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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
Failure of the Vasoconstrictor Response: | “Sympathetic escape”
- Desensitization α1-adrenoceptors | - Depletion of neurotransmitters
26
Failure of the Vasoconstrictor Response: | Metabolites and vasodilators released by ischemic tissues
- Counteract vasoconstrictor stimuli - Late phases of irreversible shock: May be completely unresponsive to vasoconstrictor drugs
27
Failure of the Vasoconstrictor Response: | Decline in plasma AVP/ADH from early peak response
- Decline in trigger to release - Depletion of AVP/ADH posterior pituitary stores - Restoration of ADH to initial peak can significantly increase BP
28
Failure of Transcapillary Refill Process: Failure of vessels to sustain resistance
- Precapillary vessels tend to fail before post capillary vessels - ↓ precapillary constricton >> ↓ postcapillary constriction - ↑ relative ratio R post/R pre--> ↑ Pc --> promotes net filtration
29
Failure of the Heart:
- Prolonged, severe hypovolemic shock --> cardiogenic shock (inadequate coronary perfusion) - Negative inotropy: - Ischemic cardiac tissue - Acidosis - Other ischemic organs may release cardiotoxic factors
30
Failure of the CNS: decreased cerebral perfusion
- detected as ↑ PCO2 and ↑ [H+]: - ↑ central chemoreceptor activation - ↑ CV control center stimulation
31
Failure of the CNS: Prolonged inadequate cerebral perfusion
- leads to ischemia - ↓ neural activity - ↓ sympathetic output - ↓ vascular and cardiac responses to hemorrhage
32
Physiologic Characteristics of Hypovolemic sock:
- Dec CVP and PCWP - Dec CO - Increased SVR - Dec Venous O2 saturation
33
Physiologic Characteristics of Cardiogenic shock:
- increased CVP and PCWP - Dec CO - Increased SVR - dec venous saturation
34
Physiologic Characteristics of Early (hyperdynamic) septic shock:
- no change in CVP and PCWP - increased CO - Dec SVR - Increased Venous O2 saturation
35
Physiologic Characteristics of Late (hypodynamic) septic shock:
- no change in CVP and PCWP - dec CO - increased SVR - no change in venous O2 saturation
36
Frank Starling Curve: Systolic Failure
- At a given EDV or Pressure: ↓ SV (↓ CO) | - ↑ EDV remaining after systole in impaired heart results in insignificant increase in SV despite ↑ LVEDP
37
What change to the curve is expected in a failing heart with cardiogenic shock?
``` ↓ SV ↓ CO ↓ MAP ↓ Tissue perfusion ↓ Inotropy ```
38
Cause of Pulmonary Edema
- ↑ pulmonary v.v. pressure--> ↑ pulmonary capillary hydrostatic pressure - Promotes filtration
39
Evidence of Pulmonary Edema in a patient
- Distended jugular veins - Mild pitting edema - Slight hepatomegaly
40
Initial DX steps of cardiogenic shock
- Hx and PE - ECG - Echo - Labs - CXR - pulmonary artery cath
41
Initial management of cardiogenic shock
- supplemental O2/mechanical ventilation - Venous access - Pain relief - Hemodynamic support (fluid if no pulmonary edema, vasopressors for hypotension unresponsive to fluids)
42
sepsis host response is initiated via:
- Pathogen Associated Molecular Patterns (PAMPs) | - Pattern Recognition Receptors
43
Activation of pattern recognition receptors such as ______ results in _____.
MyD88 / NF-kB Signaling.....Pro-inflammatory Cytokines and Vascular Adhesion Molecules
44
Acute, Local Inflammation
- Leukocyte extravasation - Alterations to endothelial cell junctions - Warmth, erythema, edema
45
Leukocyte extravasation basic steps
- rolling - integrin activation by chemokines - stable adhesion - migration through endothelium
46
Pro-Inflammatory Cytokines Involved in sepsis
- Tumor Necrosis Factor (TNF-a) - IL 1 - IL 6
47
Role of TNF alpha, IL 1, and IL 6 in inflammation
- 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
How does local, acute inflammation transitions to systemic effects?
When the concentration of Pro-Inflammatory Cytokines exceeds local boundaries
49
Systemic cellular effects of Pro-Inflammatory Cytokines
- Tissue Ischemia - Cytopathic Injury, Mitochondrial Dysfunction (NO) - Cell Death
50
Effects of Pro-Inflammatory Cytokines on Central nervous system
- Hypothalamus | - Febrile Response
51
Effects of Pro-Inflammatory Cytokines on liver
- Hepatocytes | - Acute Phase Response
52
Effects of Pro-Inflammatory Cytokines on CV system
- Vasodilation: NO and prostaglandins - Hypotension - Decreased CO - Thrombosis via activation of tissue factor
53
End organ damage from Pro-Inflammatory Cytokines Microcirculatory damage / disorder:
- CNS - Lungs - GI - Liver - Kidney

PCM III (13 decks)

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