Shock CIS (Tieman) Flashcards

(29 cards)

1
Q

capillary refill should be

A

2-3 seconds; less indicates hypoperfusion to the skin/ shunting to the organs

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2
Q

clammy skin

A

sweating; blood going to organs instead of skin

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3
Q

pulmonary pressure

A

should be about 25/15

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4
Q

Hypovolemic shock: mild, moderate, severe

A

mild: less than 20% blood volume loss, cool extremities, increased capillary refill time, diaphoresis, collapsed veins, anxiety

moderate 20-40% blood volume loss: add tachycardia, tachypnea, oliguria, postural changes

severe more than 40% blood volume loss: add hemodynamic instability, marked tachycardia, hypotension, mental status deterioration (coma)

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5
Q

Receptors which detect effects of hypotension/hypovolemia

A

High-pressure baroreceptors
Low-pressure baroreceptors
Renal Juxtaglomerular apparatus
Central and peripheral chemoreceptors

blood loss -> decreased central venous pressure –> decreased stroke volume –> decreased cardiac output –> decreased arterial pressure

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6
Q

What is the autonomic response to hypotension?

A

increased sympathetic
decreased parasympathetic

–> increased HR, contractility, TPR, circulating epinephrine, renin, and sweat gland activity (sympathetic cholinergic stimulation)

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7
Q

Humoral regulation of vascular tone in response to hypotension/hypovolemia:

A

ADH/ AVP –> vasoconstriction

ANG II –> vasoconstriction (via RAAS)

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8
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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9
Q

Which factors promote renal retention of Na+ and H2O

A

increased sympathetic activity (renal vasoconstriction–> direct stimulation of Na+ reabsorption by renal tubule cells)

increased Ang II –> aldosterone, ADH/ AVP, THIRST

Aldosterone –> Na+ reabsorption

Anti-diuretic hormone/ arginine vasopressin –> H2O reabsorption

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10
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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11
Q

Hypovolemic shock- negative-feedback (compensatory) mechanisms and positive-feedbakc (decompensatory) mechanisms

A

Hypovolemic Shock:

  • Tachycardia
  • Hypotension
  • Generalized arteriolar vasoconstriction & venoconstriction
  • Oliguria

Outcome of acute blood loss:
Depends on gains of different feedback mechanisms
Balance between positive- and negative-feedback mechanisms

Negative-feedback (compensatory) mechanisms:

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

Positive-feedback (decompensatory) mechanisms:

  • Cardiac failure
  • Acidosis
  • CNS depression
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12
Q

Irreversible Hemorrhagic Shock

A

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

Vasoconstrictor response
Capillary refill response
Heart failure
CNS response

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13
Q

Failure of the Vasoconstrictor Response

A

Prolonged hemorrhagic hypotension:
TPR: initial increase tapers off and return to pre-hemorrhage levels
Possible failures:

1. “Sympathetic escape” Desensitization α1-adrenoceptors Depletion of neurotransmitters 

2. Metabolites and vasodilators released by ischemic tissues Counteract vasoconstrictor stimuli Late phases of irreversible shock:                                                                       	May be completely unresponsive to vasoconstrictor drugs

3. 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
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14
Q

Failure of Transcapillary Refill Process

A

Failure of vessels to sustain resistance:
Precapillary vessels tend to fail before post capillary vessels

decreased precapillary constriction–> decreased postcapillary constriction

increased relative ratio Rpost/ Rpre –> increased Pc –> promotes net filtration

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15
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

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16
Q

Failure of the CNS

A

decreased cerebral perfusion detected as increased Pco2 and increased H+: increased central chemoreceptor activation, increased CV control center stimulation

prolonged inadequate cerebral perfusion –> ischemia: decreased neural activity, decreased sympathetic output, decreased vascular and cardiac responses to hemorrhage

17
Q

trachea midline means what?

A

pneumothorax is not present; usually that would cause a shift of the trachea on x-ray

18
Q

pulsus paradoxus means

A

not getting enough blood during diastole

19
Q

things that can cause obstructive shock

A

tension pneumo
foreign object
giant pulmonary embolus/ saddle, etc.

20
Q

hepatomegaly in shock/ CHF?

21
Q

Frank Starling Curve: Systolic Failure

A

at a given EDV or pressure: decreased SV (decreased CO/ CI) vs. normal

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

22
Q

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

A

decreased SV, CO, MAP, tissue perfusion, and inotropy

23
Q

Cardiorespiratory Effects of LV Heart Failure

A

increased LV pressure –> increased LA pressure–> increased pulmonary vv pressure–> increased pulmonary capillary hydrostatic pressure

promotes increased filtration –> pulmonary edema (rales!)

24
Q

MOAN therapy

A

morphine
oxygen
aspirin
nitrates

25
what should left atrial filling pressure be?
15- 18 or so
26
MOst common infections leading to sepsis
lung infection UTIs gut infections skin infections abdominal associated with the highest mortality rate gram positives: staph and strep gram negs: e coli, pseudomonas, and klebsiella
27
What drives the drop in oxygen availability during sepsis and leading, ultimately, to death?
insult--> trigger (PAMPs, DAMPs)--> complement/ coagulation system, vascular and tissue responses, blood and lymphatid responses (granulocytes,macrophages, monocytes, lymphocytes) --> confusion, respiratory distress, shock, oliguria/ anuria, liver failure, loss of barrier function in the gut and ileus, capillary lead edema, DIC
28
what type of shock is septic?
distributive
29
how do we treat septic shock?
fluids and then pressors