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Med-Surg > Sepsis / Shock > Flashcards

Sepsis / Shock Flashcards

1
Q

shock

A

complex pathophysiologic process that often results in MODS and death, all types of shock involve inadequate tissue perfusion and acute circulatory shock

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2
Q

causes of shock are classified according to

A

the pathophysiologic cause and hemodynamic profile

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3
Q

cause of shock

A
  • hypovolemic
  • cardiogenic
  • distributive; septic, anaphylactic, neurogenic
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4
Q

compensation in shock

A

neuroendocrine responses in response to ineffective circulating blood volume

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4
Q

compensation in shock

A

neuroendocrine responses in response to ineffective circulating blood volume

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5
Q

what response occurs during compensation shock

A

SNS “fight or flight”

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6
Q

why does “fight or flight” occur during compensation shock

A

compensation for increase venous return, CO, and oxygen delivery

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7
Q

progression of shock stages

A

initial stage, compensatory stage, progressive stage, refractory stage

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8
Q

progression through each stage varies with

A

the pts condition, duration of initiating event, response to therapy, and correction of underlying cause

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9
Q

clinical manifestations of all shock states are the result of

A

inadequate oxygen delivery and activation of compensatory mechanisms

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10
Q

traditional parameters for assessment of shock states

A
  • appearance
  • VS
  • LOC
  • decrease urinary output
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11
Q

objective parameters when assessing shock states

A
  • arterial pH
  • serum lactate
  • base excess and base deficit
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12
Q

how would arterial pH be affected in a pt experiencing shock

A

acid or alkaline state of the arterial output

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13
Q

how would serum lactate be affected in a pt experiencing shock

A

lactic acidosis -> anaerobic metabolism

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14
Q

how would base excess and base deficit be affected in a pt experiencing shock

A

base deficit indicates a buildup of lactic acidosis from impaired tissue oxygenation

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15
Q

general management of shock states

A
  • oxygen therapy
  • fluid resuscitation
  • vasoactive pharmacotherapy
  • nutritional support
  • hypovolemic shocl
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16
Q

why provide oxygen therapy to shock pts

A

to improve oxygen delivery to hypoxic tissues

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17
Q

why provide fluid resuscitation to shock pts

A

to restore intravascular volume (restoring preload and increase CO of oxygen delivery)

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18
Q

why provide vasoactive pharmacotherapy to shock pts

A

to restore vasomotor tone and improve cardiac function; used when fluid resuscitation has not adequately improved the pts perfusion status

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19
Q

why provide nutritional support to shock pts

A

to address the metabolic requirements which are greatly increased in shock

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20
Q

hypovolemic shock occurs when

A

inadequate circulating volume results in inadequate CO to meet tissue oxygenation

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21
Q

hypovolemic shock results from

A

an absolute fluid volume deficit or relative fluid volume deficit

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22
Q

absolute hypovolemia

A

loss of fluid from the intravascular space resulting from an external loss of fluid from the body or from internal shifting of fluid from the intravascular to the extravascular space

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23
Q

relative hypovolemia

A

vasodilation produces an increase in vascular capacitance relative to circulating volume

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24
Q

in hypovolemic shock decrease blood volume leads to ______________ leads to _____________ leads to ____________ leads to ____________

A

decrease blood volume leads to decrease venous return -> decrease SV decrease which leads to CO and results in altered tissue perfusion

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25
Q

clinical manifestations of hypovolemic shock are dependent on the

A

severity of fluid loss and the pts ability (age and health) to compensate for it

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26
Q

clinical manifestations of hypovolemic shock

A
  • increase HR
  • decrease bp as volume loss increases
  • dry mouth
  • pale
  • cool, clammy skin
  • poor cap refill
  • faint/absent peripheral pulses
  • low urine output
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27
Q

management of hypovolemic shock

A
  • secure pts airway
  • support breathing
  • control bleeding
  • restore fluid volume
  • primary prevention of shock
  • targeted treatment at the cause of shock and restoring intravascular volume
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28
Q

what is cardiogenic shock

A

occurs when the heart’s ability to contract and pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues

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29
Q

cardiogenic shock most often is seen in pts with a

A

MI

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30
Q

cardiogenic shock is decreased cardiac contractility -> ________ -> ____________ and __________

A

decrease SV and CO -> pulmonary congestion -> systemic tissue perfusion and decrease coronary artery perfusion

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31
Q

clinical manifestations of cardiogenic shock

A
  • decrease BP
  • tachypnea
  • cyanosis
  • pulmonary crackles and wheezes
  • increased respiratory distress as fluid overload occurs
  • increase HR
  • increase CVP
  • increase PAWP
  • decreased urine output
  • pale, cool, clammy skin
32
Q

goals of cardiogenic treatment

A
  • limit further myocardial damage and preserve the healthy myocardial tissue
  • improve cardiac function by ↑ myocardial contractility and ↓ ventricular afterload or both (achieved by ↑ oxygen supply to the heart muscle while ↓ oxygen demands)
33
Q

management of cardiogenic shock

A
  • prevention of cardiogenic shock
  • monitoring hemodynamic status
  • administering fluids and medications
  • enhancing safety and concern
34
Q

pharmacologic management of cardiogenic shock

A
  • oxygen
  • analgesia
  • antiplatelet and beta blockers
  • vasoactive medications
  • diuretics
  • antiarrhythmic medications
35
Q

distributive shock

A

the body’s ability to adjust vascular tone is impaired (due to endothelial insult or loss of SNS response) and blood volume is abnormally displaced in the vasculature

36
Q

classifications of distributive shock

A
  • Septic shock
  • Neurogenic shock
  • Anaphylactic shock
37
Q

septic shock is characterized by

A
  • altered fluid volume r/t vasodilation
  • increased capillary permeability
  • maldistribution of circulating volume
38
Q

bacteremia

A

presence of bacteria in the blood

39
Q

infection

A

presence of microorganisms that trigger an inflammatory response

40
Q

what does SIRS stand for

A

systemic inflammatory response syndrome

41
Q

what is SIRS

A

a syndrome resulting from a severe clinical insult that indicates an systemic inflammatory response

42
Q

sepsis

A

a systemic response to infection that may occur post burn, surgery, or serious illness

43
Q

sepsis is the presence of SIRS plus the presence of

A

an infectious source

44
Q

severe sepsis

A

defined as sepsis plus at least one of the following signs
- areas of mottled skin
- cap refill > 3 sec
- decreased urinary output
- lactate > 2mmol/L
- abrupt change in mental status
- platelet count of <100 000 or DIC
- acute lung injury (ALI) or ARDS
- cardiac dysfunction

45
Q

septic shock

A

Shock associated with sepsis; defined as severe sepsis, plus one of the following
- MAP < 60 mmHg post fluid resuscitation
- Need for vasoactive medication in order to maintain MAP of > 60 mmHg

46
Q

clinical manifestations of septic shock

A
  • Temperature (> 38.3°C or < 36°C)
  • Heart rate > 90/min
  • Tachypnea
  • Altered mental status (d/t hypoxia)
  • Significant edema or positive fluid balance (> 20 mL/kg over 24 hr)
  • Hyperglycemia (plasma glucose > 7.7 mmol/L) in the absence of diabetes
47
Q

inflammatory variables

A
  • leukocytosis - increased WBC (neutrophils)
  • elevated plasma C reactive protein
  • increase plasma procalcitonin
48
Q

goal of sepsis management

A

The goal of management is the identification and elimination of the cause of the infection and aggressive cardiopulmonary support

49
Q

managing sepsis

A
  • fluid resuscitation
  • pharmacologic therapy
  • nutritional therapy and glycemic control
50
Q

why fluid resuscitation in pts with sepsis

A

increased CVP, increased BP

51
Q

what pharmacological therapy for pts with sepsis

A
  • if fluid administration fails to increase BP and restore organ perfusion
  • vasopressor or inotropic agents
  • hydrocortisone, activated protein C
52
Q

why nutritional therapy and glycemic control for sepsis pts

A
  • malnutrition further impairs patient’s compensatory mechanisms
  • glycemic control decreased mortality
53
Q

two types of shock from spinal cord injury

A
  • spinal shock
  • neurogenic shock
54
Q

clinical manifestations of spinal and neurogenic shock are related to

A

lost sympathetic innervation & unopposed parasympathetic innervation with a triad of expected signs (hypotension, bradycardia & hypothermia)

55
Q

treatment goals of spinal and neurogenic shock

A
  • Maintain stability of spine
  • Optimize oxygen delivery
  • Restore intravascular volume
56
Q

anaphylactic shock

A
  • Severe, systemic allergic reaction to allergens including food, drugs, blood products, insect venom, and latex
  • A combination of massive vasodilation and ↑ capillary permeability results in a ↓ in venous return, ↓ in CO, and a ↓ in oxygen delivery
  • Involves multiple organ systems, but most life threatening are those involving the cardiovascular and pulmonary systems
57
Q

anaphylactic shock onsets rapidly within ________ or slowly __________

A

5-30 min ; 6-12 hrs

58
Q

clinical manifestations of anaphylaxis

A
  • Respiratory distress due to laryngeal edema, bronchospasm
  • Dizziness, chest pain, facial swelling
  • Wheezing, stridor
  • Pruritis, urticaria, angioedema
  • Anxiety
  • LIFE THREATENING
59
Q

goals of treatment for anaphylaxis

A
  • *Maintain an airway
  • *Support blood pressure
  • Oxygen as necessary
  • Early intubation if necessary, why?
  • Fluid resuscitation
  • If hypotensive, to restore vascular volume
  • Drug therapy
  • Stopping the hypersensitivity response and reversing manifestations of the response
  • Obstructive Shock
60
Q

obstructive shock

A

A physical obstruction to blood flow, either in the heart or major blood vessels resulting in a ↓ in CO and ultimately, a ↓ in tissue perfusion

61
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
61
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
61
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
61
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
61
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
62
Q

causes of obstructive shock

A
  • Pulmonary Embolism
  • Early initiation of anticoagulant therapy (heparin)
  • Tension Pneimothorax
  • Trapped air is decompressed (needle or chest tube)
  • Cardiac Tamponade
  • Emergency removal of pericardial fluid (pericardiocentesis)
  • MODS: Multiple Organ dysfunction syndrome
  • SIRS: Systemic Inflammatory response Syndrome
63
Q

SIRS stimulates an overwhelming __________

A

inflammatory, immunologic, and hormonal response similar to that seen in sepsis patients

64
Q

although SIRS presents clinically like sepsis the difference is that

A

there is NO identifiable source of infection

65
Q

SIRS -> _______ -> ________

A

SIRS -> sepsis -> septic shock

66
Q

SIRS -> _______ -> ________

A

SIRS -> sepsis -> septic shock

67
Q

SIRS can lead to

A

MODS

68
Q

This inflammatory, systemic response is manifested by two or more of the following conditions:

A
  • Temperature >38 or <36
  • HR >90
  • RR >20, or Pa CO₂ <32
  • WBC > 12,000/mm3 or < 4,000/mm3
69
Q

MODS

A

Severe organ dysfunction of at least two organ systems lasting at least 24 to 48 hours in the context of sepsis, trauma, burns, or severe inflammatory conditions

70
Q

MODS can result from SIRS or any type of

A

shock due to inadequate tissue perfusion

71
Q

two MODS pathways

A

primary
secondary

72
Q

4 factors that lead to pathologic changes associated with MODS

A

Uncontrolled systemic inflammation
- Pro-inflammatory mediators initiate a systemic, inflammatory response
Tissue hypoxia
- Patient may appear to have adequate oxygenation but regional tissue hypoxia may occur
Unregulated apoptosis (cell death)
- ↓ levels of certain immune cells (↑ susceptibility) and ↑ levels of other immune cells that ↑ tissue damage
Microvascular coagulopathy
- Abnormal clotting in the small blood vessels resulting in micro-thrombosis and obstruction of blood flow

73
Q

clinical manifestations of MODS

A
  • Difficult to identify because much of organ damage occurs at the cellular level & therefore, can’t be directly measured or observed
  • Most common types of organ dysfunction are ARF and ARDS
74
Q

focus of MODS is

A

prevention

Med-Surg (15 decks)

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