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Adv Patho > Shock-Exam 3 > Flashcards

Shock-Exam 3 Flashcards

1
Q

What is shock

A

•Inadequate tissue perfusion ànd decreased oxygen and nutrient delivery
-impaired cellular metabolism +/-
•Increased demand for oxygen and nutrients (hypermetabolic state)
•Decreased removal of cellular waste products

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2
Q

Describe the cellular changes associated with anerobic metabolism in shock states for LACTATE

A

Increased lactate&raquo_space; metabolic acidosis&raquo_space; increased oxy-Hgb dissociation

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3
Q

Describe the cellular changes associated with anerobic metabolism in shock states for PROTEIN METABOLISM

A

Increased protein metabolism&raquo_space; increased muscle wasting&raquo_space; decreased Resp and CV muscle strength

Increased protein metabolism&raquo_space; decreased immunoglobulin&raquo_space; decrease in immune response

Increase protein metabolism&raquo_space; increased cellular edema > inflammatory response&raquo_space; lysosomal enzymes OR clotting cascade

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4
Q

Describe the cellular changes associated with anerobic metabolism in shock states for ATP

A

Increase ATP&raquo_space; Increase intracellular Na and H2O&raquo_space; decrease circulating volume&raquo_space; clotting cascade&raquo_space; inflammatory response&raquo_space; lysosomal enzymes

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5
Q

Definition of Cardiogenic Shock

A

inability of heart to pump adequate blood to tissues/organs

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6
Q

Etiology of Cardiogenic Shock

A
  1. Decreased contractility (pump failure): MI, cardiomyopathy, sepsis, myocarditis,
    pericarditis, aneurysm, dysrhythmias, contusion, metabolic abnormalities, papillary muscle rupture
  2. Impaired diastolic filling: dysrhythmias
  3. Obstruction: PE, cardiac tamponade, valve disorders, tumors, wall defects
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7
Q

Defining characteristics of Cardiogenic Shock

A

hypotension and hypoperfusions despite adequate LV filling pressure and intravascular volume

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8
Q

Unique manifestations of Cardiogenic Shock

A

Related to inadequate perfusion to heart and end organs
•Chest pain, dyspnea, faintness, impending doom
•Tachycardia, tachypnea, hypotension, JVD, measures of low CO2
•Signs of poor perfusion: mottling, cyanosis, low UOP
•Extra heart sounds, pulmonary edema, hypoxemia
•Elevated end organ lab values

Treatment: support the pump, improve relaxation, or remove obstruction

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9
Q

Definition of Hypovolemic Shock

A

Loss of whole blood, plasma, or interstitial fluids in large amounts
•Symptoms with ~15% intravascular volume loss

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10
Q

Etiology of Hypovolemic Shock

A
  • Whole blood: hemorrhage
  • Plasma: Burns
  • Interstitial fluids: diaphoresis, DM, DI, emesis, diarrhea, diuresis
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11
Q

Patho of Cardiogenic Shock

A

involves a vicious spiral circle: ischemia causes myocardial dysfunction, which in turn aggravates myocardial ischemia. Myocardial stunning and/or hibernating myocardium can enhance myocardial dysfunction, thus, worsening the cardiogenic shock.

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12
Q

Unique manifestations of Hypovolemic Shock

A
  • High SVR (systemic vascular resistance): pallor and cool extremities
  • Thirst
  • Oliguria
  • Low preload (RA pressure or CVP) and tachycardia

•Treatment: fluid replacement

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13
Q

Definition of Neurogenic Shock

A

Widespread and massive vasodilation

•Related to imbalance in parasympathetic and sympathetic nervous systems

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14
Q

Etiology of Neurogenic Shock

A

-anything that stimulates parasympathetic activity and inhibits sympathetic activity
•Trauma – spinal cord or medulla
•Conditions that deprive medulla of oxygen or glucose
•Depressive drugs, anesthetic agents, severe emotional stress, pain

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15
Q

Defining Characteristics of Neurogenic Shock

A
  • Hypotension with bounding peripheral pulses and flash cap refill
  • Bradycardia
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16
Q

Patho of Hypovolemic Shock

A

shock results from significant and sudden blood or fluid losses within your body. Blood loss of this magnitude can occur because of: bleeding from serious cuts or wounds. bleeding from blunt traumatic injuries due to accidents.

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17
Q

Definition of Anaphylactic Shock

A

Inflammatory and vasodilatory reaction to an allergic antigen

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18
Q

Etiology of Anaphylactic Shock

A

-exposure to allergic antigen

Anaphylactoid type – cold, exercise and medication contaminants

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19
Q

Defining Characteristics of Anaphylactic Shock

A
  • *similar to neurogenic shock with vasodilation, peripheral pooling and tissue edema
  • Bronchoconstriction
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20
Q

Unique manifestations of Anaphylactic Shock

A
  • CV: hypotension, diaphoresis, pallor
  • Resp: SOB, cough, rhinorrhea, throat tightening, wheezing
  • GI: N/V/D, abdominal pain
  • Cutaneous: erythema, pruritis, urticaria, angioedema
  • ** ominous - anxiety, confusion, impaired mentation

Treatment: epi to stop mast cell degranulation, fluid resuscitation, antihistamines, steroids

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21
Q

Patho of Neurogenic Shock

A

combination of both primary and secondary injuries that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the vagus nerve. Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation

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22
Q

Etiology of Septic Shock

A

-infection
•Gram negative and gram positive bacteria, viruses, and fungus
•PNA, bloodstream, intravascular catheter, intraabdominal, urosepsis, surgical wound

23
Q

Defining Characteristics of Septic Shock

A
  • A vasopressor requirement to maintain MAP >65mmHG
  • low SVR and vasodilation
  • Lactate >2mmol/L
  • Without hypovolemia
24
Q

Path of Septic Shock

A

If homeostasis restored SIRS ends, if not an infectious agent cause sepsis
•Life-threatening organ dysfunction caused by a dysregulated host response to infection (Singer et al., JAMA 2016)

25
Q

Unique manifestations of Septic Shock

A

systolic hypotension (<90mmHg) and organ dysfunction (measured with LODS, SOFA, qSOFA)

26
Q

Patho of Anaphylactic Shock

A

caused by massive release of biochemical mediators from mast cell and basophils. Mast cells activation occurs mainly via antigen crosslinking of IgE bound to FcεRI receptors on cell membranes.

27
Q

What happens in SEPSIS

A

•Life-threatening organ dysfunction caused by a dysregulated host response to
infection (Singer et al., JAMA 2016)
•Commonly affects: Respiratory, hematologic, cardiac, renal, hepatic and central nervous systems

28
Q

What happens in MODS

A

•Progressive dysfunction of 2+ organ systems from uncontrolled inflammatory
response to severe illness or injury
•Sepsis or sepsis related disorders (burns, trauma, heat stroke)
•Risks for MODS: older age, significant tissue injury, pre-existing conditions

29
Q

Definition of MODS

A

•Organ dysfunction related to specific ischemia or hypoperfusion

30
Q

Patho of primary MODS

A
  • Decreased perfusion to: Local tissues (organs) or generalized hypoperfusion (typically subclinical)
  • Sets cells up for exaggerated response to secondary MODS
31
Q

Definition of secondary MODS

A
  • Excessive inflammatory reaction after a latent period following initial injury
  • Organ often distant from site of original injury
32
Q

What is the timeline symptom manifestation of MODS

A
  • 24 hours post injury: fever, tachycardia, tachypnea, dyspnea, AMS, hypermetabolic state
  • 24-72 hours: respiratory failure&raquo_space; ARDS
  • 7-10 days: hypermetabolic and hyperdynamic state bacteremia (enteric), hepatic, renal, GI failure
  • 14-21 days: worsening organ failures can evolve to death
  • 21+ days: linger: improve or die or rapidly: Improve or die
33
Q

Manifestations of sepsis

A

•General: Hypo/hyperthermia, tachycardia, tachypnea, AMS, significant edema or positive fluid balance, hyperglycemia

•Inflammatory: Leukocytosis or leukopenia (>12,000 or < 4,000, or bandemia
>10%), elevated CRP and/or Procalcitonin

•Hemodynamic: Hypotension, SvO2, Cardiac index >3.5L/min

•Organ dysfunction: PF ratio < 300, Oliguria (<0.5ml/kg/hr x 2 hours), Cr
increase coagulopathy, ileus, thrombocytopenia, hyperbilirubinemia

•Tissue perfusion: Lactic acidosis, decreased cap refill

34
Q

What is the basic patho of shock?

A
  • Mismatch of oxygen and glucose delivery/demand

* Inadequate perfusion

35
Q

What happens in SEPTIC SHOCK

A

Progressive dysfunction in response to an infection that can lead to organ failure

36
Q

How can organ failure be evaluated/quantified?

A

-Using the SOFA Scores
***Sequential Organ Failure Assessment (SOFA)
•P/F ratio +/- mechanical ventilation
•Plt count
•GCS
•Bilirubin
•MAP
•Creatine

***+ if score increases 2 points = organ
dysfunction due to hypoperfusion

***Quick SOFA (qSOFA)
•RR >22
•GCS < 15 (or lower than baseline)
•SBP < 100mmHg

***+ if 2/3 criteria true
•Best measure outside of ICU

37
Q

What is the basic patho of shock?

A
  • Mismatch of oxygen and glucose delivery/demand
  • Inadequate perfusion

***the patho of shock is the same regardless of etiology

38
Q

Patho of primary MODS

A

Primary MODS is the direct result of a well-defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself.

  • Decreased perfusion to: Local tissues (organs) or generalized hypoperfusion (typically subclinical)
  • Sets cells up for exaggerated response to secondary MODS
39
Q

Path of secondary MODS

A

Secondary MODS develops as a consequence of a host response and is identified within the context of SIRS.

40
Q

What is the basic patho of shock?

A
  • Mismatch of oxygen and glucose delivery/demand
  • Inadequate perfusion

***the patho of shock is the same regardless of etiology

41
Q

How do you treat shock?

A

Treatment depends on addressing the underlying cause, then:
•Improve tissue perfusion
•Improve oxygen delivery
•Manage hyperglycemia

42
Q

When figuring out what shock a person may be in, what do you look at?

A
  • Consider patient history
  • Risk factors and
  • Clinical situation
43
Q

Who is at greater risk for MODS?

A

older age, significant tissue injury, pre-existing coniditions

44
Q

Criteria for SIRS

A

Must meet at least 2 or more of the following

  1. Temp >38 or <36
  2. Heart rate >90
  3. RR >20
  4. PaCo2 <32
  5. WBC >12,000 or <4,000
  6. Band cell >10%
45
Q

What is sepsis

A

SIRS + confirmed infection

46
Q

Cellular changes are caused by

A

anaerobic metabolism

47
Q

Stages of shock

A
  1. Compensated
  2. Decompensated
  3. Irreversible
48
Q

What happens in compensated shock?

A

Compensated
• Shock in which the body is still able to compensate for absolute or relative fluid loss
• Patient is still able to maintain an adequate blood pressure and cerebral perfusion

49
Q

What happens in irreversible shock?

A

• Irreversible
• a rapid deterioration of the cardiovascular system and the compensatory mechanisms
have failed and the patient will die

50
Q

What happens in decompensated shock?

A

• Decompensated
• the late phase of shock in which the body’s compensatory mechanisms are unable to
maintain adequate perfusion to the brain and vital organs

51
Q

SIRS can be infectious or noninfectious?

True or false

A

True

example: pt on echmo when tubing and lines are changed

52
Q

If we don’t reduce the inflammation in SIRS it can lead to

53
Q

What is underlying causes of sepsis

A

bacteremia

54
Q

What is the causes of septic shock?

Adv Patho (23 decks)

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