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Pathophysiology > Shock > Flashcards

Shock Flashcards

1
Q

definition of shock

A

A physiological state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products, resulting in tissue injury.

not necessarily decreased perfusion (sometimes perfusion even increases in shock), but definitely decreased O2 delivery

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2
Q

4 things that perfusion requires

A
  1. properly beating heart
  2. adequate transport medium, blood, and hemoglobin
  3. intact and functioning vessel system
  4. functioning respiratory system
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3
Q

What does short-term hypoperfusion cause?

long term = shock

A

Syncope, orthostatic collapse, carotis hyperesthesia, electric shock, spinal cord injury, etc

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4
Q

Perfusion is what?

A

O2 , nutrient, delivery and CO2 elimination

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5
Q

Normal blood volume

A

5-6 liters

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6
Q

3 Stages of shock:

A
  1. Compensated
  2. Progressive
  3. Irreversible

(note that 2 and 3 are normally considered “decompensated” and fall into 3 categories: subacute reversible, subacute irreversible, and acute irreversible.)

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7
Q

What is the final change to note of irreversible shock before cellular death?

A

Cellular membrane injury

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8
Q 
Clinical markers of shock, what are:
BP
HR
Sock Index
Resp Rate
A

BP: systolic <110
Sinus tach, at least > 90 BPM
Sock index: BPsys/pulse < or equal to 1 (normal is 2)
Resp rate: <7 or >29 breaths/min

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9
Q

Clinical markers of shock:
Urine output
Bicarbonate
pO2

A

Urine output: <0.5mL/kg/hr
Bicarbonate: metabolic acidemia, [HCO3] <31mEq/L or base deficit >3mEq/L
pO2: hypoxemia, depends on age. <80mmHg or <70mmHg

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10
Q

What mental changes are seen as a clinical marker of shock?

A

Beginnning: Anxiousness, agitation,

End: Indifference, lethary, obtundation

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11
Q

What are the 2 general causes of hypovolemic shock?

A

Hemorrhage

Dehydration (diarrhea, sweating..)

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12
Q

What are major causes of obstructive shock?

A
  1. pulmonary embolism
  2. tension pneumothorax
  3. cardiac tamponade
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13
Q

What occurs with cardiogenic shock?

A

Pump failure. (i.e. 40% of myocardium damaged by AMI)

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14
Q

What does distributive shock mean?

A

No fluid loss, but it’s being distributed poorly or is not oxygenated. Perfusion is actually increasing, but extreme vasodilation may -> shock.

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15
Q

What may cause and what occurs in neurogenic shock?

A

Spinal cord injury, drug overdose or poisoning that -> neural deficits -> inability to maintain vascular tone -> vasodilation

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16
Q

Generally, what occurs in anaphylactic shock?

A

IgE -> Vasodilation and fluid shifting from capillary to the cell. Leads to micro clotting and smooth muscle contraction

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17
Q

What may cause and what occurs in septic shock?

A

Overwhelming infection -> lot of NO produced + bacterial toxins -> vasodilation and fluid shifting

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18
Q

What may cause urinary tract fluid loss that can cause hypovolemic shock?

A

Diabetes insipidus or mellitus, salt-wasting disorders, adrenocortical insufficiency, diuretics

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19
Q

What may cause fluid loss from the skin that may cause hypovolemic shock?

A

Excessive burns, skin inflammation (generalized exfoliative dermititis)

20
Q

What may cause internal sequestration of fluid that may cause hypovolemic shock?

A

Loss of volume into interstitial space or body cavities. Chronic liver disease, acute pancreatitis, angioedema

21
Q

What part of cardiac output is affected by hypovolemia?

A

Preload is decreased -> CO decreased

22
Q

How is the body’s response during the compensated stage of hemorrhagic shock?

A

Volume depletion -> CO decreased -> body detects and increases sympathetic tone -> vasoconstriction + bronchodilation and cardiac stimulation

23
Q

What happens to the capillary pressure and blood glucose level during compensated hemorrhagic shock?

A

Capillary pressure decreases, causing interstitial fluid to build up in the vascular compartment

Blood glucose level increases (bc metabolism increases from beta 2 effect), causing osmotic effect that brings fluid to the vascular compartment as well

24
Q

What are the humoral or delayed responses of compensated hemorrhagic shock?

A

ADH, aldosterone, renin-angiontensin II

25
Q

Which organs are vasoconstricted in the compensated hemorrhagic shock response?

A

Kidney, splanchnic area, muscle, adipose tissue

26
Q

What are 2 consequences of hemorrhagic shock?

A
  1. almost normal cerebral and cardiac circulation (systolic BP 70-90 mmHg)
  2. circulation to other organs decreased (pale skin, decreased urine output, muscle weakness)
27
Q

What is the result of prolonged peripheral hypoperfusion during the progressive stage of hemorrhagic shock?

A

Hypoperfusion -> metabolic acid build up -> autoregulation causes vasodilation in periphery, constriction in lung

28
Q

What is the mechanism in irreversible hemorrhagic shock?

A

Compensatory mechanisms fail -> precapillary sphincters open, releasing metabolic acids, microemboli, and other waste into circulation -> cell damage, organ failure, death

29
Q

What is myocardial “stunning?”

A

Reperfusion of ischemic myocardium w/in 6 hours of a coronary thrombosis takes a while to regain function, often delayed for hours to weeks. Cause is unknown, maybe free ROS release or alteration of intracellular calcium..

30
Q

What is “hibernating myocardium?”

A

Chronic myocardial ischemia -> chronic lower contractility in order to reduce myocardial oxygen demands

31
Q

What happens to cardiac output in cardiogenic shock?

A

Preload is decreased. Fluid replacement doesn’t help much bc there isn’t a problem with fluid volume

32
Q

Distributive shock: what happens to
BP
TPR
CO

A

BP: normal
TPR: decreased (general vasodilation)
CO: increased 2-3 x

33
Q

Hyperdynamic stage of distributive shock, what occurs:
acid balance?
amino acid metabolism?

A

Lactic acid accumulates in periphery

Liver metabolism changes. Tyrosine -> octopamine, inhibiting alpha receptors

34
Q

Why might cardiac failure result from distributive shock?

A

Very fast heart rate -> shorter diastolic time -> no time for coronary filling -> hypoxia in heart

35
Q

What causes anaphylactic shock?

A

Sensitized individual exposed to antigen, triggering an IgE-mediated activation of mast cells

Decreased symp tone on vasculature (from drugs or food)

Direct smooth muscle relaxation (from endotoxins, endotoxin-induced cytokine release)

36
Q

Late Reperfusion injury: why is it so dangerous?

A

Once blood flow is restored, the products from the injured area induce systemic inflammation

37
Q

What is the “reflow paradox” in early reperfusion

A

Somehow, inflammatory rxn is going to cause an increased filtration in the postcapillary venules (? can’t understand audio too well)

38
Q

What are some enzymes that are activated in tissue damage?

A

PLA 2, XOR, iNOS

39
Q

What are some primary mediators in tissue damage?

A

Histamine, eicosanoids, NO, peptides, IL’s, TNFalpha, PAF, etc..

40
Q

What % of body mass is muscle?

What are some cytokines that muscle can release?

A

30-40%

TNF, IL-1, IL-6, GIF

41
Q

What are some affects of TNF on muscle metabolism?

A

Inhibits pyruvate dehydrogenase.

Causes glucose uptake increase, glucose oxidation decrease, protein degradation increase, alanine in plasma increases

42
Q

What is secreted by the pancreas during shock and effects the heart and bowel?

A

Myocardial Depressing Factor (MDF)

43
Q

What type of kidney necrosis can develop from shock?

A

Low bp -> Tubular necrosis, causing acute kidney failure

44
Q

What lung problem might occur a few days after shock that can kill people?

A

ARDS: waste product washed from periphery to central circulation activates lung inflammation, causing edema and pulmonary failure

45
Q

Why may obesity be more of a problem during shock?

A

Adipose is affected by alpha receptors, meaning they get constricted and can become necrotic -> lipid peroxidation -> acid components that later get released into bloodstream

46
Q

What amino acid levels may change during shock?

A

Ones with aromatic ring (Tyr and Phe) are less metabolized, and so their serum level increases. Often in lab these are compared to leucine level to see if they’re changed from normal.

47
Q

What happens to fibrinogen level in shock?

A

Increases, as well as other acute phase proteins

Pathophysiology (14 decks)

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