  • Alveolar edema
  • Decrease in surfactant
  • Increase in shunt
  • V/Q mismatch
  • End result: ARDS

*Read notes

117
Q

SIRS and MODS Pathophysiology: Cardiovascular System

A
  • Myocardial depression and massive vasodilation
  • Results in decreased SVR and BP
  • Baroreceptors respond to enhance CO
  • Albumin and fluid move out of blood vessels

*Look at notes

118
Q

SIRS and MODS Pathophysiology: Neurologic System

A
  • Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion
  • Often early sign of MODS

*Look at notes

119
Q

SIRS and MODS Pathophysiology: Renal System

A

AKI:

  • Hypoperfusion
  • Release of mediators
  • Activation of renin-angiotensin-aldosterone system
  • Nephrotoxic drugs, especially antibiotics

*Look at notes

120
Q

SIRS and MODS Pathophysiology: GI System

A
  • Motility decreased: abdominal distention and paralytic ileus
  • Decreased perfusion: risk for ulceration and GI bleeding
  • Potential for bacterial translocation

*Look at notes

121
Q

SIRS and MODS Pathophysiology: Hypermetabolic State

A
  • Hyperglycemia-hypoglycemia
  • Insulin resistance
  • Catabolic state
  • Liver dysfunction
  • Lactic acidosis

*Look at notes

122
Q

SIRS and MODS Pathophysiology: Others

A
  • Hematologic System (DIC)
  • Electrolyte imbalances
  • Metabolic acidosis

*READ NOTES

123
Q

SIRS and MODS Prognosis

A

Poor or MODS

124
Q

SIRS and MODS Interprofessional Care Goals

A

Prevent the progression of SIRS to MODS

125
Q

Interprofessional Care for patients with MODS focuses on

A
  • Prevention and treatment of infection
  • Maintenance of tissue oxygenation
  • Nutritional and metabolic support
  • Appropriate support of individual failing organs
126
Q

SIRS and MODS Interprofessional Care: Prevention and treatment of infection

A
  • Aggressive infection control strategies to decrease risk for nosocomial infection (Strict asepsis and assess need for invasive lines)
  • Once an infection is suspected, institute interventions to control source

*Read notes

127
Q

SIRS and MODS Interprofessional Care: Maintenance of tissue oxygenation

A

Decrease O2 demand and increase O2 delivery:

  • Sedation
  • Mechanical ventilation
  • Analgesia
  • Rest
128
Q

SIRS and MODS Interprofessional Care: Goals for Nutritional and Metabolic Needs

A
  • Preserve organ function

- Total energy expenditure is often increased 1.5 to 2.0 times

129
Q

SIRS and MODS Interprofessional Care: Nutritional and Metabolic Needs

A
  • Use of the enteral route is preferred to parenteral nutrition
  • Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis
  • Provide glycemic control
130
Q

SIRS and MODS Interprofessional Care: Support of failing organs

A
  • ARDS: aggressive O2 therapy and mechanical ventilation
  • DIC: appropriate blood products
  • Renal failure: continuous renal replacement therapy or dialysis

*Look at notes

NURS 425 (19 decks)

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