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POD Test Two > Hemodynamic 3 Lecture > Flashcards

Hemodynamic 3 Lecture Flashcards

1
Q

Define hemorrhage

A

Extravastion of blood due to vessel rupture

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2
Q

What causes hemorrhages?

A 
Trauma
Neoplastic Erosion
Atherosclerosis
Inflammation
Bleeding disorders (increase fragility of vessels, platelet deficiency or dysfunction, derangement of coagulation)
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3
Q

What are characteristics of hemmorrhages?

A

Erythrocytes in these lesions are degraded and phagocytosed by macrophages
The hemoglobin is converted to bilirubin and eventually to hemosiderin accounting for the golden brown color in a bruise
Extensive hemorrhages occasionally develop jaundice from the massive red cell breakdown and systemic release of bilirubin

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4
Q

Define punctate petechial hemorrhage

A

Hemorrhages of the colonic mucosas due to thrombocytopenia (reduced platelet number)

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5
Q

What are the normal counts?

A

150,000-300,000

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6
Q

What are thrombocytopenia counts?

A

<100,000

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7
Q

What are spontaneous bleeding counts?

A

<20,000

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8
Q

What are post-traumatic bleeding counts?

A

20,000-50,000

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9
Q

Define hematoma

A

The accumulation of extravascular blood within a tissue

- Large accumulation of blood in the body cavities is named after the cavity site

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10
Q

Examples of names based on the cavity site?

A

Hemothorax
Hemopericardium
Hemoperitoneum
Hemarthrosis (in the joints)

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11
Q

What is the clinical significance of hemorrhages?

A

Depends on the site, the rate, and the amount of blood loss

  • Vary from trivial (small subcutaneous hemorrhage) to critical (a large hemorrhage in the brain)
  • Large loss (>20% of blood) can lead to shock
  • Small vessel rupture can lead to local ischemia and cell death
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12
Q

What happens to RBC that leak out?

A

Broken down

  • Leading to the release of vasoactive substances –> strong vasoconstriction and cellular injury
  • Where there is chronic and severe vasoconstriction of the arteries of the brain there will be neuronal death
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13
Q

Define Infarction

A

an infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or venous drainage in a tissue
- Most cardiovascular disease are due to myocardial or cerebral infarcts

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14
Q

What do nearly all infarcts arise from?

A

Thrombi or embolic events and result from arterial occlusion

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15
Q

What is the morphology of an infarct?

A

Classified by color

  • Reflecting the amount of hemorrhage
  • Presence or absence of microbial infection (may be hemorrhagic: red or anemic: white)
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16
Q

What are hemorrhagic infarct associated with?

A

Venous occlusions
Loose tissue allowing blood to collect in the infarct area
Tissue with dual circulation (small intestine)
Reperfusion to a site of arterial occlusion and necrosis

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17
Q

What are ischemic (anemic) infarct associated with?

A

Arterial occlusions in solid organs (heart, kidney, spleen)

- Solid state of the tissue limit the hemorrhage to leak into the area of ischemic necrosis

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18
Q

What is acute transmural myocardial infarction?

A

Schematic representation of sequential progression of coronary artery lesion morphology, beginning with stable chronic plaque responsible for typical angina and leading to the various acute coronary syndromes

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19
Q

How does myocardial necrosis progress?

A
  • Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone
  • Narrow zone of myocardium beneath the endocardium is spared from necrosis because it can be oxygenated by ventricular diffusion
  • Perfusion from the coronary artery obstructed leads to blood flow obstruction
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20
Q

Define cerebral infarcation

A

Results fro focal obstruction of blood flow caused by either thrombotic or embolic arterial occlusion
- Usually a stroke syndrome –> the sudden onset of a neurological deficit within clinical manifestations

21
Q

What are two groups of cerebral infarctions

A

Hemorrhagic infarction associated with embolism

Nonhemorrhagic infarction usually associated with thrombosis

22
Q

What four things influence the effects of infarct?

A
  • The nature of the blood supply
  • The rate of development of the occlusion
  • The vulnerability of the tissue to hypoxia
  • Oxygen content of blood
23
Q

What does the nature of the blood supply mean?

A

Availability of collaterals

  • Dual circulations (lung, liver)
  • Anastomosing circulations (radial arteries, small intestine)
  • End-arterial vessels generally causes infarction (spleen, kidney)
24
Q

What does the rate of development of the occlusion mean?

A

Slowly developing occlusions may not cause infarction because it provide time to develop alternate perfusion pathways (collateral coronary circulation)

25
Q

What does the vulnerability of the tissue to hypoxia mean?

A

Neurons undergo irreversible damage after 3-4 minutes of ischemia
Myocardial cells die after 20-30 minutes after ischemia
Fibroblasts within ischemic myocardium survives for many hours

26
Q

What does the oxygen content of blood means?

A

Anemia, cyanosis, or CHF (with hypoxia) can cause infarction (otherwise inconsequential blockage)

27
Q

Define shock

A

Is the final common pathway for a series of very serious clinical events
Includes: severe hemorrhage, serious trauma or burns, large myocardial infarction, massive pulmonary embolism, microbial sepsis

28
Q

Define cardiogenic shock

A

Results form heart pump failure
- Caused by: intrinsic myocardial damage (infarction or ventricular rupture), arrhythmias, extrinsic compression (cardiac tamponade), outflow obstruction (pulmonary embolism)

29
Q

Define hypovolemic shcok

A

Results from loss of blood or plasma

- Caused by hemorrhage, fluid loss from burns, vomiting, diarrhea, trauma

30
Q

Define septic shock

A

Results from overwhelming systemic microbial infection
Caused by: peripheral vasodilation and pooling of blood, endothelial activation and injury, leukocyte-induced damage, intravascular coagulation, activation of cytokine cascades

31
Q

What is activation of cytokine cascades?

A

Most commonly seen with gram-negative infections (endotoxic shock) but also with gram positive infections and fungal infections

32
Q

Define neurogenic shock

A

Resulting from anesthetic accident or spinal cord injury leading to loss of vascular tone and peripheral pooling of blood

33
Q

Define anaphylactic shock

A

Initiated by generalized IgE-mediated hypersensitivity and resulting in systemic vasodilation and increased capillary permeability
- Increase in systemic capacitance leads to hypotension, tissue, hypoperfusion and cellular anoxia or hypoxia

34
Q

What are the stages of shock?

A

Initially stage: non-progressive phase
Second stage: progressive phase
Final stages: irreversible phase

35
Q

What happens during the non-progressive phase?

A

Reflex mechanisms are activated and organ perfusion is maintained

36
Q

What do reflex mechanisms include?

A 
Baroreceptors reflexes
Release of catecholamines 
Activation of the renin-angiotensin
Aldosterone axis
Increased sympathetic activation
37
Q

What are the net effects of reflex mechanisms?

A

Tachycardia, peripheral vasoconstriction, renal conservation of fluid

38
Q

What happens during the progressive phase is characterized by?

A

Tissue hypoperfusion
Worsening of circulation
Metabolic imbalances

39
Q

What are the net effects of the progressive phase?

A

Tissue hypoxia and lactic acidosis
Lowers the tissue pH
The acidosis blunts the body’s vasomotor response

40
Q

What happens in the irreversible phase

A

Sets in once the body has sustained severe cellular/tissue injury that even with correction of hemodynamic deficits, survival cannot be possible
- There is complete shut down of the kidney and ischemic damage to the brain kidneys and liver

41
Q

What is Lipopolysaccharide Mediated Activators??

A

LPS initiates the cytokine cascade in addition: LPS and various downstream factors can directly stimulate downstream cytokine production
- Secondary effectors that become important include: NO and platelet-activating factor

42
Q

Define endotoxins

A

Bacterial wall LPS that are released when cell walls are degraded during the immune, inflammatory response

43
Q

What is the ultimate effect of hypoperfusion?

A

Hypoperfusion produced by the hypotension, heart failure, and DIC leads to multiorgan failure

44
Q

Brain ultimate effects?

A

Ischemic encephalopathy

45
Q

Heart ultimate effects?

A

Focal and widespread coagulation necrosis

46
Q

Liver ultimate effects?

A

Fatty change with perfusion deficits and hemorrhagic necrosis

47
Q

Kidneys ultimate effects?

A

Extensive tubular ischemic injury

48
Q

Lung ultimate effects?

A

Diffused alveolar damage

49
Q

GI tract ultimate effects?

A

Patchy mucosal hemorrhage

POD Test Two (8 decks)

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