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Parker Pathology Block 2 > Hemodynamics 2 > Flashcards

Hemodynamics 2 Flashcards

1
Q

What is shock?

A

Systemic hypoperfusion and cardiovascular collapse

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2
Q

3 causes of shock?

A
  1. Decreased circulating blood volume
  2. Decreased cardiac output
  3. Sepsis
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3
Q

3 other causes of shock (much less common)?

A
  1. Anaphylaxis
  2. SIRS
  3. Neurogenic causes
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4
Q

Hypovolemic shock (decreased circulating blood volume) is due to?

A
  1. Bleeding
  2. Fluid loss from vomiting
  3. Diarrhea
  4. Extensive burns
    * All these things would lead to loss of fluid!
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5
Q

Cardiogenic shock (decreased cardiac output) is due to?

A
  1. MI
  2. Arrhythmia
  3. Pulmonary embolism
  4. Hemopericardium
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6
Q

When a hemopericardium (hemmorhage in the heart) is squeezing the cardiac filling chambers and obstructing filling, what is this called?

A

Cardiac tamponade

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7
Q

Shock due to widespread vasodilation, where not enough blood is returned to the heart and lungs?

A

Septic shock

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8
Q

Can a patient have more than one type of shock at a given time?

A

Of course, Hickam’s dictum

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9
Q

What blood pressure defines “shock”?

A

None, shock is a syndrome, not a number

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10
Q

First symptoms of shock?

A

Agitation… Nervous, fidgety, irritable

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11
Q

Clinical manifestations of shock?

A

Decreased mental status, eventually coma

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12
Q

A patient has a weak rapid (“thready”) pulse, with cool, clammy, cyanotic skin. What kind of shock do they have?

A

Hypovolemic or cardiogenic shock

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13
Q

Patient has warm, flushed skin. What type of shock?

A

Septic shock

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14
Q

7.6% increase in mortality unless an antibiotic is given is a characteristic of?

A

Septic shock

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15
Q

Should you rely on vital signs to indicate shock?

A

No, vital signs are late responders to shock

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16
Q

Why should you be weary of a young trauma or post-op patient with regards to shock?

A

Young ppl are better at compensating. One minute, they fine. The next, cardiac arrest due to painless bleeding into the abdomen or retroperitoneum

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17
Q

Least common of the three major types of shock?

A

Cardiogenic shock

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18
Q

Failure of heart as a pump due to intrinsic heart disease is what type of shock?

A

Cardiogenic

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19
Q

Bleeding into pericardial sac (hemopericardium) prevents the heart from filling and can lead to cardiogenic shock. This is known as?

A

Cardiac tamponade

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20
Q

How do you treat cardiac tamponade?

A

remove the blood from the pericardial sac

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21
Q

A large pulmonary thromboembolus has obstructed the pulmonary trunk. What type of shock are you concerned about?

A

Cardiogenic

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22
Q

Some would put shock from pulmonary embolism or cardiac tamponade into a fourth category of shock known as?

A

Obstructive shock

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23
Q

Explain septic shock?

A

Systemic vasodilation leads to too much blood “pooled” in the periphery and not enough returning to the heart for adequate perfusion

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24
Q

Anaphylactic shock has the same feature as septic shock and these two are sometimes put into a broad group of shock called?

A

Vasogenic shock

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25
Q

Should the ever changing fashion in the terminology of shock come as a shock to you?

A

No, no Nichols, it shouldn’t. Thanks

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26
Q

A type of vasogenic shock due to spinal cord injury or spinal anesthesia causing acute loss of sympathetic nervous system maintenance of normal levels of vasoconstriction?

A

Neurogenic shock

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27
Q

Trauma patients can have shock that is partly hemorrhagic and partly more like septic shock. Why?

A

Increased production of pro inflammatory cytokines such as TNF, IL-1, IL-6

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28
Q

Most common of the three major types of shock?

A

Hypovolemic shock

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29
Q

Is it important to categorize shock? Why?

A

Very important! The type of shock determines the treatment

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30
Q

How much blood loss causes hemorrhagic shock?

A

25-30%

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31
Q

Life threatening shock if not immediately diagnosed and treated?

A

35-45%

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32
Q

Dividing line between life and death?

A

50%

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33
Q

This 50% number comes with caveats. If a very slow hemorrhage occurs in a healthy person, will losing 50% of their blood kill them?

A

No

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34
Q

If someone with MI and narrowing of several large coronary arteries loses 5% of their blood through hemorrhage will they die?

A

Possibly

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35
Q

How is sepsis defined?

A

SIRS with suspected infection

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36
Q

What are the two subsets of sepsis?

A

Severe sepsis and septic shock

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37
Q

Define SIRS

A

2 or more of the following criteria:

  1. Temp above 38 or below 36
  2. HR > 90
  3. Tachypnea > 20 or arterial pCO2 12000 or <4000
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38
Q

Of the three: sepsis, severe sepsis, septic shock, which is most likely to have a positive blood culture?

A

Septic shock: 69% For the others, a positive blood culture is in the minority

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39
Q

A new conference in 2003. Lots of docs made a new list of what qualifies as “sepsis” and “SIRS”. What did they add to the list?

A

About 15 new things.. altered mental status, HR >2 st dev above normal, “significant edema”, positive fluid balance >20ml/kg, lots of others…

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40
Q

What can we take from the fact that tons of doctors couldn’t agree on a concise list of symptoms and signs for sepsis?

A

In diagnosis, there is no substitute for experience

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41
Q

General, overall view of the molecular mechanism of sepsis?

A

PRR’s (on TLR’s, NOD’s and others) bind PAMPs (bacterial cell wall lipoproteins, lipopolysacs). This activates inflammatory cells which release cytokines (TNF, IL-1, 6, 8, 12, 18, INF, HMGB-1). Cytokines upregulate endothelial adhesion molecules that bind leukocytes directing them to site of infection

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42
Q

What molecule is 100-1000 times more potent at inducing vascular dilation and increasing vasc perm than histamine?

A

Platelet activating factor (PAF)

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43
Q

Other functions of PAF?

A
  1. Promotes leukocyte adhesion to endothelial cells
  2. Chemotaxis
  3. Degranulation
  4. Oxidative burst that enables microbial killing in leukocytes
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44
Q

What components of the complement system increase vasc perm and cause vasodilation by inducing mast cells to release histamine?

A

C3a and C5a

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45
Q

According to Nichols (who suuuucks at teaching Immunology), what results in T-cell activation and proliferation?

A

Binding of CD80 (on APC’s) to CD28 (on T-cells)

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46
Q

What sustains expression of CD80 on the surface of APC’s?

A

The release of IL-12 from Th1 cells that have been activated by the APC

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47
Q

Which interleukins (IL) causes release of histamine from mast cells?

A

IL-1 and IL-8

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48
Q

Histamine is released from mast cells and basophils, but also from ?

A

Platelets

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49
Q

What cells can do the arachidonic acid pathway and create prostaglandins?

A

Activated macrophages, neutrophils, mast cells, and endothelial cells

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50
Q

What are prostaglandins?

A

Short lived lipid mediators that bind to G-coupled receptors on many cell types and have a variety of effects.

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51
Q

Which prostaglandins cause vasodilation?

A
  1. PGI2 (prostacyclin)
  2. PGD2
  3. PGE1
  4. PGE2
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52
Q

Which prostaglandins cause an increase in vascular permeability?

A

PGD2 and PGE2

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53
Q

What cells can release PAF?

A

macrophages, neutrophils, mast cells, endothelial cells, platelets

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54
Q

What does PAF do?

A

Increases vascular permeability

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55
Q

What chemical that is a potent vasodilator is released from activated endothelial cells?

A

Nitric oxide (NO)

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56
Q

What cells can produce NO?

A

Endothelial cells, macrophages, neutrophils

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57
Q

How can too much NO cause problems?

A

It would cause too much vasodilation which would damage endothelial cells. Damaged endothelial cells would lead to increased vascular permeability which would allow fluid to leak out of the blood vessels. This would decrease blood volume leading to septic shock

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58
Q

What activates Hagaman factor (XII)?

A

Activated platelets, basement membrane, collagen

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59
Q

Hageman factor is the king activator of what pathways?

A

Kinin, Clotting, Fibrinolytic, Complement

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60
Q

What does activated factor X do?

A

Causes increased vascular permeability and leukocyte emigration from blood vessels

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61
Q

Who is the king of clotting?

A

Thrombin

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62
Q

What does Thrombin generate that causes increased vascular permeability and is chemotactic for leukocytes?

A

Fibrinopeptides

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63
Q

How does Thrombin link the clotting and complement cascades?

A

Thrombin cleaves C5 which releases C5a

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64
Q

Can a medical student memorize all the interconnections of these pathways in a month?

A

No

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65
Q

Will we have to memorize all the interconnections of these pathways in a month if we want to do well on the test?

A

Yes

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66
Q

Endothelial cells, when activated by sepsis, promote what?

A

Increased vascular permeability, dilation, and thrombosis

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67
Q

Does sepsis cause clotting?

A

Yes, it indirectly inhibits fibrinolysis

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68
Q

How does sepsis indirectly inhibit fibrinolysis?

A
  1. Increases plasminogen activator inhibitor-1
  2. Decreases tissue factor pathway inhibitor
  3. Decreases thrombomodulin
  4. Decreases protein C
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69
Q

What is a common complication (50%) in sepsis patients?

A

Unlocalized disseminated intravascular coagulation (DIC)… Septic patients are DICs haha (but it helps doesn’t it…)

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70
Q

Is lipoxin inflammatory or anti-inflammatory?

A

Anti-inflammatory

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71
Q

How is lipoxin anti-inflammatory? What does it do?

A

inhibits neutrophil adhesion to endothelial cells

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72
Q

What is lipoxin generated from ?

A

Arachidonic acid

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73
Q

What are the anti-inflammatory molecules of the complement system?

A

Factor H, DAF, C1 inhibitor, lipoxins

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74
Q

What is anti-inflammatory for macrophages?

A

IL-10

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75
Q

What makes IL-10

A

Macrophages.. It “calms” itself down

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76
Q

What blocks the inflammatory actions of TNF?

A

sTNFR (soluble TNF receptor)

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77
Q

What do you call the anti-inflammatory mechanism that leads to apoptosis of lymphocytes and GI epithelial cells that leads to immunosuppression?

A

Counter-regulatory mechanism

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78
Q

What are some results of immunosuppression?

A

Opportunistic infections, reactivation of latent infections, GI hemorrhage

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79
Q

Can sepsis be fatal due to the counter-regulatory mechanism “overshooting”?

A

You betcha

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80
Q

Whats the acronym for the counter-regulatory mechanism?

A

CARS: compensatory anti-inflammatory response syndrome

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81
Q

When a patient swings back and forth between pro-inlfammatory response and anti-inflammatory response what do you call that?

A

MARS: mixed antagonistic response syndrome

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82
Q

Infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira) block what cytokine?

A

TNF-alpha

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83
Q

What drug blocks IL-6 receptors?

A

Tocilizumab

84
Q

What have these cytokine blocking drugs been used to treat?

A

Autoimmune diseases

85
Q

Extensive trauma or burns, acute pancreatitis, extensive multi-organ ischemic necrosis, and infection can all cause?

A

SIRS

86
Q

Antigens that promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity

A

Superantigens

87
Q

Toxic shock syndrome toxin-1 (TSST-1) activates what percentage of T cell clones?

A

5-20% (the normal is 0.001%)

88
Q

Give the generalized steps going from super antigen to toxic shock syndrome

A

Superantigens activate tons of T-cells. T-cells release tons of cytokines (IL-1 and TNF). Cytokine storm ensues leading to SIRS and toxic shock

89
Q

Toxic shock is due to a nonspecific immunologic over-reaction to a bacterial product produced by?

A

Staphylococci or streptococci

90
Q

Staph aureus has overgrown in a superabsorbent tampon. What is this called?

A

Menstrual toxic shock syndrome

91
Q

First step in treating menstrual toxic shock syndrome?

A

Remove the tampon containing overgrown bacteria. Then give antibiotics

92
Q

Is menstrual toxic shock syndrome due to infection?

A

No, its due to bacteria

93
Q

An infection of what bacteria in the skin or pharynx produces streptococcal pyrogenic exotoxin A (SPEA) acting as a superantigen?

A

Streptococcus pyogenes

94
Q

Is disease racist? Give 2 examples

A

Yes, 90% of toxic shock syndrome occurs in whites. Chinese are more likely to get severely ill with influenza

95
Q

How is severe sepsis/SIRS different from sepsis/SIRS?

A

ACUTE ORGAN DYSFUNCTION!!

96
Q

What’s MOF?

A

Multiple organ failure

97
Q

Can hypovolemic and cardiogenic shock also cause MOF?

A

Yes

98
Q

Does the MOF become its own syndrome with a life of its own?

A

Yes

99
Q

What are the 3 stages of shock?

A
  1. Non-progressive
  2. Progressive
  3. Irreversible
100
Q

Which stage has manifestations of decompensating organ function?

A

Progressive

101
Q

Which stage has reflex compensatory mechanisms that maintain perfusion of vital organs?

A

Non-progressive

102
Q

Which stage of shock causes death even if the cause of shock is reversed?

A

Irreversible

103
Q

What are the compensatory responses to shock?

A
  1. Sympathetic nervous system responses
  2. Fluid shifts within the body
  3. Neuroendocrine stress responses
104
Q

Does the sympathetic nervous system and neuroendocrine system response increase or decrease the heart rate?

A

Increase

105
Q

What are the molecular mediators to neuroendocrine response to shock?

A

Epinepherine/norepinepherine (from adrenal medulla), vasopressin (from pituitary), and renin (from kidneys)

106
Q

Describe the fluid shift response

A

Movement of water from extravascular compartment to the blood. This dilutes the blood, but it keeps the blood pressure up

107
Q

Continue the fluid shift response…

A

Kidneys stop making urine. Body shuts down perfusion to periphery (last to go is heart and brain)

108
Q

Last to go if cerebral shutoff is slow enough?

A

Deeply emotional memories and central “tunnel” vision

109
Q

Cells are deprived of adequate oxygen so they resort to anaerobic metabolism generating lactic acid. What stage of shock are we in?

A

Progressive

110
Q

What are the biomarkers for the “point of no return”?

A

Blood levels of TNF-alpha, IL-1, and IL-6

111
Q

Pathology of shock in brain?

A

Cerebral necrosis with red (dead) neurons and cerebral edema

112
Q

Pathology of shock in intestines?

A

Hemorrhagic ischemic enteritis

113
Q

Pathology of shock in kidneys?

A

Renal acute tubular necrosis

114
Q

Pathology of shock in adrenals?

A

Adrenal cortical lipid depletion and necrosis

115
Q

Pathology of shock in liver?

A

Centrilobular hepatic necrosis

116
Q

Pathology of shock in lungs?

A

Pulmonary diffuse alveolar damage

117
Q

Pathology of shock in heart?

A

Myocardial necrosis

118
Q

Are cerebral necrosis and edema common outcomes of shock?

A

Yes

119
Q

How long after death do the neurons in the brain develop condensed cytoplasm rendered hypereosinophilic?

A

12 hours

120
Q

What is the name for these hypereosinophilic (in the cytoplasm) neurons?

A

Red neurons

121
Q

The dead red neurons shrink and their nuclei become shrunken and condensed and hyper basophilic. What is this clumping of the nucleus called?

A

Pyknosis

122
Q

People that are resuscitated from shock or cardiac arrest can have return of all organ function except the brain. Why?

A

Neurons do not regenerate

123
Q

Shutting off the bowel can convert hypovolemic shock to?

A

Septic shock

124
Q

Ischemic bowel mucosa becomes?

A

Leaky and sticky

125
Q

What all leaks into the bowel/mucosa during bowel ischemia/necrosis?

A

Bile pigment, fibronectin (which causes stool to stick to bowel linings), blood

126
Q

Whats the pathologic appearance of ischemic bowel?

A

Dusky

127
Q

How do you cure septic shock from ischemic bowel?

A

Remove the portion of ischemic bowel

128
Q

Acute kidney injury (AKI) caused by shock is irreversible? T/F

A

False, it is reversible

129
Q

Gross pathology of AKI?

A

swollen kidney with pale cortex and congested medulla

130
Q

AKI “hits” primarily in the?

A

Tubules

131
Q

What does AKI do to the tubules?

A

Loss of proximal tubule epithelial cell brush borders, then epithelial cell swelling and vacuolization. Finally, epithelial cell necrosis and sloughing into tubular lumen

132
Q

What are the two possible elements of tubular obstruction in the case of AKI?

A
  1. Eosinophilic hyaline material (Tamm-Horsfall protein)
  2. If shock has resulted in rhabdomyolysis (skeletal muscle breakdown), then myoglobin casts may also obstruct the tubules
133
Q

Leukocytes in the vasa recta (small blood vessels of adrenal medulla) is associated with?

A

AKI

134
Q

What does shock initially do to the adrenal glands?

A

Makes them deplete their cholesterol making stress hormones which enter the bloodstream

135
Q

Adrenal necrosis is frequently accompanied by?

A

Hemorrhage

136
Q

What is a big infectious concern in children that can lead to massive adrenal hemorrhage and necrosis?

A

Neisseria meningitidis

137
Q

Adrenal hemorrhage and necrosis (most commonly due to Neisseria meningitidis) is known as?

A

Waterhouse-Friderichsen syndrome

138
Q

Gross path of shock liver?

A

Nutmeg liver

139
Q

Microscopic pathology of shock liver?

A

Coagulative necrosis of hepatocytes in the center of hepatic lobules

140
Q

Vulnerability of hepatocytes to ischemia is directly proportional to their proximity to?

A

Hepatic lobular central veins

141
Q

What is the popular thing to call shock lung?

A

ALI (acute lung injury)

142
Q

Gross path of shock lung (ALI)?

A

Firn, edematous, congested, beefy, red organ

143
Q

Microscopic path of ALI?

A

Increased neutrophils in the capillaries in the septa between alveoli

144
Q

Whats the chemotactic for the neutrophils that invade the lung after ALI? What produces these chemokines?

A

IL-8, produced by macrophages

145
Q

What kind of damage do the neutrophils do to the lung?

A

Release substances (oxidants, proteases, PAF, leukotrienes) that damage alveolar epithelial cells and increase permeability of air/blood barrier

146
Q

With typical ALI, alveolar adema fluid condenses into eosinophilic hyaline membranes lining the airspaces. What does this cause?

A

Can block diffusion of oxygen resulting in hypoxemia (decreased oxygen loading of the blood passing thru the lungs)

147
Q

Severe end of ALI?

A

ARDS (acute respiratory distress syndrome)

148
Q

Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in absence of evidence for cardiogenic pulmonary edema?

A

ARDS

149
Q

Is disease racist? Give 2 examples

A

Yes, 90% of toxic shock syndrome occurs in whites. Chinese are more likely to get severely ill with influenza

150
Q

How is severe sepsis/SIRS different from sepsis/SIRS?

A

ACUTE ORGAN DYSFUNCTION!!

151
Q

What’s MOF?

A

Multiple organ failure

152
Q

Can hypovolemic and cardiogenic shock also cause MOF?

A

Yes

153
Q

Does the MOF become its own syndrome with a life of its own?

A

Yes

154
Q

What are the 3 stages of shock?

A
  1. Non-progressive
  2. Progressive
  3. Irreversible
155
Q

Which stage has manifestations of decompensating organ function?

A

Progressive

156
Q

Which stage has reflex compensatory mechanisms that maintain perfusion of vital organs?

A

Non-progressive

157
Q

Which stage of shock causes death even if the cause of shock is reversed?

A

Irreversible

158
Q

What are the compensatory responses to shock?

A
  1. Sympathetic nervous system responses
  2. Fluid shifts within the body
  3. Neuroendocrine stress responses
159
Q

Does the sympathetic nervous system and neuroendocrine system response increase or decrease the heart rate?

A

Increase

160
Q

What are the molecular mediators to neuroendocrine response to shock?

A

Epinepherine/norepinepherine (from adrenal medulla), vasopressin (from pituitary), and renin (from kidneys)

161
Q

Describe the fluid shift response

A

Movement of water from extravascular compartment to the blood. This dilutes the blood, but it keeps the blood pressure up

162
Q

Continue the fluid shift response…

A

Kidneys stop making urine. Body shuts down perfusion to periphery (last to go is heart and brain)

163
Q

Last to go if cerebral shutoff is slow enough?

A

Deeply emotional memories and central “tunnel” vision

164
Q

Cells are deprived of adequate oxygen so they resort to anaerobic metabolism generating lactic acid. What stage of shock are we in?

A

Progressive

165
Q

What are the biomarkers for the “point of no return”?

A

Blood levels of TNF-alpha, IL-1, and IL-6

166
Q

Pathology of shock in brain?

A

Cerebral necrosis with red (dead) neurons and cerebral edema

167
Q

Pathology of shock in intestines?

A

Hemorrhagic ischemic enteritis

168
Q

Pathology of shock in kidneys?

A

Renal acute tubular necrosis

169
Q

Pathology of shock in adrenals?

A

Adrenal cortical lipid depletion and necrosis

170
Q

Pathology of shock in liver?

A

Centrilobular hepatic necrosis

171
Q

Pathology of shock in lungs?

A

Pulmonary diffuse alveolar damage

172
Q

Pathology of shock in heart?

A

Myocardial necrosis

173
Q

Are cerebral necrosis and edema common outcomes of shock?

A

Yes

174
Q

How long after death do the neurons in the brain develop condensed cytoplasm rendered hypereosinophilic?

A

12 hours

175
Q

What is the name for these hypereosinophilic (in the cytoplasm) neurons?

A

Red neurons

176
Q

The dead red neurons shrink and their nuclei become shrunken and condensed and hyper basophilic. What is this clumping of the nucleus called?

A

Pyknosis

177
Q

People that are resuscitated from shock or cardiac arrest can have return of all organ function except the brain. Why?

A

Neurons do not regenerate

178
Q

Shutting off the bowel can convert hypovolemic shock to?

A

Septic shock

179
Q

Ischemic bowel mucosa becomes?

A

Leaky and sticky

180
Q

What all leaks into the bowel/mucosa during bowel ischemia/necrosis?

A

Bile pigment, fibronectin (which causes stool to stick to bowel linings), blood

181
Q

Whats the pathologic appearance of ischemic bowel?

A

Dusky

182
Q

How do you cure septic shock from ischemic bowel?

A

Remove the portion of ischemic bowel

183
Q

Acute kidney injury (AKI) caused by shock is irreversible? T/F

A

False, it is reversible

184
Q

Gross pathology of AKI?

A

swollen kidney with pale cortex and congested medulla

185
Q

AKI “hits” primarily in the?

A

Tubules

186
Q

What does AKI do to the tubules?

A

Loss of proximal tubule epithelial cell brush borders, then epithelial cell swelling and vacuolization. Finally, epithelial cell necrosis and sloughing into tubular lumen

187
Q

What are the two possible elements of tubular obstruction in the case of AKI?

A
  1. Eosinophilic hyaline material (Tamm-Horsfall protein)
  2. If shock has resulted in rhabdomyolysis (skeletal muscle breakdown), then myoglobin casts may also obstruct the tubules
188
Q

Leukocytes in the vasa recta (small blood vessels of adrenal medulla) is associated with?

A

AKI

189
Q

What does shock initially do to the adrenal glands?

A

Makes them deplete their cholesterol making stress hormones which enter the bloodstream

190
Q

Adrenal necrosis is frequently accompanied by?

A

Hemorrhage

191
Q

What is a big infectious concern in children that can lead to massive adrenal hemorrhage and necrosis?

A

Neisseria meningitidis

192
Q

Adrenal hemorrhage and necrosis (most commonly due to Neisseria meningitidis) is known as?

A

Waterhouse-Friderichsen syndrome

193
Q

Gross path of shock liver?

A

Nutmeg liver

194
Q

Microscopic pathology of shock liver?

A

Coagulative necrosis of hepatocytes in the center of hepatic lobules

195
Q

Vulnerability of hepatocytes to ischemia is directly proportional to their proximity to?

A

Hepatic lobular central veins

196
Q

What is the popular thing to call shock lung?

A

ALI (acute lung injury)

197
Q

Gross path of shock lung (ALI)?

A

Firn, edematous, congested, beefy, red organ

198
Q

Microscopic path of ALI?

A

Increased neutrophils in the capillaries in the septa between alveoli

199
Q

Whats the chemotactic for the neutrophils that invade the lung after ALI? What produces these chemokines?

A

IL-8, produced by macrophages

200
Q

What kind of damage do the neutrophils do to the lung?

A

Release substances (oxidants, proteases, PAF, leukotrienes) that damage alveolar epithelial cells and increase permeability of air/blood barrier

201
Q

With typical ALI, alveolar adema fluid condenses into eosinophilic hyaline membranes lining the airspaces. What does this cause?

A

Can block diffusion of oxygen resulting in hypoxemia (decreased oxygen loading of the blood passing thru the lungs)

202
Q

Severe end of ALI?

A

ARDS (acute respiratory distress syndrome)

203
Q

Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in absence of evidence for cardiogenic pulmonary edema?

A

ARDS

204
Q

Subendocardial myocyte blood supply is cut off, how long until they begin dying?

A

20 minutes

205
Q

Person sustains a subendocardial MI but is resuscitated they tend to have?

A

A circumferential infarct involving anterior left ventricle, left lateral ventricle, and posterior left ventricle

Parker Pathology Block 2 (2 decks)

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