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NSG 478 > Shock, Sepsis, MODS > Flashcards

Shock, Sepsis, MODS Flashcards

1
Q

Stages of shock

A

Stage I: Initial/Compensatory
Stage II: Progressive
Stage III: Irreversible

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2
Q

Stage I of shock (Compensatory stage): Patient presentation

A
  • Vitals
    • Increased HR
    • Increased RR
    • Blood pressure is normal
    • Increased Diastolic pressures
  • Increased CO (May be less volume or less resistance so more blood has to be pumped)
  • Lactic acidosis
  • Cool extremities
  • Low UOP
  • Hypoactive howel sounds
  • Change in LOC
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3
Q

Stage I shock, compensatory: Nursing assessment

A
  • Watch for subtle changes in LOC
  • VS
  • Pulse pressure (diastolic is on the rise)
  • Stroke volume (Narrowing PP is an indicator of decreasing stroke volume)
  • Capillary refill
  • RR
  • Lab values
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4
Q

Nursing mgmt of compensatory stage I shock

A
  • Identify the cause of shock
  • Correct the underlying cause of shock
    • Fluid
    • Supplemental O2
    • Meds to maintain an adequate BP
    • Obtain lab test
      • Blood cultures
      • Lactate levels
      • CBC
      • BMP
    • Monitoring tissue perfusion
      Main focus is to decrease tissue demand for O2 and deliver more O2 to tissue by increasing perfusion
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5
Q

Neural response

A
  • Baroreceptor reflex: Detects changes in arterial BP, activating vasomotor center of the medulla
  • Sympathetic nervous system (SNS): activated by hypovolemia and hypotension causing peripheral vasoconstriction and shunts blood to vital organs (autoreg)
  • Reduction in renal blood flow activates hormonal response

These activate to compensate for decreased CO

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6
Q

Hormonal response to shock

A
  • Increased production of catecholamines and ACTH activate the RAAS system
  • Angiotensin I and II direct peripheral vasoconstriction and release aldosterone (ADH)
  • This causes the Na and K retention, increased ADH, and increased circulating catecholamines, increasing intravascular volume, HR, BP and decreasing urine output
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7
Q

Chemical response to shock

A
  • Related to ventilation perfusion imbalance (Result of sympathetic stimulation, redistribution of blood flow and decreased pulmonary perfusion)
  • Respiratory alkalosis
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8
Q

Nursing priority interventions and actions: Stage I, compensatory

A
  • Main
    • Supplemental O2/ventilation
    • IV fluids
    • Blood transfusions
    • Control dysrhythmias
    • Increase CO
  • Specific to cause
    • Antibiotics if septic
    • Blood pressure mgmt: depending on type
  • Other
    • Clarify advanced directives
    • Sedation pain mgmt
    • Consider Central venous access for meds and monitoring / art line
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9
Q

Medical actions: passive leg raising

A
  • Only to be performed by a provider
  • Nurse assist with implementation operates and troubleshoots equipment
  • Nurse monitors patients response (Pre, intra, post PLR)
  • Goal is determined if patient will benefit from a fluid bolus
  • Looking for increase with preload, CO and BP
  • Must be mechanically vented,sedated and have an art line
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10
Q

Shock progressive phase: Stage II, Patient presentation

A
  • Compensation phase has failed
  • Blood pressure hypotensive (<100 SBP or <40 from baseline)
  • Map is below normal (70-100)
  • Mental status declining
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11
Q

Shock progressive phase: Stage II, FIRST PHASE

A
  • Heart becomes dysfunctional from overworked heart
  • Unable to meet the O2 demands
  • Ischemia that causes release of biochemical mediators causing myocardial depression
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12
Q

Shock progressive phase: Stage II: SECONDARY PHASE

A
  • Increased capillary permeability
  • Arteriolar and venous constriction in bowel, kidney and lungs
  • Interstitial edema causing a decreased return to the heart
  • Inflammatory response is active releasing both proinflammatory and anti inflammatory mediators and this activates the coagulation system in effort to correct homeostasis
  • Body mobilizes energy stores causing an increase in O2 consumptoms to an already compromised tissue vicious cycle causing shock to progress to MODS
  • Essentially your body freaks out and kills itself
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13
Q

Shock progressive phase: Stage II: Interventions

A
  • Assessment and identifying changes
  • Early interventions
    • Hemodynamic monitoring
    • Meds/fluids
    • Labs
    • Supportive treatment: vent, dialysis, intraaortic balloon pump
    • Collab with healthcare team
    • Preventing further complications
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14
Q

Shock progressive phase: Stage II, Clinical presentation: Resp

A
  • Compromised early and often require intubation and mechanical ventilation
  • Assess anterior and posterior, often you can hear crackles due to the decreased blood flow to the lungs you are hypoxic and retain CO2
  • Alveoli in the lungs become boggy and are unable to allow diffusion, they shunt blood and your alveoli collapse causing ALI or ards PF ratio
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15
Q

Shock progressive phase: Stage II, Clinical presentation: Cardio

A
  • Bad CO means arrhythmias and ischemia to heart
  • Troponin 1 will increase
  • Myocardial depressant factor is a peptide released in various types of shock and is a massive vasodilator and can cause ventricular dilation and decrease contractility of heart
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16
Q

Shock progressive phase: Stage II, Clinical presentation: Neuro

A
  • Decreased blood flow to brain, hypoxemia
  • Very subtle at first to agitation, to lethargy and becoming unresponsive
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17
Q

Shock progressive phase: Stage II, Clinical presentation: Renal

A
  • MAP below 65, your GFT drops and your kidneys don’t make urine
  • Watch your labs for elevated BUN and creatinine
  • I+O and electrolytes are shifting
  • Acid base imbalances and you lose the hormone that regulates BP as you enter AKI
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18
Q

Shock progressive phase: Stage II, Clinical presentation: Liver

A
  • Unable to metabolize meds and metabolic waste like ammonia and lactic acid
  • Risk for infections because of the metabolic activity of the liver doesn’t function like gluconeogenesis
  • Looks at AST/ALT+bilirubin which are all elevated
  • Assess for jaundice
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19
Q

Shock progressive phase: Stage II, Clinical presentation: GI

A
  • Once of the first organs to vasoconstrict
  • Stress of infection can cause GI bleeding, bloody stools
  • Bacteria toxins from bowel can enter the bloodstream through the lymphatic system
  • all this can cause further inflammation, vasodilation and increased capillary permeability and more biochemical mediators
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20
Q

Shock progressive phase: Stage II, Clinical presentation:Heme

A
  • Blood is sluggish, hypoerfusing
  • Metabolic acidosis
  • Colagupathy
  • General hypoxemia
  • Because of inflammatory cytokines activation of the clotting cascade occurs and you consume all the clotting factors causing consumption coagulopathy or DIC
  • Assess pt for ecchymoses, petechiae, review labs, PT, PTT and plts are depeleted
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21
Q

Shock progressive phase: Stage II, Nursing interventions

A
  • Assessment
  • Assess perfusion
  • Assess O2
  • Assess infection
  • Prevent complications and progression
  • Promote rest and comfort
  • Support the family
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22
Q

What 3 agents are given for shock

A
  • Inotropic agents
  • Vasodilators
  • Vasopressor agents
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23
Q

Inotropic agents

A
  • Improve contractility, increase stroke volume, increase CO
  • But it increases O2 demand of the heart
  • Examples
    • Dobutamine
    • Dopamine
    • Epi
    • Milrinone
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24
Q

Vasodilators

A
  • Reduce preload and afterload, reduce o2 demand of the heart
  • Can cause hypotension
  • Examples
    • Nitroglycerine
    • Nitroprusside
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25
Q

Vasopressor agents

A
  • Increase blood flow by vasoconstriction
  • However, it increases afterload, increasing cardiac workload, which can limit perfusion to skin, kidney, lungs and GI
  • Examples
    • Norepi
    • Dopamine
    • Phenylephrine
    • Vasopressin
    • Epi
    • Angiotensin II
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26
Q

Alpha cell innervation

A
  • Causes constriction of the cardiopulmonary, GI , Skin and Kidney
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27
Q

Beta I receptor innervation

A

Causes increased heart rate and myocardial contraction

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28
Q

Beta II receptor innervation

A

Causes vasodilation in the heart and skeletal muscles as the bronchioles relax

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29
Q

Stage III shock: irreversible shocl

A
  • Refractory to all treatment
  • BP not sustainable with life (No perfusion)
  • Respiratory, needs max support with massive hypoxemia
  • Multiple pressors
  • Metabolic acidosis
  • MODS
  • Anaerobic metabolism worsens and elevated lactate levels
  • All reserves are depleted (no mo ATP) and any potential of new energy stores are destroyed (Cells have no energy and no way to get more)
  • Death is immanent
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30
Q

Multiple Organ dysfunction syndrome: MODS

A
  • Hemostasis cannot be maintained
  • Progressive and potential reversible physiological dysfunction of two or more organs
  • Each organ involved increases mortality rate
  • Mortality rate is 27-100% depending on organs involved
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31
Q

Your patient is in shock and is attempting to compensate for shock. The adrenal cortex releases aldosterone due to the presence of angiotensin II. Select all the effects aldosterone will have on the body in attempt to increase cardiac out put and maintain tissue perfusion.
1. Increase blood volume
2. Causes kidneys to keep sodium and water
3. Causes the kidney to excrete sodium and water
4. Causes the urine to have low osmolarity

A
  1. Increase blood volume
  2. Causes kidneys to keep sodium and water

RAAS system, increases your blood volume by preventing the excretion of urine. This causes retention of sodium. This in turn causes the urine to have a high osmolarity as it is much more concentrated

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32
Q

Select all the complications a patient may encounter from Progressive Shock.
1. ARDS
2. Extreme Edema
3. Elevated Ammonia and Lactate levels
4. MI
5. GI bleeding and ulcers
6. Dysrhythmias
7. Acute tubular necrosis
8. DIC

A

ALL options are correct. All these conditions can occur in the progressive stage of shock

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33
Q

A 74-year-old patient is extremely confused and does not respond to commands or stimulation. The patient respiratory rate is 28 and labored, oxygen saturation 86%, heart rate 120, blood pressure 70/40, mean arterial pressure is 50 mmHg, and temperature is 97 F. The patient’s heart rhythm is atrial fibrillation. The patient’s urinary output is 5 mL/hr. The patient’s labs: blood pH 7.15, serum lactate 15 mmol/L, BUN 55 mg/dL, Creatinine 6 mg/dL. In addition, the patient is now starting to have slight oozing of blood around puncture sites.
1. Initial/Compensatory
2. Progressive
3. Refractory

A

The answer is B. This is the progressive stage. There are four stages of shock (in order): initial, compensatory, progressive, and refractory. The patient’s body is experiencing major signs and symptoms of shock. This is not found in the initial stage of shock because the signs and symptoms are subtle. During the compensatory stage, the body (for a while) can compensate so major organs are not showing major signs and symptoms of failure as they are in this scenario (the kidneys are starting to fail based on the BUN, creatinine, urinary output). In addition, the body is no longer compensating because the blood pressure is very low along with the MAP (mean arterial pressure). A big sign is that the patient’s mental status is altered. This represents that the brain is not being perfused very well. The MAP should be 60 or greater to provide adequate perfusion. The MAP here is 50 and this shows us the body is NOT perfusing the organs, so the cells will experience hypoxic injury. The patient is also starting to show early signs and symptoms of DIC due to the slight oozing of blood around puncture sites. The next stage (which is the last) is the refractory and this is where organs have failed or are about too. Death is imminent. This patient is not at that point but is getting close. This patient needs very dynamic treatment in order to survive

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34
Q

_______________ is a stage of shock that the body attempts to utilize the hormonal, neural, and biochemical responses in the body.
Refractory
Progressive
Proliferation
Compensatory

A

Compensatory

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35
Q

4 types of shock

A
  • Hypovolemic
  • Cardiogenic
  • Obstructive
  • Distributive
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36
Q

Hypovolemic shock causes

A
  • Sudden loss of intravascular volume, whether externally or interstitially
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37
Q

Hypovolemic shock causes: External

A
  • Trauma
  • Surgery
  • Vomiting
  • Diarrhea
  • Diuresis
  • DKA
  • DI
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38
Q

Hypovolemic shock causes: Internal fluid shift

A
  • Hemorrhage
  • Burns
  • Ascites
  • Peritonitis
  • Dehydration
  • Necrotizing pancreatitis
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39
Q

Hypovolemic shock: Patho

A
  • Decreased intravascular volume
  • Decreased venous return
  • Decreased Filling pressures (PAD,PCWP), decreased blood in the heart
  • Decreased Stroke volume
  • decreased CO
  • Decreased Tissue perfusion> Starving cell
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40
Q

Hypovolemic shock: Nursing interventions

A
  • Primary prevention: Closely monitoring a patient at risk
  • safe admin of meds: Vasopressors
  • Safe admin of fluid and or blood replacement
  • O2 admin
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41
Q

Crystalloid fluids

A
  • LR
    • Buffers metabolic acidosis
    • Can cause pulmonary edema and abdominal compartment syndrome, may need central
  • 0.9% NS
    • Can cause hypernatremia
    • Hypokalemia
    • Hyperchloremic metabolic acidosis
    • ALI
    • ACS
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42
Q

Colloid Fluids

A
  • Albumin
  • Plasma expander: Rapidly expands plasma volume
  • Can cause HF
  • Expensive
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43
Q

Blood products

A
  • Rapidly replaces volume due to hemorrhage
  • Can consider MTP
  • TRALI or TACO
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44
Q

Cardiogenic shock

A
  • Hearts inability to contract and pump
  • O2 is inadequate for heart and tissue
45
Q

Types of cardiogenic shock

A
  • Coronary
  • Noncoronary
46
Q

Coronary:cardiogenic shock

A
  • Acute MI with dmg to the LV
  • Anterior wall MI most common for cardiogenic shock due to dmg to the left ventricle and occlusion to the left anterior descending CA
47
Q

Noncoronary: cardiogenic shock

A
  • Stess to the myocardium
  • From hypoxia, acidosis , hypoglycemia, tension pneumo, Cardiomyopathies, valvular dmg, cardiac tamponade, arrhythmia
48
Q

Cardiogenic shock presentation: LV failure

A
  • Tachycardia
  • Dysrhythmias
  • Pulsus alternans: poor prognosis
  • Tachypnea
  • S3
  • Crackles
49
Q

Cardiogenic shock presentation: RV failure

A
  • JVD
  • Peripheral edema
  • Hepatosplenomegaly
50
Q

Cardiogenic shock nursing interventions:

A
  • Prevention: Decrease work demand of pt, admin O2
  • Monitoring Hemodynamics
  • Intra-aortic balloon pump
  • Administering meds and fluids: need to see how they tolerate them Fluids arent as effective as other forms of shock
  • Maintaining safety and comfort
51
Q

Obstructive shock

A
  • Vital organs and tissue do not get enough blood flow
  • Blood can’t get in or out
  • No CO, but the heart muscle is usually ok
  • Rare type
  • Highest rate of survival if identified and treated early
52
Q

Obstructive shock examples

A
  • Large blood clot in the PA
  • Pericardial tamponade
  • aortic stenosis
  • Aortic dissection
  • Constrictive pericarditis
  • Vena cava compression syndrome
  • Tension pneumo
  • Tension hemothorax
  • Tumors
  • High PEEP (Barotrauma)
53
Q

Two types of obstructive shock

A
  • Pulmonary Vascular
  • Mechanical
54
Q

Pulmonary Vascular: Obstructive shock

A
  • RV fails, can’t pump into the lungs because it doesn’t have enough pressure to go against pulmonary resistance
  • PE
  • Pulmonary hypertension
  • Severe stenosis, acute obstruction of the pulmonary or tricuspid valve
55
Q

Mechanical: Obstructive Shock

A
  • Presents as hypovolemic shock, with decreased preload
  • Tension Pneumo
  • Pericardial tamponade
  • Constrictive pericarditis
  • Restrictive cardiomyopathy
56
Q

Nursing actions obstructive shock

A
  • Assess: With stethoscope, both resp and cardio
  • Obtain medical assistance immediately (Medical emergency)
  • Prepare: IV insertion and O2
  • Prepare: bedside ultrasound, echo and ekg
  • Prepare: med admin (fluids, blood, vasoactive meds)
57
Q

Distributive shock

A
  1. A precipitating event causes **massive vasodilation, **
  2. which triggers the inflammatory response to try and fix it (it doesn’t).
  3. leading to the maldistribution of intravascular volume.
  4. Less volume means less venous return
  5. Less venous return return means less preload leading to reduced CO
  6. No CO means no tissue perfusion
58
Q

Three types of distributive shock

A
  • Neurogenic
  • Anaphylactic
  • Septic
59
Q

Neurogenic shock

A
  • Type of distributive shock
  • loss of the parasympathetic and sympathetic stimulation
  • Caused by
    • Spinal cord injury
    • Spinal anesthesia
    • Nervous system dmg
    • Meds
    • Hypoglycemia
60
Q

How does the presentation of neurogenic shock differ from other forms of shock

A
  • Usually with forms of shock with the hypotension, it is accompanied with tachycardia and cool moist skin.
  • With neurogenic shock your sympathetic nervous system is unable to react leading to hypotension, with bradycardia and dry warm skin (Idk about hypoglycemia tho)
61
Q

Mgmt of neurogenic shock: General

A
  • Restore sympathetic tone
  • Stabilize the spine
  • Patient proper positioning
  • Define underlying cause
62
Q

Mgmt of neurogenic shock: Nursing actions

A
  • Support cardiovascular and neuro function until the shock resolves
  • HOB 30 degrees
  • Immobilization of pt
  • Assess for any lower extremity pain, redness, tenderness and warmth
  • Complete passive rom to increase circulation
  • Application of pneumatic compression devices
  • Antithrombotic agents
  • Prepare to assist provider with stabilization of the spine
63
Q

Anaphylactic shock

A
  • Form of distributive shock
  • Ig-E mediated allergic reactions
  • Drug and toxin induced
    • SIRS like syndromes
    • Narcotics, snake and insect bites, transfusion reactions
    • Heavy metal poisoning , toxic shock
  • Endocrine
    • Addisonian crisis (Adrenal failure due to mineralocorticoid deficiency)
64
Q

Anaphylactic shock presentation

A
  • Onset of 2-30 min
  • S+S include resp distress, decreased BP, GI, skin and mucosal tissue irritation
  • Feeling of impending doom
65
Q

Anaphylactic shock mgmt

A
  • Know the cause, and stop it! remove the antigen
  • IV access
  • IV fluids
  • Epinephrine (Epi pen)
  • Diphenhydramine IV (benadryl)
  • Albuterol
  • CPR
66
Q

Anaphylactic shock: Nursing action

A
  • Prevention and early intervention is key
  • Being aware of S+S anaphylactic shock
  • Asking about any allergies
  • Knowing how the patient has reacted in the past to any reactions
  • Being aware of all risk factors
    • Meds
    • Foods
    • Contrast
67
Q

A 32-year-old patient is admitted after falling from a second-story balcony. The patient has a fractured femur, several fractured ribs, and possible head injury.
The primary provider has prescribed lactated Ringer’s solution to be infused at 250 mL/hr to maintain a blood pressure >120 mm Hg and urine output >50 mL/h.
Two large-bore IVs are started in each arm and IV fluids are initiated. The patient is alert to name only. The patient is typed and crossed for blood products, and a series of metabolic labs and a lactate level are drawn for analysis.
The patient becomes unresponsive to name and begins moaning and grimacing.
Vital signs are as follows: BP 92/72, HR 132 bpm, RR 32 breaths/min, SpO2 92% on 40% FiO2 via a facemask with a urine output of 15 mL over the last hour.

Place each of the interventions in priority order

  1. Prepare to administer vasoactive medications
  2. Prepare to administer IV Fluid
  3. Prepare to administer Blood Transfusion
  4. Notify Provider
  5. Prepare to administer pain medication
  6. Prepare for further diagnostics ( ABG, Chest x-ray, Cardiac markers
A

4
2
1
3
6
5

68
Q

The nurse is concerned that a client is developing multiple organ dysfunction syndrome (MODS). Place the signs/symptoms in the classic sequence in which this syndrome develops. Use all options.

  1. Cardiovascular instability
  2. Hypermetabolism
  3. Bleeding disorder
  4. Neurologic deterioration
  5. Lung dysfunction
  6. Liver dysfunction
  7. Fluid balance
  8. Kidney dysfunction
A

The classic pattern for the development of MODS begins with the lungs as the client experiences progressive dyspnea and respiratory failure. Increasing amounts of IV fluids and vasoactive agents are then needed to support blood pressure and cardiac output. Signs of a hypermetabolic state occur next, which is characterized by hyperglycemia, hyper lactic acidemia, and an increased blood urea nitrogen level. After 7 to 10 days, signs of liver dysfunction (elevated bilirubin and liver function tests) and kidney dysfunction (elevated creatinine and anuria) develop. As the lack of tissue perfusion continues, the hematologic system becomes dysfunctional, which increases the risk of bleeding. The cardiovascular system becomes unstable and unresponsive to vasoactive medications, and the neurologic system deteriorates to a state of unresponsiveness or coma.
5
2
6
8
3
1
4

69
Q

The nurse is assessing a 6-year-old child in the emergency department (ED) who was brought in by the parent. The child was stung by a bee and the child is now having trouble breathing. Review patient information below. What does the nurse suspect is wrong with this child?

Temp-unable to obtain
HR 127
RR 33
BP 80/42
Urticaria over entire body

This child is having an allergic reaction and going into ________________ Shock.

What medications would the Provider order for this child?
1.) ____________________
2.) ____________________
3.) ____________________

A

Anaphylactic shock

EPI
IV fluids
Albuterol

70
Q

The nurse is caring for a client in the irreversible stage of shock. The nurse is explaining to the client’s family the poor prognosis. Which would the nurse be most accurate to explain as the rationale for imminent death?

  1. Endotoxins in the system
  2. Limited gas exchange
  3. Brain Death
  4. Multiple organ failure
A

In the irreversible stage of shock, significant cells and organs are damaged. The client’s condition reaches a “point of no return” despite treatment efforts. Death occurs from multiple system failure as the kidneys, heart, lungs, liver, and brain cease to function.

4

71
Q

You are caring for a client in the compensation stage of shock. You know that in this stage of shock adrenaline and noradrenaline are released into the circulation. What positive effect does this have on your client?
1. Increased myocardial contractility
2. Decreases blood return to the heart
3. Decreases carbon dioxide exchanges
4. Contracts bronchioles

A

Increased myocardial contractility

72
Q

Septic shock

A
  • Most common type of distributive shock
  • Dmged capillaries
  • maldistribution of blood flow
  • Vasodilation
  • Poor O2 utilization
  • High mortality risk
73
Q

Septic shock, risk factors: Host related

A
  • Age under 1, over 65
  • Malnutrition
  • Debilitation
  • Immunocompromise
    • Hepatic dysfunction, CD, DM, renal disease, ETOH abuse, HIV cancer
  • Pregnancy
74
Q

Septic shock, risk factors: treatment related

A
  • Invasive procedures and cath (Central line, cath, dialysis, advanced airway, surgical procedures
  • Immunosuppression meds: Steroids, chemo, biologics
  • Wounds
  • Traumatic injury
  • Antibiotic resistance
75
Q

Sepsis: causative microorganisms: Gram Negative

A
  • E coli
  • Klebsiella: Mouth and intestines
  • Pseudomonas aeruginosa
  • Bacteroids
  • Proteus
76
Q

Sepsis: Causative microorganisms: Gram positive

A
  • Staph aureus
  • Strep pyogenes
  • Strep Pneumoniae
  • Pneumococcus
  • Clostridium
77
Q

Systemic Inflammatory response syndrome (SIRS)

A
  • Physiologic response to an insult or injury from an infectious or noninfectious source
    • Temp greater than 38 or less than 36
    • HR greater than 90
    • RR greater than 20, or PaCO2 less than 32, or need for mechanical venting due to resp failure
    • White blood cells: greater than 12k or less than 4k
78
Q

Innate immune system

A
  • Physical barriers
  • Skin, organ mucosal layers
79
Q

Chemical barriers (Immune system)

A

Stomach acid, lysozymes in eye

80
Q

Innate response(Immune system):

A

Inflammatory response cells
(Mast, neutrophils, macrophages, Natural killer cells)

81
Q

Adaptive immune system

A
  • Cell mediated response+ humoral response
  • Cell mediated
    • T lymphocytes: to CD4 and CD8 cells
  • Humoral response
    * B-lymphocytes: antibodies
82
Q

Appropriate inflammatory response

A
  • Immune system responds to invading microorganism without causing dmg to its own tissue
  • Limited number of microbes, local responses are sufficient to clear the pathogen and the body returns to homeostasis
  • High microbial load, host genetics and other issues can lead to an exaggerated response, which can lead to collateral tissue dmg and cell death (Starts to be an issue)
  • Necrotic cell death causes a release of DAMP that act on the pRR that were triggered by initial pathogens
  • Inflammatory process continues
  • Complex array of intersecting pathways become dysfunctional
    • Excessive function
    • Depressed function
  • Results in a self destructive process that can be fatal
83
Q

Patho alterations of septic shock as the process continues: Increased capillary permeability

A
  • Activation of the complement system and subsequent release of vasoactive substances
  • Activation of kinin system
  • Histamine release
84
Q

Patho alterations of septic shock as the process continues: Microemboli

A
  • Activation of the clotting system
  • Aggregation of neutrophils due to increased C5
  • Plt aggregation due to increased Thromboxane A2 and Prostacyclin
85
Q

Patho alterations of septic shock as the process continues: Vasoconstriction of pulmonary, renal and splenic vasculature

A
  • Increased prostaglandin F
  • Decreased Prostacyclin
  • Norepi, Epi, Angiotensin release
  • Myocardial depressant factor released
86
Q

Patho alterations of septic shock as the process continues: Decreased myocardial contractility

A
  • Activation of the complement system
  • Release of myocardial depressant factor
  • Endorphin release secondary to LEM
  • Histamine release
87
Q

Septic Shock: Massive vasodilation effect

A
  • Venous
    • Dilation of the veins and venules
    • Venous pooling
    • Decreased Venous return
    • Decreased Filling pressure
    • Decreased Preload
  • Arterial
    • Dilation of arterioles
    • Increased lumen diameter
    • Decreased SVR
    • Decreased afterload
88
Q

Septic Shock: Maldistribution of blood volume

A
  • Select vasoconstriction
    • Blood vessels in the pulmonary renal and gut constrict
    • This occurs as a result of increased catecholamines and angiotensin release myocardial depressant factor
    • This causes increased pulmonary vascular resistance, causing pulmonary hypertension (oh no)
    • Decreased renal blood flow, increased GFR and urine output
89
Q

SIRS criteria

A
  • Any two of the 2 criteria for both a new or existing pt
    • Temp <36 or >38
    • HR over 90
    • RR over 20 or PaCO2 under 32
    • WBC under 4000 or over 12k
90
Q

CMS Sep-1

A
  • All or nothing in order to be compliant you need to meet the measures. for severe sepsis
91
Q

CMS Sep-1: Within 3 hours of presentation

A
  • Measure serum lactate
  • Obtain blood cultures prior to antibiotics
  • Admin antibiotics
92
Q

CMS Sep-1: Within 6 hours of presentation

A
  • Repeat serum lactate if initial lactate is >2
93
Q

CMS Sep-1: Septic shock within 3 hours of presentation

A
  • Measure serum lactate
  • Obtain blood cultures prior to antibiotics
  • Admin antibiotics
  • Resuscitation with 30ml/kg crystalloid fluids
94
Q

CMS Sep-1: Septic shock within 6 hours of presentation

A
  • Repeat column status and tissue perfusion assessment
  • Vasopressor admin (If hypotension persist after fluid)
95
Q

CMS Sep-1: Repeat assessment

A
  • Repeat assessment of volume status and tissue perfusion is required for patients with septic shock
  • This is done when a pt has persistent hypotension after fluid resuscitation (Can be done with a focused assessment or using physiologic parameters)
  • Pts who are transferred from another acute care facility are not included in this
96
Q

CMS Sep-1: Repeat assessment: Focused exam must include

A
  • Vitals
  • Cardiopulmonary exam
  • Cap refill
  • Peripheral pulse eval
  • Skin exam
97
Q

CMS Sep-1: Repeat assessment: Physiologic parameters

A
  • Can be done instead of a physical exam but it must include 2 of the following
    • Central venous pressure
    • Central venous oxygen
    • Bedside cardiovascular ultrasound
    • Passive leg raise or fluid challenge
98
Q

Sepsis: WBC

A
  • Leukopenia, occurs early during septicemia
  • Resultant of the coherence of the endotoxins to the walls of the circulatory white blood cells (Neutrophils or PMN)
  • Leukocytes are sequestered in the spleen and removed from circulation
  • As immune defenses are mobilized a rebound leukocytosis (Increased WBC) occurs.
99
Q

Sepsis: Lactate

A
  • Indirect identification of tissue perfusion
  • Increase can indicate hypoxia
  • >2mmol/L remeasure in 2-4 hours
  • Lactate guided resuscitation is shown to decrease mortality
100
Q

Sepsis: Blood cultures

A
  • Obtain prior to antibiotics
    • Sterilization of cultures can occur within min of first dose of antibiotic
    • Optimize pathogen identification and improve outcomes
  • Obtain 2 sets of blood cultures (anaerobic and aerobic)
  • Admin of appropriate antibiotics should not be delayed in order to obtain cultures
101
Q

Sepsis: Broad spectrum antibiotics

A
  • Should be started asap to cover all possible pathogens
  • Therapy should be narrowed once pathogen is established
  • Discontinue if pt does not have an infection
  • Potent antibiotics can cause large amount of exotoxins from dying bacteria, this can make the hypotension and vasodilation worse
102
Q

Sepsis: IV fluids

A
  • Sepsis induced hypoperfusion or septic shock is a medical emergency, need to start effective fluid resuscitation immediately
  • Hypotension and elevated lactate
  • 30ml/kg IV crystalloid
  • Fluid admin beyond initial resuscitation requires careful assessment and patient fluid responsiveness should be eval (FVE)
  • Some evidence says sustained positive fluid balance during icu is harmful
103
Q

Sepsis: Vasopressors

A
  • Restore adequate perfusion pressure to the vital organs
  • Start vasopressors within the first hour to achieve MAP> 65
  • Norepinephrine is pressor of choice
104
Q

Hour one bundle:

A
  • Initial resuscitation for sepsis and septic shock
    1. Measure lactate level (Remeasure if >2)
    2. Obtain blood cultures before antibiotics
    3. Admin broad spectrum antibiotics
    4. Begin rapid admin of 30ml/kg crystalloid for hypotension or lactate greater than 4
    5. Apply vasopressors if hypotensive during or after to maintain a map of greater than 65
105
Q

The nurse is caring for a client whose worsening infection places the client at high risk for shock. Which assessment finding would the nurse consider a potential sign of shock?

  1. Elevated systolic blood pressure
  2. Elevated mean arterial pressure
  3. Shallow, rapid respirations
  4. Bradycardia
A
  1. Shallow, rapid respirations
106
Q

The intensive care unit nurse is caring for a client with sepsis whose tissue perfusion is declining. What sign would indicate to the nurse that end-organ damage may be occurring?
1. Urinary output increases
2. Skin becomes warm and dry
3. Adventitious lung sounds occur in the upper airway
4. Heart and respiratory rates are elevated

A

As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the client begins to show signs of organ dysfunction. The cardiovascular system also begins to fail, the blood pressure does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., acute kidney injury, pulmonary failure, hepatic failure). As sepsis progresses to septic shock, the blood pressure drops, and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs. Adventitious lung sounds occur throughout the lung fields, not just in the upper fields of the lungs.

107
Q

A nurse is providing care to all of the following clients. Which client would be most at risk for septic shock?

  1. The patient with left lower lobe pneumonia
  2. The patient with a BMI of 25 who has been vomiting and lost 3 lbs.
  3. The 45-year-old patient with sudden onset of frequent PVC’s
  4. The patient with testicular cancer who is receiving IV Chemotherapy
A

Just a guess but 4

108
Q

A nurse is assessing a client who is experiencing significant stress due to septicemia. Choose 3 options from below
1. Administer supplemental 02
2. Maintain prone position
3. Monitor temperature
4. Increase oral (PO) intake
5. Obtain Lactate level

A

1
3
5

The nurse should expect to administer oxygen therapy to support perfusion, monitor temperature to assess metabolic response, and obtain lactate levels, which serve as a critical predictor of the client’s metabolic stress response. The nurse should not place a client with septicemia in a prone position because this would lead to further respiratory compromise. The nurse should not increase PO fluid intake because this would also lead to respiratory compromise and fluid volume overload

109
Q

Combined shock states

A
  • Need to be able to critically think, there might be more than one source of the cause, or one may transfer to another
  • Look at the diagram in lecture it displays it well

NSG 478 (23 decks)

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