Hemodynamics II Lecture (Dr. Galbraith) TEST 1 Flashcards

1
Q

Defects of Secondary Hemostasis

A
  • Often present with BLEEDING into Joints (Hemarthrosis) or soft tissue
  • Due to Coagulation factor DEFICIENCIES, which may be Hereditary or acquired
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2
Q

PT

A
  • Extrinsic Pathway

- VII, X, V, II, Fibrinogen

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3
Q

PTT

A
  • Intrinsic Pathway

- XII, XI, IX, VIII, X, V, II, Fibrinogen

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4
Q

Acquired Coagulation Protein Deficiencies

A
  • Consumptive Coagulopathy (DIC)
  • Liver Disease
  • Vitamin K Deficiency
  • Massive Transfusion
  • Coagulation Protein Inhibitors
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5
Q

Disseminated Intravascular Coagulation

A
  • Activation of the Coagulation and Fibrinolysis Systems –> simultaneous production of THROMBIN and PLASMIN
    a) Widespread Microthrombi
    b) Consumption of Coagulation factors
    c) Consumption of platelets
  • Is not a single disease, but rather, a complication arising from different causes:
    a) Sepsis, complications related to childbirth, massive trauma, malignancy
  • Lab studies show ELEVATED PT and PTT, Low Fibrinogen, Increased Fibrin Degradation products (D-Dimers), and THROMBOCYTOPENIA
  • What begins as widespread Thrombosis may evolve into Widespread Hemorrhage, due to consumption of factors and platelets
  • May also result in Intravascular Hemolysis
    a) Schistocytes

** Mostly occurs is SEPSIS!!!!!!**

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6
Q

Liver Disease

A
  • Most coagulation factors are made in the Liver
  • Severely Decreased liver function —> Decreased Synthesis
    a) ELEVATION of PT and PTT
  • Abnormal factors may be Synthesized
    a) Dysfibrinogenemias
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7
Q

Vitamin K Deficiency

A
  • Lipid soluble vitamin, found in Leafy greens and synthesized by Gut Flora
  • Essential for production of functional factors X, IX, VII, II (Prothrombin) (“1972”), Proteins C and S

Deficient:

a) In patients receiving WARFARIN/ Coumadin
b) Malnourished or prolonged parenteral Nutrition
c) Prolonged antibiotics

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8
Q

Massive Transfusion

A
  • Has been defined as replacement of 1.5x blood Volume in 24h
  • Results from DILUTION of factors by replacing with packed RBC and Normal Saline
    a) Increased PT and PTT, Decreased Fibrinogen and Platelets
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9
Q

Acquired Factor Inhibitors

A
  • Antibody to a coagulation factor
  • Most common factor to be clinically significantly INHIBITED is Factor VIII !!!!!!!!!!!!!
  • May occur in Multiple Clinical scenarios, such as:
    a) B Cell Lymphoma/ Plasma Cell Neoplasms
    b) Amyloidosis
  • Mixing study may help determine whether abnormal clotting times are due to a decreased amount of actor, or presence of an Inhibitor
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10
Q

Embolism

A
  • DEFINITION:
    “An Embolus is a detached Intravascular Solid, Liquid, or Gaseous mass that is carried by the blood from its point of Origin to a distant site, where it often causes tissue dysfunction or infarction”
  • Most arise from a THROMBUS
  • Clinical importance depends on the size and the location of the Embolus
    a) It will travel until it reaches a vessel with a Lumen too small to admit its passage
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11
Q

Pulmonary Embolism (PE)

A
  • Embolus lodged within the Pulmonary Arterial Vasculature
  • Greater than 95% arise from DEEP VENOUS THROMBI (DVT) of the Legs
    a) The Embolus travels through the Venous System to the right side of the Heart and out of the Pulmonary Artery
  • The Embolus can be a single large fragment of Thrombus or a shower of smaller fragments
  • History of having a PE is a risk factor for RECURRENCE
  • Most are silent, due to SMALL SIZE
  • Sudden death or Right Heart Failure may occur when at least 60% of the Pulmonary Arterial circulation is obstructed
  • Multiple small Emboli over time may organize and lead to Pulmonary Hypertension and subsequent Right Heart Failure
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12
Q

Systemic Thromboembolism

A
  • Approximately 80% arise from the HEART
  • Other sources include:
    a) Thrombi from AORTIC ANEURYSM

b) Thrombi from ATHEROSCLEROTIC Plaques
c) CARDIAC Valves (“Vegetations”)
d) PARADOXICAL Emboli

  • May lodge in a variety of sites:
    a) Major go to LOWER EXTREMITIES
    b) Brain
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13
Q

Fat and Marrow Embolism

A
  • Usually caused by BONE FRACTURE, the trauma of which translocates Marrow/ Fat globules into Venous Sinuses and then travel to the LUNGS
  • In the vast majority of cases it is Subclinical, but a MINORITY (about 10%) experience FAT EMBOLISM SYNDROME

Results:

a) PULMONARY INSUFFICIENCY
- Dyspnea, Tachypnea, Tachycardia

b) NEUROLOGIC SYMPTOMS:
- Irritability, Delirium, Coma

c) ANEMIA and THROMBOCYTOPENIA (Diffuse PETECHIAL RASH)
- Platelets and Erythrocytes through to aggregate around FAT GLOBULES and become Sequestered/ removed in the Spleen or otherwise OCCLUDE MICROVASCUALTURE in the Lungs and Brain

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14
Q

Air Embolism

A
  • Gas Bubbles can OBSTRUCT Small Vessels
  • May be introduced Surgically
    a) Vascular, Neurosurgical, Laparoscopic
  • Decompression Sickness
    a) The Bends, seen in divers who ascend too quickly
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15
Q

Amniotic Fluid Embolism

A
  • RARE but serious complication of Childbirth
    a) Incidence 1 in 40,000 deliveries, mortality up to 80%
  • Amniotic fluid and/or fetal tissue enter Maternal Circulation and may cause Obstructive Effects, but much of the MORBIDITY may be due to development of DIC
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16
Q

Infarction

A
  • A relatively discrete are of Ischemic Necrosis caused by Vascular Occlusion (Usually Arterial)
  • Most cases arise from Aterial Thrombosis or Thromboembilusm, but less common causes include:
    a) Torsion
    b) Vessel Trauma
    c) Compression due to Tumor or Edema
    d) Herniatoin
17
Q

Infarct Morphology

A

1) RED (Hemorrhagic) Infarcts:
- In tissue with a DUAL BLOOD SUPPLY (Lung)

  • Venous Occlusion (Torsion)
  • Previosly congested Tissue
  • REPERFUSED Necrotic Tissue AFTER Arterial Occlusion

2) WHITE (Anemic) Infarcts:
- Arterial Occlusions in SOLID ORGANS with end-arterial circulation
a) Spleen, Kidney, Heart

18
Q

Infarct Morphology

A
  • Wedge-shaped, involving the geographic distribution of the occluded vessel
  • Microscopically: ISCHEMIC Coagulative Necrosis
    a) EXCEPT Brain: LIQUEFACTIVE!!!!!!!!!
  • Most infarcts ultimately replaced by SCAR!!!!
19
Q

Infarct Morphology

A
  • SEPTICT INFARCT: may occur when the Necrotic Tissue is INFECTED, or when an Infected Heart Valve VEGETATION BREAKS OFF and Embolizes (Septic Embolus)
    a) Infarct —–> ABSCESS!!!!!!
20
Q

Development and course of an Infarct

A
  • Anatomy of affected Vessels
    a) Presence/ absence of a Dual Blood Supply
  • Rate of Occlusion
    a) SLOW rate of occlusion may allow time for Collateral Circulation to develop
  • Tissue Vulnerability to HYPOXIA
21
Q

Shock

A
  • Significant decreased Tissue Perfusion and resultant HYPOXIA secondary to:
    a) DECREASED Cardiac Output (CARDIOGENIC Shock)

b) DECREASED Circulating Blood Volume (HYPOVOLEMIC Shock)
c) Systemic Inflammatory Effects (SEPTIC Shock)

22
Q

Septic Shock

A
  • Most common cause of death in US ICUs, with a Mortality rate of Greater than 20%
  • Causative Organisms are many, although GRAM POSITIVE bacteria are MOST COMMON
23
Q

Septic Shock Pathogenetic Factors

A

1) Release of Inflammatory Mediators
- Microbial products induce Innate Immune Cells to release Cytokines (TNF, IL-1, among many others)

2) Endothelial Activation and Injury
- VASODIALTION—> Decreased blood Pressure

  • INCREASED PERMEABILITY —> Leakage and Edema, impeding perfusion

3) Procoagulant State
- Systemic INCREASE of Thrombin

24
Q

Septic Shock Pathogenetic Factors

A

1) METABOLIC Disturbances
- Insulin resistance and Hyperglycemia

2) ORGAN Dysfunction
- Accumulated damage secondary to HYPOXIA (Decreased PERFUSION secondary to Decreased Blood Pressure, Vascular Leakage, Stasis, Thrombi)

25
Q

Shock- Clinical Course

A

1) Initial Stage characterized by Compensatory Mechanisms
- Sympathetic Discharge —> Catecholamines

  • Renal Conservation of Volume

2) A subsequent progressive stage characterized by Increased Tissue Hypoperfusion and widespread Hypoxia
- Aerobic —-> Anaerobic Metabolism

  • Further Vasodilation, peripheral pooling and Stasis

3) Irreversible Stage
- Irreversible Organ Failure

4) Cariogenic/ Hypovolemic shock may present differently than Septic Shocl
- Cool, Clammy and Cyanotic as opposed to Warm and Flushed

  • Both may be HYPOTENSIVE and TACHYCARDIC
    5) Treatment and outcome depend on the Nature of the insult and the underlying condition of the patient