Hypotensive shock Flashcards

1
Q

Define circulatory shock

A

Generalized inadequate blood flow through body resulting in significant decreased tissue/organ perfusion

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2
Q

What are the types of shock?

A
  1. Cardiogenic
  2. Hypovolemic
  3. Obstructive
  4. Distributive
    A. Neurogenic
    B. Anaphylactic
    C. Septic
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3
Q

What is compensated shock?

A

Normal circulatory compensatory mechanisms take over

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4
Q

What is progressive shock?

A

Shock progressively worsens

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5
Q

What is decompensated shock/Irreversible?

A

Leads to death

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6
Q

What is the pathophys of compensated shock?

A
  1. Compensatory mechanisms activated to maintain cardiac output & perfusion to brain & heart
  2. Baroreceptors sense drop in BP
    A. Epi & NE released
  3. ↑ peripheral resistance, BP, & contractility
  4. RAAS activated
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7
Q

What is the pathophys of progressive shock?

A
  1. Tissue hypoxia
  2. Cells switch to anaerobic metabolism
    A. Lactic acid accumulates
  3. Endothelial mediators released 2° to hypoxia
    A. Venous pooling & ↑ capillary permeability
    B. Sluggish blood flow increases risk of DIC
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8
Q

What is the pathophys of irreversible shock?

A
  1. Inadequate perfusion damages cell membranes
    A. Lysosomal enzymes released, energy stores depleted, leading to cell death
  2. Perfusion to coronary arteries reduced due to low BP
  3. Decreased CO
  4. Circulatory & respiratory failure follow
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9
Q

What is cardiogenic shock?

A
  1. Low output cardiac failure resulting from inadequate cardiac pumping (MI)
  2. Survival rate often less than 15%
  3. Most common cause of shock in hospital setting
  4. Vicious cycle which is difficult to change
  5. In ischemic heart, BP as low as 80-90 mm Hg can set off vicious cycle leading to cardiac deterioration
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10
Q

What are the causes of cardiogenic shock?

A
  1. Arrhythmias
  2. MI
  3. Heart failure
  4. Valve disorders
  5. Cardiomyopathies
  6. HTN
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11
Q

What is the results of cardiogenic shock?

A

Often a patient dies of cardiogenic shock before normal compensatory mechanisms begin

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12
Q

What are the general treatment guidelines for cardiogenic shock?

A
  1. Treatment extremely important in management of acute MI’s

2. Treatment includes inotropic drugs & pressors

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13
Q

What are the sxs of cardiogenic shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
  6. JVD
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14
Q

What dx studies are used for cardiogenic shock?

A
  1. EKG
  2. ECHO
  3. ABG
  4. CBC, PT, PTT, thrombin time, Plts
  5. BMP
  6. Trop, CK MB
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15
Q

What is seen on an echo in cardiogenic shock?

A
  1. Decreased left ventricular contractility
  2. Seen as hypokinesis of ventricular wall
  3. Decreased ejection fraction (EF)
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16
Q

What is seen on ABG in cardiogenic shock?

A

Metabolic acidosis

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17
Q

What is the most common cause of hypovolemic shock?

A
  1. Hemorrhage
  2. Hemorrhage decreases venous return & filling pressure
  3. As a result, cardiac output decreases
  4. End result is shock
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18
Q

What is the pathophys of hemorrhagic hypovolemic shock?

A
  1. Decrease in arterial pressure w/ hemorrhage causes sympathetic stimulation
    A. Baroreceptors
  2. Leads to vasoconstriction throughout body
  3. Heart rate also increases
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19
Q

What is involved in compensated hemorrhagic hypovolemic shock?

A
  1. Several feedback mechanisms attempt to return cardiac output & arterial pressure back to normal
  2. These include:
    A. Baroreceptor reflexes
    -Powerful sympathetic stimulation of CNS
    B. CNS ischemic response
    -Powerful sympathetic stimulation when SBP
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20
Q

What is involved in decompensated hemorrhagic hypovolemic shock?

A
  1. Decompensated shock
    A. Decreased BP leads to decreased blood flow to myocardium -> decreased cardiac output
  2. Vasomotor failure
    A. Due to decreased BP, there is decreased perfusion of brain, specifically, the vasomotor center
    B. Leads to decrease in sympathetic stimulation
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21
Q

What is involved in progressive hemorrhagic hypovolemic shock?

A
  1. Blockage of small vessels with sludge
  2. Increased capillary permeability
  3. Release of toxins by ischemic tissue
  4. Cardiac depression caused by endotoxin
  5. Generalized cellular deterioration
  6. Tissue necrosis
  7. Metabolic acidosis
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22
Q

What are the sxs of hemorrhagic hypovolemic shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool and mottled extremities
  6. JVD
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23
Q

What are the dx studies for hemorrhagic hypovolemic shock?

A
  1. EKG
  2. TEE
  3. ABG
  4. CBC, PT, PTT, thrombin time, plts
  5. BMP
  6. Trop, CK MB
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24
Q

What are the TEE results in hemorrhagic hypovolemic shock?

A
  1. Decreased left ventricular volume due to decreased filling
  2. Contractility preserved
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25
Q

What are the ABG results in hemorrhagic hypovolemic shock?

A

Metabolic acidosis

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26
Q

What can non-hemorrhagic hypovolemic shock results from?

A
1. Can result from:
A. Intestinal obstruction
B. Severe burns
C. Dehydration
2. Similar to hemorrhage except blood viscosity now significantly increased
27
Q

What is the pathophys of intestinal obstruction causing hypovolemic shock?

A
  1. Distention of intestine partly blocks venous flow in intestinal wall
  2. Results in increased capillary pressure which causes fluid to leak into interstitial spaces & intestinal walls/lumen
  3. Because interstitial fluid has high concentration of protein, there is reduced blood plasma protein leading to decreased blood volume
28
Q

What is the pathophys of severe burns causing hypovolemic shock?

A
  1. Significant amount fluid is lost through burned skin

2. Results in markedly reduced plasma volume

29
Q

What is the pathophys of dehydration causing hypovolemic shock?

A
  1. Reduces plasma volume which can lead to hypovolemic shock
  2. Can result from:
    A. Excessive sweating
    B. Severe vomiting/diarrhea
    C. Excessive loss of fluid by kidneys in nephrotic syndrome
    D. Destruction of adrenal cortex
30
Q

What are the sxs of non-hemorrhagic hypovolemic shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
31
Q

What dx studies are used for non-hemorrhagic hypovolemic shock?

A
  1. EKG
  2. ECHO
  3. ABG
  4. CBC, PT, PTT, thrombin time, plts
  5. BMP
  6. Trop, CK-MB
32
Q

What are the echo results in non-hemorrhagic shock?

A
  1. Significant collapse of SVC/IVC

2. Obliteration of LV cavity @ end of systole

33
Q

What are the ABG results in non-hemorrhagic hypovolemic shock?

A

Metabolic acidosis

34
Q

What causes obstructive shock?

A
  1. Cardiac tamponade
  2. Tension Pneumothorax
  3. Massive PE
  4. Causes acute decrease in CO -> shock
35
Q

What are the sxs of obstructive shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
36
Q

What are the dx studies for obstructive shock?

A
  1. EKG
  2. ECHO
  3. ABG
  4. CBC, PT, PTT, thrombin time, plts
    5 .BMP
  5. Trop, CK MB
37
Q

What are the echo results in obstructive shock?

A
  1. Pericardial effusion

2. Right atrial or R ventricle collapse

38
Q

What are the ABG results in obstructive shock?

A

Metabolic acidosis

39
Q

What are the types of distributive shock?

A
  1. Septic shock
  2. Anaphylactic shock
  3. Neurogenic shock
40
Q

What causes distributive shock?

A
  1. Sepsis
  2. Anaphylaxis
  3. Pancreatitis
  4. Burns
  5. Traumatic spinal cord injury
  6. Severe systemic vasodilation results in inadequate CO & tissue hypoperfusion despite normal circulatory volume
41
Q

What are the sxs of distributive shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
42
Q

What is the pathophys of neurogenic shock?

A
  1. Sudden loss of vasomotor tone throughout the body
    A. Venous pooling of blood
  2. Reduces mean systemic filling pressure
  3. Reduces venous return to heart
43
Q

What is the etiology of neurogenic shock?

A
1. Deep general anesthesia
A. Depresses vasomotor center
2. Spinal anesthesia
A. Blocks sympathetic nervous outflow tract
3. Brain damage involving the medulla
A. Causes vasomotor paralysis
44
Q

What are the sxs of neurogenic shock?

A
1. Hypotension without compensatory tachycardia
A. Low BP
B. Oliguria
C. Altered mental status
D. Cool & mottled extremities
45
Q

What is the etiology of anaphylaxtic shock?

A
  1. Allergic condition in which cardiac output & arterial pressure decrease significantly
  2. Results from antigen-antibody reaction
46
Q

What is the pathophys of anaphylactic shock?

A
  1. Leads to histamine release
    A. Vasodilation: Decrease in venous return to heart, Decreased arterial pressure
  2. Increased capillary permeability
    A. Leads to rapid loss of fluid & protein in interstitial spaces
47
Q

What are the sxs of anaphylactic shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
48
Q

What cause septic shock?

A
  1. Shock secondary to disseminated bacterial infection
    A. Peritonitis 2° to uterine/fallopian tube infection
    B.Peritonitis 2° to rupture of organ(s) of GI system
    C. Disseminated strep or staph skin infection
    D. Disseminated gangrenous infection
    E. Urosepsis
49
Q

What type of shock causes the most deaths in a hospital setting?

A

Septic

50
Q

What are the sxs of septic shock?

A
  1. Low BP
  2. Tachycardia
  3. Oliguria
  4. Altered mental status
  5. Cool & mottled extremities
    ADDITIONALLY
  6. High fever
  7. Marked vasodilation, especially in infected tissues
  8. Sludging of blood
  9. Development of micro blood clots in widespread areas of body ( DIC-disseminated intravascular coagulation)
51
Q

What are the general treatment measure for shock?

A
  1. ABC’s
  2. Oxygen
  3. Fluids
    A. CVC for infusion of fluids & hemodynamic measuring
    B. CVP: 18 mm Hg suggests volume overload, HF, tamponade, pulmonary HTN
    D. Treatment aimed at CVP 8-12 mm Hg
  4. Monitor I’s & O’s
  5. Telemetry
52
Q

What volume replacement methods are used to treat shock?

A
  1. If shock 2° to hemorrhage, transfuse whole blood
  2. If shock 2° to plasma loss, administer fresh frozen plasma (FFP)
  3. If shock 2° to dehydration, administer appropriate isotonic crystalloid
    A. 0.9% Normal saline
    B. Lactated Ringer’s
53
Q

What vasoactive agents are used to treat shock?

A
1. Vasopressors & inotropic agents
A. Administered only after fluid resuscitation
2. Vasopressors 
A. Support vasomotor tone
B. If persistent hypotension w/high CO after volume resuscitation
3. Inotropic agents
A. Improve contractility
B. Low CO
54
Q

What is dobutamine used for?

A
1. Vasoactive Agent
A. Predominantly beta adrenergic agonist
B. 1st line for cardiogenic shock
C. ↑ contractility 
D. ↓ afterload
55
Q

What are sympathemimetics used for?

A
  1. Drug that mimics sympathetic stimulation
  2. Include epinephrine & norepinephrine
  3. Used when increased vasoconstriction is required
  4. Beneficial when treating:
    A. Neurogenic shock
    B. Anaphylactic shock
    C. Epinephrine drug of choice
56
Q

What are the effects of a low dose of dopamine?

A
  1. (2-5 mcg/kg.min) stimulates dopaminergic & beta adrenergic receptors
  2. ↑ GFR, HR & contractility
57
Q

When are the effects of a medium dose of dopamine?

A
  1. (5-10 mcg.kg.min) beta 1 adrenergic receptors effects predominate
  2. ↑ HR & contractility
58
Q

When are the effects of a high dose of dopamine?

A
  1. (> 10 mcg/kg/min) alpha adrenergic effects predominate -> peripheral vasoconstriction
59
Q

When is vasopressin (ADH) used?

A
  1. Often used as adjunctive therapy with NE or epi for distributive shock
  2. Causes peripheral vasoconstriction (vasoactive drug)
60
Q

When are corticosteroids indicated in the treatment of shock?

A

Tx of choice in pts w/ shock 2° to adrenal insufficiency

61
Q

When are abx indicated in the treatment of shock?

A

Empiric broad spectrum abx after cultures for pts w/ septic shock

62
Q

Why is the trendelenburg position used to help treat shock?

A
  1. Promotes venous return

2. ↑ cardiac output

63
Q

Why is oxygen used to help treat shock?

A

Although underlying problem is circulatory, increased oxygenation may improve overall oxygenation slightly