Lecture 12: Blood Flow Alterations, Shock

Question 1

Primary hemostasis includes:

1. Coagulation cascade
2. Activation of thrombin
3. Fibrinolysis
4. Platelet aggregation

Answer 1

Platelet aggregation

Question 2

Brick is to mortar as platelets are to:

1. Thrombin
2. Factor VII
3. Fibrin
4. Plasminogen

Answer 2

Fibrin

Fibrin is the glue that helps stabilize the platelets

Question 3

1. what is this
2. How can you tell this is formed antemortem

Answer 3

1. Arterial thrombus (saddle thrombus)
2. firm
   • Other clotted blood easily washed out
   • True thrombus stays behind
   • pale regions, dark red regions

Question 4

1. Where is an arterial thrombus initiated at?
2. does it grow upstream or downstream?
3. Will it always be completely occlusive?

Answer 4

1. Initiated at areas of endothelial damage
2. Downstream growth (away from site of attachment)
   
   • There’s the attachment site, and then the growth of thrombus continues away from the heart
3. can be completely occlusive, but often times are not
   • Remember it’s a higher pressure vessel, so blood will blast through to some degree
   • If it’s a fully occlusive thrombus, then death will come rapidly

Question 5

1. if a tail of an arterial thrombus breaks off and lodge in other places what will that be called?
2. what does it prevent?

Answer 5

1. Called a thromboembolism
2. will prevent oxygenated blood from entering a site

Question 6

1. What is this called?
2. What distinguishes it?
3. What necrosis will this be classified as?

Answer 6

1. renal arterial infarct
2. often have a wedge shaped outline
   
   • Subtle elevation of the cortex here, so it’s slightly swollen,
   • it’s pale
   • we can still see the linear structures that represent the nephrons
3. Coagulative necrosis

Question 7

1. Where would venous thrombi form?
2. Are they sometimes or often occlusive?
3. Will it have upstream or downstream growth?
4. What will it prevent?

Answer 7

1. venous thrombi are most likely to occur in areas of stasis
   
   • Blood pooling is a risk factor
   • Remember there’s less pressure, less vascular tone in the venous system
   • So you have the greater likelihood that the blood may pool
2. Often occlusive
3. Upstream growth
   
   • Have a site of attachment, and that thrombus is going to grow in front of that attachment
4. prevent the venous blood from leaving a site

Question 8

1. Would this be an arterial or venous thrombi?
2. why?

Answer 8

1. venous thrombi
2. Blood can’t escape so the Lesion will be dark red to black in color

Question 9

1. what kind of infarct would this be
2. why is this happening

Answer 9

1. venous infarct
2. there’s s twist or impingement that’s impeding the venous return

Question 10

1. What kind of clot is this?
2. What is in the yellowish color
3. Red?
4. is this normal?

Answer 10

1. Chicken fat clot (post mortem, normal)
2. Yellow material is a combination of fibrin, WBC, other proteins
3. Red, jelly-like material - Remnants of RBC
4. it is normal

Question 11

What happens in deep vein thrombosis?

Answer 11

• Sitting allows for stasis of blood to form in the long, deep veins of your leg when you sit for a long period of time,
• If you suddenly get up and start moving around, the large thrombus can break loose, will go straight to your heart, to the lungs
• Large caliber vessels, therefore really good at making large caliber thrombi
• Can be a rapid cause of death

Question 12

what are 5 other forms of emboli

Answer 12

1. Bacteria - mats of fibrin seeded with bacteria makes for a great embolus
2. Fat
3. Cartilage - as we saw earlier this semester, can serve as an embolus if it gets into the bloodstream
4. Air- from an IV apparatus
5. Parasites - heartworms

Question 13

Describe the steps of what happens in DIC, disseminated intravascular coagulation

Answer 13

1. Often secondary to some other primary disease
   
   • Ex: septic, undergoing widespread metastatic event leading to
2. endothelial damage (widespread)
3. Allows for the formation of microthrombi
   • Ischemic injury to organs
     
     • Could lead to multiple organ failure
   • ​Consumption of platelets and coagulation factors
     
     • ​When you’re creating lots of small thrombi throughout your body, you’re also using up platelets and coagulation factors
     • ​​Which means that if you need to stop hemorrhaging somewhere, you can’t
     • All the factors have been used up
     • So spontaneous hemorrhage may be the next step
   • Activation of fibrinolysis
     
     • In addition, once you have the presence of thrombi in the vascular system, fibrinolysis kicks off
     • Body will do what it knows to do, with is to break down thrombi
     • Leads to multiple FDP, or fibrin degradation products
     • Leads to hemorrhagic diathesis (diathesis = exiting of blood from a space. Nice way of saying bleeding out, or uncontrolled bleeding)
     • See petechiae and ecchymoses in skin or gums, on serosal surfaces

Question 14

1. What is hemorrhagic diathesis?
2. What will you see grossly when this happens in DIC?

Answer 14

1. diathesis = exiting of blood from a space. Nice way of saying bleeding out, or uncontrolled bleeding)
2. See petechiae and ecchymoses in skin or gums, on serosal surfaces

Question 15

Can you run one test to diagnose DIC?

Answer 15

• DIC is not something we can run one test for and know that DIC is going on
• Harder to pinpoint
• More of knowing the risks, and what risk factors are present such that DIC may occur

Question 16

What are some diagnostic tests that can be done that shows risk factors of DIC from happening?

(basically know the 3 risk factors)

Answer 16

1. thrombocytopenia
   
   • Generally, when you get to less than 50,000 platelets, that animal could be at risk for DIC
2. Increased fibrin degradation products (FDPs) or D-dimers
3. Increased clotting time
   
   • test would be PT/PTT ( prothrombin time/partial thromboplastin time)

Question 17

What are the 2 major consequences of DIC

Answer 17

1. Hemorrhage
   
   • Loss of ability to coagulate anything
   • Due to Dysregulation and misuse of clotting factors
   • So while the body is busy making microthrombi where it shouldn’t, all those factors are being used up and that body can’t response where it should, like in surgery, or even through simple procedures like putting in an iv
   • May cause a hemorrhage that an animal can’t stop on their own
2. Multiple organ failure due to ischemia
   
   • If you’re sending microthrombi out into microvasculature will have an effect on everything
   • Hypovolemic shock may also be a consequence
   • If you’re bleeding or hemorrhaging even into internal cavities, that’s still a lack of blood that’s there to provide any kind of vasomotor tone to the vascular system

Question 18

what is shock?

Answer 18

Widespread hypoperfusion of cells and tissues due to inadequate effective circulating blood volume.

Question 19

What are the 4 types of shock?

Answer 19

1. Hypovolemic
2. Cardiogenic
3. Distributive (endotoxic, anaphalactic, septic)
4. Neurogenic

Question 20

During normal cell metabolism what should the general levels of the following substances be at (high or low)

1. O2
2. Glucose
3. ATP
4. Lactic acid

Answer 20

1. O2- high
2. Glucose- high
3. ATP- high
4. Lactic acid- low

Question 21

1. During shock what does the heart do to compensate?
2. microcirculation?

Answer 21

1. Cardiac output and rate will increase to compesate
2. microcirculation will constrict

Question 22

1. If shock goes on for more than 24-48 hours what will happen to cardiac output and rate?
2. microcirculation
3. cell metabolism? (O2, glucose, ATP and lactic acid levels)
4. cell morphology?

Answer 22

1. Cardiac output and rate have tanked
2. Microcirculation constriction compensation cannot keep up
3. Increased lactic acid
   
   • decreased O2, glucose and ATP
4. Cell swelling, and then leading to necrosis

Question 23

1. What is generally happening in hypovolemic shock?
2. What are some reasons for it to happen?

Answer 23

1. .Hypovolemia – loss of circulating fluid
   
   • Decreased blood volume leads to decreased venous return, and It all leads to decreased cardiac output
2. Loss of fluid may be
   
   • internal reasons for hypovolemia
     
     • Maybe HBC, dog kicked by horse…. Bleeding into abdominal cavity
     • Internal hemorrhage
   • external reasons for hypovolemia
     
     • Burns
     • Animal that’s been vomiting or diarrhea for a long time

Question 24

1. during hypovolemic shock what happens initially?
2. later?

Answer 24

1. Initially there is peripheral vasoconstriction
   
   • Trying to get all the blood back into the main organs
2. Later there is peripheral vasodilation
   
   • Loss of vasomotor tone

Question 25

What leads to cardiogenic shock?

give 2 examples

Answer 25

1. Pump failure for any reason
2. Arrhythmia or Cardiac tamponade

Question 26

How can cardiac tamponade happen?

Answer 26

• You’re a dog that’s suffering from hemangiosarcoma of the right auricle, and that tumor ruptures through, so that all the blood that’s currently in the right auricle can freely move into the pericardial sac. That’s going to happen fast
  
  • Or anykind of injury to heart, knife, bullet wound
• Decreased output. The heart can no longer expand to take in more blood.

Question 27

What are the steps in cardiogenic shock that lead to decreased cardiac output?

Answer 27

Cardiogenic shock is a direct step to decreased cardiac output

Question 28

1. Generally what is happening in distributive shock
2. What are the 3 types of shock classified under distributive shock?

Answer 28

1. Pooling of blood in microvasculature
2. Endotoxic shock
   • Septic shock
   • Anaphylactic shock

Question 29

How does endotoxic shock happen

Answer 29

• Gram neg - release of LPS that has a negative effect on endothelial cells
• Has the potential of causing systemic endothelial damage

Question 30

How does septic shock happen

Answer 30

1. The presence of other bacterial toxins, and/or the bacteria themselves in the vasculature
   
   • Can happen with both gram neg or pos
2. Leads to increased TNF and cytokines
3. widespread endothelial damage
   
   • Either DIC or
     
     • DIC leads to hypoxic cell injury
     • then heatfailure and renal failure
     • leads to metabolic acidosis and decreased cardiac output
   • increase vascular permeabliity
     
     • Leads to decreased blood volume
     • deacreased venous return
     • deacreased cardiac output

Question 31

how does anaphalactic shock happen

Answer 31

Systemic Type 1 hypersensitivity

• IgE is the big mediator for this
• Will result in systemic vasodilation
• Have no vasomotor tone at all, have opened up miles of space in your vascular system that the same volume of blood now needs to fill

Question 32

How can neurogenic shock happen (give 4 examples)

Answer 32

1. Blunt force trauma to spinal cord
2. fear
3. lightening strike
4. emotional stress

Question 33

How does neurogenic shock lead to decreased cardiac output

Answer 33

1. Loss of sympathetic tone
2. neural-induced vasodilation and then peripheral vasodilation
3. Reduced blood pressure
4. Reduced venous return
5. decreased cardiac output

Question 34

what are 8 clinical findings of shock

Answer 34

1. Muddy cool mucous membranes
2. Increased capillary refill time
3. Cool skin
4. Increased heart rate—weak thready pulse
5. Increased respiratory rate
6. Hypotension
7. Oliguria- lack of urine formation
8. Metabolic acidosis

Question 35

Why are LPS so bad

Answer 35

• LPS initiates a highly activated state of endothelial cells, and everything else
• It’s very efficient at activated endothelial cells and beginning an inflammation cascade that has such rapid and wide reaching effects that in the end has a very negative outcome for the animal