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PCM III Exam I > SHOCK - SRS > Flashcards

SHOCK - SRS Flashcards

1
Q

What is normal CO?

A

4-8 L/min

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2
Q

What is normal cardiac index?

A

2.6 - 4.2 (L/min)/m2

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3
Q

What is normal stroke volume?

A

50-100 ml/beat

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4
Q

What is normal SVR?

A

700-1600 dynes*s/cm5

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5
Q

What is the normal pulmonary vascular resistance?

A

30-130 dynes*s/cm5

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6
Q

What is the normal left ventricular stroke work?

A

60 - 80 g-m/beat

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7
Q

What is the normal right ventricular stroke work?

A

10-15 g-m/beat

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8
Q

At what % of nl blood volume are people considered to be in mild, moderate and sever hypovolemic shock?

A

Mild: <20% blood volume loss

Moderate: 20-40% blood volume loss

Severe: >40% blood volume loss

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9
Q

What are five presentations associated with mild hypovolemic shock?

A
  1. Cool extremities
  2. increased capillary refill time
  3. diaphoresis
  4. collapsed veins
  5. anxiety
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10
Q

What are 9 clinical presentation items associated with moderate hypovolemic shock?

(hint: 5 are the same as in mild)

A

Same as in mild…

  1. Cool extremities
  2. increased capillary refill time
  3. diaphoresis
  4. collapsed veins
  5. anxiety

NEW FOR MODERATE

  1. Tachycardia
  2. tachypnea
  3. oliguria
  4. postural changes
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11
Q

Severe hypovolemic shock has the same presentations as mild and moderate PLUS what other four things?

And for the hell of it, what are the other 9 items that it has in common with mild and moderate hypovolemic shock?

A

NEW for severe…

  1. hemodynamic instability
  2. marked tachycardia
  3. hypotension
  4. mental status deterioration

Same as in mild…

  1. Cool extremities
  2. increased capillary refill time
  3. diaphoresis
  4. collapsed veins
  5. anxiety

Same as in MODERATE

  1. Tachycardia
  2. tachypnea
  3. oliguria
  4. postural changes
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12
Q

Again, because it sounded like a test item, what is the normal SVR?

A

700-1600

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13
Q

What are the ATLS classifications of shock by blood loss?

A

I: up to 750 ml (~15%)

II: 750-1500 ml (15-30%)

III: 1500-2000 ml (30-40%)

IV: >2000 ml (>40%)

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14
Q

What is the urine output in class IV haemorrhagic shock?

A

Negligible

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15
Q

What are the CNS/mental status changes for class I-IV hemorrhagic shock?

A

I: SLightly anxious

II: Mildly anxious

III: anxious and confused

IV: Confused and lethargic

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16
Q

What receptors detect hypotension and hypovolemia? 4

A
  1. •High-pressure baroreceptors
  2. •Low-pressure baroreceptors
  3. •Renal Juxtaglomerular apparatus
  4. •Central and peripheral chemoreceptors
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17
Q

What is the autonomic efferent response to hypotension?

A

•↑ sympathetic

↓ parasympathetic

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18
Q

What are the components of the effector response to hypotension?

Specifically for the heart, vasculature, adrenals, kidney and skin.

A
  • ↑ HR (nodal cells)
  • ↑ contractility (↑ [Ca2+]i in contractile myocytes)
  • ↑ TPR (VSMC contraction; veno- and vasoconstriction)

–Attempt re-establish MAP

  • ↑ Circulating epinephrine (Adrenal medulla)
  • ↑ Renin (Granular cells in the renal JXG apparatus)
  • ↑ Sweat gland activity (Sympathetic cholinergic stimulation; clammy extremities)
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19
Q

What effect will hypotension/hypovolemia have on humoral regulation of vascular tone?

A

↑ ADH/AVP –> ↑ vasoconstriction

↑ ANG II by activation of RAAS –> ↑ vasoconstriction

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20
Q

By what two ways is renin upregulated in response to hypotension/hypovolemia?

A

(1) Sympathetic stimulation of juxtaglomerular granular cells –> renin
(2) Renal vasoconstriction –> ↓ renal pressure –> ↑ renin

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21
Q

What are three ways that the body tries to correct lost blood volume?

A
  1. Renal fluid conservation
  2. Stimulation of thirst –> water intake
  3. Net capillary reabsorption (Starling’s forces)

•“Transcapillary refill”

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22
Q

Hypotension/hypovolemia leads to ↓ renal blood flow which leads to ↓ filtration rate & ↓ Na+ and H2O excretion. Which leads to the dark side. How does a Jedi (and all the rest of us) promote renal retention of Na+ and H20?

A
  • ↑ Sympathetic activity
  • ↑ ANG II = ↑ Aldosterone, ↑ ADH/AVP secretion, ↑ Thirst stimulation
  • ↑ Aldosterone = ↑ Na+ reabsorption
  • ↑ Anti-diuretic hormone/Arginine Vasopressin = ↑ H2O reabsorption
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23
Q

Transcapillary refill is a mechanism the body uses to correct for volume loss, how does this work?

What is the result?

A

–Net reabsorption of fluid: from interstitial fluid –> capillaries

–Reabsorption of interstitial fluid helps replace lost blood volume

Result: initial hemodilution

24
Q

The effect of normal capillary hydrostatic pressure is net filtration. What is the effect of intial hypotension after hemorrhage?

How about following compensation (↑↑↑ arteriolar & ↑ venular resistance)?

A

In both cases, there is a shift to net reabsorption

25
Q

The outcome of hypovolemic shock depends on balance between negative-feedback (compensatory) mechanisms, and positive-feedback (decompensatory) mechanisms.

What are four examples of negative-feedback mechanisms?

A
  1. –Baroreceptor reflexes
  2. –Chemoreceptor reflexes
  3. –Transcapillary reabsorption of interstitial fluid
  4. –Renal conservation of salt and water
26
Q

The outcome of hypovolemic shock depends on balance between negative-feedback (compensatory) mechanisms, and positive-feedback (decompensatory) mechanisms.

What are three examples of positive-feedback mechanisms?

A
  1. –Cardiac failure
  2. –Acidosis
  3. –CNS depression
27
Q

After temporary improvement, hemorrhagic shock may become irreversible (even with transfusion) due to what?

A

Multiple failures, specifically in…

  1. Vasoconstrictor response
  2. Capillary refill response
  3. Heart failure
  4. CNS response
28
Q

Failure of the vasoconstrictor response produces prolonged hemorrhagic hypotension. With TPR increases tapering off and returning to prehemorrhage levels. What are 3 possible causes of this type of failure?

A
  1. Sympathetic escape
  2. metabolites and vasodilators released by ischemic tissues
  3. decline in plasma AVP/ADH from early peak response
29
Q

Sympathetic escape can cause failure of the vasoconstrictor response, how? 2 things

A
  1. –Desensitization α1-adrenoceptors
  2. –Depletion of neurotransmitters
30
Q

metabolites and vasodilators released by ischemic tissues can cause the vasoconstrictor response to fail. How does this happen? In late phases of irreversible shock, what will this manifest as?

A

These metabolites counteract the vasoconstrictor response (pretty straight forward)

In late phase, may be completely unresponsive to vasopressors

31
Q

A decline in plasma AVP/ADH from the early peak response can lead to failure of the vasoconstrictor response. How does this come about? 2

A
  1. –Decline in trigger to release
  2. –Depletion of AVP/ADH posterior pituitary stores
32
Q

Failure of transcapillary refill can lead to irreversible shock. Which vessels tend to fail first?

What does this lead to?

A

Precapillary vessels tend to fail before post capillary vessels.

•↑ relative ratio Rpost/Rpre –> ↑ Pc –> promotes net filtration

33
Q

Failure of the heart can also push for irreversible shock, what is the mechanism behind this?

A

Prolonged, severe hypovolemic shock –> cardiogenic shock (inadequate coronary perfusion)

34
Q

Failure of the CNS response can lead to irreversible shock, how does this goes down?

A

Prolonged inadequate cerebral perfusion –> ischemia

Which causes:

  1. ↓ neural activity
  2. ↓ sympathetic output
  3. ↓ vascular and cardiac responses to hemorrhage
35
Q

What is pulsus paradoxus?

A

Decrease of SBP by more than 10 mmHG on inspiration

36
Q

What is pulsus paradoxus often associated with?

A

Cardiac tamponade

37
Q

Identify the types of shock based on the changes depicted in the chart

(definitely Test questions here)

A
38
Q

In hypovolemic shock what happens to the following parameters?

  1. CVP and PCWP
  2. CO
  3. SVR
  4. Venous O2 saturation
A
  1. CVP and PCWP: Decrease
  2. CO: Decrease
  3. SVR: Increase
  4. Venous O2 saturation: Decrease
39
Q

In cardiogenic shock what happens to the following parameters?

  1. CVP and PCWP
  2. CO
  3. SVR
  4. Venous O2 saturation
A
  1. CVP and PCWP: Increase
  2. CO: Decrease
  3. SVR: Increase
  4. Venous O2 saturation: Decrease
40
Q

In neurogenic shock what happens to the following parameters?

  1. CVP and PCWP
  2. CO
  3. SVR
  4. Venous O2 saturation
A
  1. CVP and PCWP: Decrease
  2. CO: Decrease
  3. SVR: decrease
  4. Venous O2 saturation: Decrease
41
Q

In hyperdynamic septic shock what happens to the following parameters?

  1. CVP and PCWP
  2. CO
  3. SVR
  4. Venous O2 saturation
A
  1. CVP and PCWP: Decrease or increase
  2. CO: increase
  3. SVR: decrease
  4. Venous O2 saturation: increase
42
Q

In hypodynamic septic shock what happens to the following parameters?

  1. CVP and PCWP
  2. CO
  3. SVR
  4. Venous O2 saturation
A
  1. CVP and PCWP: Decrease or increase
  2. CO: decrease
  3. SVR: increase
  4. Venous O2 saturation: decrease or increase
43
Q

What changes to the cardiovascular system are expected in cardiogenic shock?

A

–↓ SV

–↓ CO

–↓ MAP

–↓ Tissue perfusion

–↓ Inotropy

44
Q

In LV heart failure, there is increased LA pressure which leads to increased pulmonary vascular pressure. What does this lead to?

A

promotes filtration and pulmonary edema formation

(will hear rales)

45
Q

What is the effect of pulmonary edema on the right side of the heart?

A
  • ↑ RV volume and pressure
  • ↑ RA volume and pressure
46
Q

What are three clinical signs of right heart failure?

A

–Distended jugular veins

– Mild pitting edema

– Slight hepatomegaly

47
Q

What is the progression from pulmonary edema/pHTN to hepatomegaly, ascites and peripheral edema?

A

•Pulmonary edema/hypertension: RV Failure –> RA Failure –> Venous Distension (Vena Cava) –> Hepatomegaly, Ascites, Peripheral Edema

48
Q

What triggers the initation of the host response to bacterial organisms?

A

–Pathogen Associated Molecular Patterns (PAMPs) OR damage associated molecular patterns (DAMPs)

–Pattern Recognition Receptors

49
Q

When pattern recognition receptors are activated, what signaling pathway upregulates proinflammatory cytokines and vascular adhesion molecules?

A

MyD88/NF-kB

50
Q

What are the proinflammatory cytokines initiated by PAMPS/DAMPS?

A

TNF-alpha

IL-1

IL-6

51
Q

What are three actions of TNF-alpha?

A
  1. •Stimulates the recruitment and activation of neutrophils and monocytes
  2. •Activates vascular endothelial cells to express cellular adhesion molecules
  3. •Can induce extrinsic apoptosis
52
Q

What are the actions of IL-1 and IL-6?

A

Similar to and redundant of TNF-alpha

  1. •Stimulates the recruitment and activation of neutrophils and monocytes
  2. •Activates vascular endothelial cells to express cellular adhesion molecules
  3. •Can induce extrinsic apoptosis
53
Q

At what point does the transition to systemic effects occur from TNF and friends?

A

When concentration exceeds local boundaries

54
Q

What are the systemic cellular effects of the response to bacterial infection? 3

A
  1. –Tissue Ischemia
  2. –Cytopathic Injury
    • Mitochondrial Dysfunction (NO)
  3. –Cell Death
55
Q

How does the CNS respond to infection?

A

Hypothalamus produces the febrile response

56
Q

How does the liver respond to bacterial infection?

A

hepatocytes produce the acute phase response/reactants

57
Q

How does the cardiovascular system respond to infection?

A
  1. –Vasodilation
    • NO and prostaglandins
  2. –Hypotension
  3. –Decreased Cardiac Output
  4. –Thrombosis
    • Activation of tissue factor

PCM III Exam I (9 decks)

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