Hemodynamics II Lecture (Dr. Galbraith) TEST 1 Flashcards
Defects of Secondary Hemostasis
- Often present with BLEEDING into Joints (Hemarthrosis) or soft tissue
- Due to Coagulation factor DEFICIENCIES, which may be Hereditary or acquired
PT
- Extrinsic Pathway
- VII, X, V, II, Fibrinogen
PTT
- Intrinsic Pathway
- XII, XI, IX, VIII, X, V, II, Fibrinogen
Acquired Coagulation Protein Deficiencies
- Consumptive Coagulopathy (DIC)
- Liver Disease
- Vitamin K Deficiency
- Massive Transfusion
- Coagulation Protein Inhibitors
Disseminated Intravascular Coagulation
- 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!!!!!!**
Liver Disease
- 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
Vitamin K Deficiency
- 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
Massive Transfusion
- 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
Acquired Factor Inhibitors
- 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
Embolism
- 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
Pulmonary Embolism (PE)
- 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
Systemic Thromboembolism
- 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
Fat and Marrow Embolism
- 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
Air Embolism
- 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
Amniotic Fluid Embolism
- 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
Infarction
- 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
Infarct Morphology
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
Infarct Morphology
- Wedge-shaped, involving the geographic distribution of the occluded vessel
- Microscopically: ISCHEMIC Coagulative Necrosis
a) EXCEPT Brain: LIQUEFACTIVE!!!!!!!!! - Most infarcts ultimately replaced by SCAR!!!!
Infarct Morphology
- 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!!!!!!
Development and course of an Infarct
- 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
Shock
- 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)
Septic Shock
- 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
Septic Shock Pathogenetic Factors
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
Septic Shock Pathogenetic Factors
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)
Shock- Clinical Course
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
