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850-Exam 2 material > 850-IP8 Pathophysiology of Shock > Flashcards

850-IP8 Pathophysiology of Shock Flashcards

1
Q

Shock definition:

A

Mediated by many different mechanisms each with their own specific treatment but all are characterized by the hypo-perfusion of tissues leading to aerobic metabolism–>anaerobic metabolism (impaired cellular metabolism).

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2
Q

Clinical endpoints used to identify patients in shock:

-Hemodynamic instability

A
  • Systolic blood pressure(SBP) <90mmHg

- Mean arterial pressure(MAP) <65mmHg

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3
Q

Clinical endpoints used to identify patients in shock:

-Signs of poor tissue perfusion/anaerobic metabolism

A
  • Elevated lactate >4mmol/L
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4
Q

Impaired oxygen utilization:

A
  • aerobic becomes anaerobic metabolism (less efficient)
    1. Cells burn ATP stores faster than able to replenish
    2. Increased Na+ inside cell
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5
Q
  1. Cells burn ATP stores faster than able to replenish
A
  • Sodium/potassium ATPase pump unable to maintain resting membrane potential –> decrease amplitude of action potential
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6
Q
  1. Increased Na+ inside cell
A
  • Intracellular edema causes cellular membrane dysfunction and leaking lysosomal enzymes –> damage
    cells further
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7
Q
  1. Decreased circulatory volume causes:
A
  • Sluggish capillary blood flow –> decreased O2 delivery

o Activation of clotting cascade

  1. Acute Tubular Necrosis (ATN)
  2. Acute Respiratory Distress Syndrome (ARDS)
  3. Disseminated Intravascular Coagulation (DIC)

o Anaerobic metabolism –> Metabolic acidosis/acidemia

  1. Disrupts membrane (releases more lysosomal enzymes) 2. Enzyme disassociation
  2. Decreases oxygen carrying capacity
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8
Q

Impaired glucose utilization:

A
  1. Decreased delivery (poor circulation/perfusion)

2. Increased cortisol, growth hormone, catecholamines

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9
Q

Increased cortisol, growth hormone, catecholamines:

A
  • Hyperglycemia/insulin resistance
  • Glycogenolysis, gluconeogenesis and lipolysis –> high energy costs contribute to cells failure
  • Gluconeogenesis:
    1. Protein used for fuel no longer available to maintain cellular structure, function, repair, replication
    2. Protein breakdown
    3. Skeletal muscle wasting (diaphragm) and cardiac muscle wasting
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10
Q

Increased cortisol, growth hormone, catecholamines

-Gluconeogenesis: Protein breakdown

A
  1. Decrease albumin = decreased oncotic pressure
  2. Decrease immunoglobulins = immunosuppression
  3. Releases alanine –> pyruvate –> lactate
  4. Byproducts ammonia (toxic to living cells) and urea (disrupts cellular metabolism)
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11
Q

Increased cortisol, growth hormone, catecholamines

-Gluconeogenesis: Skeletal muscle wasting (diaphragm) and cardiac muscle wasting

A
  1. Respiratory dysfunction –> reduced oxygen/CO2 exchange
  2. Myocardial dysfunction –> glucose delivery (exacerbates vicious cycle)
  3. Decreased removal of waste products
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12
Q

Shock is driven by??

A

REDUCED Cardiac Output (CO) or REDUCED Systemic Vascular Resistance (SVR) or Both

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13
Q

Blood Pressure = CO x SVR

A

-Is a function of CO and SVR

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14
Q

CO = stroke volume (SV) X heart rate (HR)

A

-Liters of blood flow the heart pumps per minute

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15
Q

Central venous pressure (CVP)

A

-Pressure of blood returning to the heart through

the venous system; Preload

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16
Q

MAP = (1/3) X SBP + (2/3) X DBP

A
  • Average of systolic and diastolic pressure in the
    arterial system
  • Surrogate marker of tissue perfusion
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17
Q

SVR = 80 X (MAP – CVP)/CO

A
  • The total resistance of the circulatory system (the

heart must overcome this to create forward flow)

18
Q

Cardiogenic shock: “problem with the pump”

A
  1. Etiology of cardiac dysfunction will guide treatment:

2. Compensatory INCREASE in SVR further REDUCES Cardiac Output

19
Q

-Etiology of cardiac dysfunction will guide treatment:

A
  • Decompensated heart failure –> inotrope + diuresis (usually)
  • Myocardial ischemia/infarction –> PCI or CABG
  • Pulmonary arterial hypertension –> pulmonary artery dilation (iNO)/milrinone
  • Massive Pulmonary Embolism (PE) –> remove clot thrombectomy/thrombolysis/VA-ECMO
  • Valvular dysfunction –> replace valve
  • Dysrhythmias –> correct underlying cause (electrolytes/ischemia)
  • Myocarditis –> LVAD, steroids, heart transplant
20
Q

Hemodynamic Components starting from aorta and ending at the inferior vena cava?

A

Aorta –> CO –> MAP –> SVR –> CVP –> Inferior vena cava

21
Q

Common Pathway of Shock:

A
  1. Heart –> Baroreceptor Dysfunction –> Brain (decrease afferent inhibitory signals)
  2. Brain –> increase vasopressin secretions & increase sympathetic nervous system activity
  3. Increase vasopressin secretions –> kidney (decrease renal flow, increase aldosterone, increase sodium reabsorption, increase H2O reabsorption)
  4. Increase sympathetic nervous system activity –> decrease limb blood flow & increase renin secretion
  5. Increase renin secretions –> increase angiotensin II –> Kidney (decrease renal flow, increase aldosterone, increase sodium reabsorption, increase H2O reabsorption)
22
Q

(Aerobic cellular metabolism):

A

Differentiated tissue –> +02 –> Glucose –> Pyruvate (lactate leaves pyruvate) goes into the mitochondrion and O2 is added –> CO2
(oxidative phosphorylation ~36 mol ATP/mol Glucose)

23
Q

(Anaerobic cellular metabolism):

A

Differentiated tissue –> -O2 –> Glucose –> Pyruvate –> Lactate
(Anaerobic glycolysis: 2 mol ATP/mol glucose)

24
Q

Hypovolemic

A

Is a consequence of decreased preload due to intravascular volume loss. During hypovolemic shock, the diminished preload decreases the CO and the SVR increases in an effort to compensate for diminished CO and maintain perfusion to the vital organs. The PCWP is decreased.

25
Q

Aldosterone:

A

A corticoid hormone which stimulates absorption of sodium by the kidneys and so regulates water & salt balance.

26
Q

Renin:

A

the enzyme secreted by and stored in the kidneys which promotes the production of the protein angiotensin

27
Q

Angiotensin II:

A

a naturally occurring peptide hormone of the renin-angiotensin-aldosterone-system (RAAS) that has the capacity to cause vasoconstriction and an increase in blood pressure in the human body

28
Q

Treatment for Cardiogenic shock:

A

“Make it pump!”

  • Inotrope
  • Vasopressor
  • Cautious diuresis
  • Correct underlying cause
29
Q

Hypovolemic shock “blank”?

A

“there’s hole in the bucket”

30
Q

Hypovolemic shock treatment:

A

“Plug the hole! Fill the bucket!”

  • Stop bleeding/fluid loss
  • Fluids
  • Vasopressors (temporize)
31
Q

Hypovolemic shock

Types of fluid loss and cause:

A
  1. Hemorrhage:
    - Whole blood: RBCs, Clotting factors, Platelets
    - Burn: Plasma
    - Diaphoresis, emesis, diarrhea, diuresis, diabetes mellitus/insipidus: interstitial fluid
32
Q

Neurogenic shock “blank”:

A

“Profound vasodilation and lack of compensatory tachycardia”

  • Too much parasympathetic –> bradycardia
  • Too little sympathetic stimulation of vascular smooth muscle –> decreased SVR
  • Most common cause spinal cord injury: 1. C-Spine 2. High T-spine (T1-T6)
33
Q

Neurogenic shock treatment:

A

Fluids, vasopressors (increased vascular tone), inotropes (bradycardia), stabilized spine (if injured)

  1. Fluids
  2. Vasopressors
  3. Inotropes
34
Q

Anaphylactic shock (distributive shock):

A
  1. Allergic –> immune/inflammatory response
    - Snake venom, insect venom, pollen, shellfish, tree nuts, penicillin, animal sera
    - IgE mediated
  2. Vasodilation (decreased SVR) and vascular permeability (tissue edema/hypovolemia)
  3. Extra-vascular smooth muscle constriction –> bronchoconstriction/laryngospasm
35
Q

Anaphylatic shock treatment:

A
  • Remove antigen or anti-venom (if available)
    1. Glucocorticoids, antihistamine –> blunt inflammatory response
    2. Fluid resuscitation –> correct hypovolemia
    3. Epinephrine –> vasoconstriction (alpha 1 agonist) bronchodilation (beta 2 agonist)
36
Q

Septic shock (distributive shock):

A

Bacteremia –> endo/exo-toxins, lipopolysaccharide (LPS) gram negative, peptidoglycan and lipoteichoic acid gram positive

**Extremely complex host response designed to eliminate invading organism –> dysregulation and overactive immune response leads to host morbidity/mortality **

37
Q

Septic shock treatment:

A

“remove/suppress infection”

  • Source control: drain abscess, remove infected heart valve, debridement/amputation
  • Antimicrobials
  • Supportive care: fluid resuscitation, vasopressors, renal replacement therapy, mechanical ventilation
38
Q

What are the 4 anaphylactic shock treatments?

A
  1. Remove antigen
  2. Fluids
  3. Epinephrine
  4. Steroids/Antihistamines
39
Q

What are the 4 septic shock treatments?

A
  1. Fluids
  2. Vasopressors
  3. Antibiotics
  4. Source control
40
Q

Sustained shock –> Multi-Organ Dysfunction Syndrome (MODS):

A

-the progressive dysfunction of two or more organ systems resulting from uncontrolled inflammatory response to severe illness or injury

41
Q

Sustained shock –> Multi-Organ Dysfunction Syndrome (MODS):

Common triggers:

A
  1. Severe trauma
  2. Major surgery
  3. Burns
  4. Shock
  5. Pancreatitis
  6. AKI
  7. ARDS

850-Exam 2 material (19 decks)

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