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PCM III > Shock Simulation cases > Flashcards

Shock Simulation cases Flashcards

1
Q

Normal CO value

A

4-8 L/min

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2
Q

Normal Systemic Vascular Resistance (SVR) value

A

700-1600 Dynes x sec/cm^5

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3
Q

Mild Hypovolemic Shock presentation (

A
  • Cool extremities
  • increased capillary refill time
  • diaphoresis
  • collapsed veins
  • anxiety
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4
Q

Moderate Hypovolemic Shock presentation (20-40% blood loss)

A

same as mild Hypovolemic Shock presentation plus:

  • Tachycardia
  • tachypnea
  • oliguria
  • postural changes
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5
Q

Severe Hypovolemic Shock presentation ( > 40% blood loss)

A

Same as Moderate Hypovolemic Shock presentation plus:

  • hemodynamic instability
  • marked tachycardia
  • hypotension
  • mental status deterioration/coma
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6
Q

Receptors which detect effects of hypotension/hypovolemia?

A
  • High-pressure baroreceptors
  • Low-pressure baroreceptors
  • Renal Juxtaglomerular apparatus
  • Central and peripheral chemoreceptors
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7
Q

Autonomic response to hypotension effect on sympathetics/parasympathetics?

A

↑ sympathetic

↓ parasympathetic

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8
Q

Autonomic response to hypotension effect on effectors?

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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9
Q

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

A

↑ ADH/AVP

↑ vasoconstriction

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10
Q

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

A
  • ↑ ANG II by activation of RAAS
  • ↑ vasoconstriction
  • Sympathetic stimulation of juxtaglomerular granular cells –>renin
  • Renal vasoconstriction –> ↓ renal pressure –> ↑ renin
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11
Q

How can loss of blood volume be corrected?

A
  1. Renal fluid conservation
  2. Stimulation of thirst –> water intake
  3. Net capillary reabsorption (Starling’s forces)
    “Transcapillary refill”
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12
Q

Which factors promote renal retention of Na+ and H2O?

A
  • ↑ Sympathetic activity
  • ↑ ANG II
  • ↑ Aldosterone
  • ↑ Anti-diuretic hormone/Arginine Vasopressin
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13
Q

How does sympathetic activity promote renal retention of Na+ and H2O?

A

↑ Sympathetic activity

  • Renal vasoconstriction (↓ RBF) –>↓ filtration rate –> ↓ Na+ excretion
  • ↑ Renin (Activation of RAAS)
  • Direct stimulation of Na+ reabsorption by renal tubule cells
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14
Q

How does ANG II/aldosterone promote renal retention of Na+ and H2O?

A

↑ ANG II:
↑ Aldosterone
↑ ADH/AVP secretion
↑ Thirst stimulation

↑ Aldosterone:
↑ Na+ reabsorption

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15
Q

How does ADH/Vasopressin promote renal retention of Na+ and H2O?

A

↑ Anti-diuretic hormone/Arginine Vasopressin:
↑ by ANG II and osmoreceptors
↑ H2O reabsorption

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16
Q

Transcapillary Refill: correction for volume loss

A
  • Net reabsorption of fluid: from interstitial fluid  capillaries
  • Reabsorption of interstitial fluid helps replace lost blood volume
  • Result: initial hemodilution
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17
Q

Effect of normal Pc on capillaries?

A
  • net filtration
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18
Q

Effect of initial hypotension after hemorrhage on capillaries?

A
  • Net reabsorption
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19
Q

Effect on capillaries following compensation for volume loss (↑↑↑ arteriolar & ↑ venular resistance):

A
  • Net reabsorption
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20
Q

Hypovolemic Shock:

A
  • Tachycardia
  • Hypotension
  • Generalized arteriolar vasoconstriction & venoconstriction
  • Oliguria
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21
Q

Negative-feedback (compensatory) mechanisms for Hypovolemic Shock:

A
  • Baroreceptor reflexes
  • Chemoreceptor reflexes
  • Transcapillary reabsorption of interstitial fluid
  • Renal conservation of salt and water
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22
Q

Positive-feedback (decompensatory) mechanisms for Hypovolemic Shock:

A
  • Cardiac failure
  • Acidosis
  • CNS depression
23
Q

After temporary improvement: hemorrhagic shock may become irreversible (even with transfusion) due to the following multiple failures:

A
  1. Vasoconstrictor response
  2. Capillary refill response
  3. Heart failure
  4. CNS response
24
Q

Failure of the Vasoconstrictor Response:

Prolonged hemorrhagic hypotension:

A

TPR: initial increase tapers off and return to pre-hemorrhage levels

25
Q

Failure of the Vasoconstrictor Response:

“Sympathetic escape”

A
  • Desensitization α1-adrenoceptors

- Depletion of neurotransmitters

26
Q

Failure of the Vasoconstrictor Response:

Metabolites and vasodilators released by ischemic tissues

A
  • Counteract vasoconstrictor stimuli
  • Late phases of irreversible shock: May be completely unresponsive to vasoconstrictor drugs
27
Q

Failure of the Vasoconstrictor Response:

Decline in plasma AVP/ADH from early peak response

A
  • Decline in trigger to release
  • Depletion of AVP/ADH posterior pituitary stores
  • Restoration of ADH to initial peak can significantly increase BP
28
Q

Failure of Transcapillary Refill Process: Failure of vessels to sustain resistance

A
  • Precapillary vessels tend to fail before post capillary vessels
  • ↓ precapillary constricton&raquo_space; ↓ postcapillary constriction
  • ↑ relative ratio R post/R pre–> ↑ Pc –> promotes net filtration
29
Q

Failure of the Heart:

A
  • Prolonged, severe hypovolemic shock –> cardiogenic shock (inadequate coronary perfusion)
  • Negative inotropy:
    • Ischemic cardiac tissue
    • Acidosis
    • Other ischemic organs may release cardiotoxic factors
30
Q

Failure of the CNS: decreased cerebral perfusion

A
  • detected as ↑ PCO2 and ↑ [H+]:
  • ↑ central chemoreceptor activation
  • ↑ CV control center stimulation
31
Q

Failure of the CNS: Prolonged inadequate cerebral perfusion

A
  • leads to ischemia
  • ↓ neural activity
  • ↓ sympathetic output
  • ↓ vascular and cardiac responses to hemorrhage
32
Q

Physiologic Characteristics of Hypovolemic sock:

A
  • Dec CVP and PCWP
  • Dec CO
  • Increased SVR
  • Dec Venous O2 saturation
33
Q

Physiologic Characteristics of Cardiogenic shock:

A
  • increased CVP and PCWP
  • Dec CO
  • Increased SVR
  • dec venous saturation
34
Q

Physiologic Characteristics of Early (hyperdynamic) septic shock:

A
  • no change in CVP and PCWP
  • increased CO
  • Dec SVR
  • Increased Venous O2 saturation
35
Q

Physiologic Characteristics of Late (hypodynamic) septic shock:

A
  • no change in CVP and PCWP
  • dec CO
  • increased SVR
  • no change in venous O2 saturation
36
Q

Frank Starling Curve: Systolic Failure

A
  • At a given EDV or Pressure: ↓ SV (↓ CO)

- ↑ EDV remaining after systole in impaired heart results in insignificant increase in SV despite ↑ LVEDP

37
Q

What change to the curve is expected in a failing heart with cardiogenic shock?

A 
↓ SV
↓ CO
↓ MAP
↓ Tissue perfusion
↓ Inotropy
38
Q

Cause of Pulmonary Edema

A
  • ↑ pulmonary v.v. pressure–> ↑ pulmonary capillary hydrostatic pressure
  • Promotes filtration
39
Q

Evidence of Pulmonary Edema in a patient

A
  • Distended jugular veins
  • Mild pitting edema
  • Slight hepatomegaly
40
Q

Initial DX steps of cardiogenic shock

A
  • Hx and PE
  • ECG
  • Echo
  • Labs
  • CXR
  • pulmonary artery cath
41
Q

Initial management of cardiogenic shock

A
  • supplemental O2/mechanical ventilation
  • Venous access
  • Pain relief
  • Hemodynamic support (fluid if no pulmonary edema, vasopressors for hypotension unresponsive to fluids)
42
Q

sepsis host response is initiated via:

A
  • Pathogen Associated Molecular Patterns (PAMPs)

- Pattern Recognition Receptors

43
Q

Activation of pattern recognition receptors such as ______ results in _____.

A

MyD88 / NF-kB Signaling…..Pro-inflammatory Cytokines and Vascular Adhesion Molecules

44
Q

Acute, Local Inflammation

A
  • Leukocyte extravasation
  • Alterations to endothelial cell junctions
  • Warmth, erythema, edema
45
Q

Leukocyte extravasation basic steps

A
  • rolling
  • integrin activation by chemokines
  • stable adhesion
  • migration through endothelium
46
Q

Pro-Inflammatory Cytokines Involved in sepsis

A
  • Tumor Necrosis Factor (TNF-a)
  • IL 1
  • IL 6
47
Q

Role of TNF alpha, IL 1, and IL 6 in inflammation

A
  • Stimulates the recruitment and activation of neutrophils and monocytes –> Leads to the production of IL-1
  • Activates vascular endothelial cells to express cellular adhesion molecules
  • Can induce extrinsic apoptosis
48
Q

How does local, acute inflammation transitions to systemic effects?

A

When the concentration of Pro-Inflammatory Cytokines exceeds local boundaries

49
Q

Systemic cellular effects of Pro-Inflammatory Cytokines

A
  • Tissue Ischemia
  • Cytopathic Injury, Mitochondrial Dysfunction (NO)
  • Cell Death
50
Q

Effects of Pro-Inflammatory Cytokines on Central nervous system

A
  • Hypothalamus

- Febrile Response

51
Q

Effects of Pro-Inflammatory Cytokines on liver

A
  • Hepatocytes

- Acute Phase Response

52
Q

Effects of Pro-Inflammatory Cytokines on CV system

A
  • Vasodilation: NO and prostaglandins
  • Hypotension
  • Decreased CO
  • Thrombosis via activation of tissue factor
53
Q

End organ damage from Pro-Inflammatory Cytokines Microcirculatory damage / disorder:

A
  • CNS
  • Lungs
  • GI
  • Liver
  • Kidney

PCM III (13 decks)

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