HEMODYNAMIC DISORDERS Flashcards
Accumulation of fluid in tissues or body cavities
Edema (tissues)
Effusion (body cavities)
Increased blood volume within tissues
hyperemia and congestion
pathologic counterpart of hemostasis
thrombosis
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
embolus
Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage
infarct
State in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia
shock
4 main mechanisms of edema formation
- Increased hydrostatic pressure
- Decreased oncotic pressure
- Increased vascular permeability
- Lymphatic obstruction
General morphologic appearance of edema
- Clearing and separation of ECM
2. Subtle cell swelling
58/M, with history of MI, presented with paroxysmal nocturnal dyspnea and orthopnea. CXR showed bilateral pleural effusion. What is the diagnosis, the mechanism of edema in this case, and the kind of effusion?
Congestive heart failure; Increased hydrostatic pressure; Transudate
32/M, with history of remittent fever and productive cough, developed dyspnea. CXR showed right pleural effusion with left parenchymal infiltrates. What is the mechanism of edema in this case, and what is the kind of effusion?
Parapneumonic effusion; CAP MR; Increased vascular permeability; Exudate
57/M, chronic alcoholic, presented with increase in abdominal girth. Chemistry showed low serum albumin and elevated ALT and AST. Abdominal UTZ showed moderate ascites. What is the mechanism of edema in this case?
Decreased oncotic pressure
Decreased oncotic pressure
34/F, known case of breast cancer stage 2 (T2N0M0), s/p MRM, left, developed left arm swelling. What is the mechanism of edema in this case?
lymphatic obstruction
It is an active process resulting from augmented blood flow due to arteriolar dilation or increased oxygen demand; affected tissue is redder than normal, because of engorgement with oxygenated blood
HYPEREMIA
It is a passive process resulting from impaired venous return out of a tissue; tissue has a blue-red color due to accumulation of deoxygenated blood in the affected tissue
CONGESTION
24/M, with a large left atrial myxoma that obstructed flow of blood into the left atrium, subsequently died. Autopsy of the lung showed engorged alveolar capillaries, alveolar septal edema, and focal intra-alveolar hemorrhage. What is the diagnosis?
Acute pulmonary congestion
34/F, died from acute right-sided heart failure secondary to saddle embolus. Autopsy of the liver showed distended central vein and sinusoids, centrilobular ischemic necrosis, and periportal fatty change. What is the diagnosis?
Acute hepatic congestion
55/M, died of complications from congestive heart failure. Autopsy of the lung showed thickened and fibrotic alveolar septa, and hemosiderin-laden macrophages. What is the diagnosis?
Chronic passive congestion, lung
60/M, died of complications from heart failure. On autopsy, liver is heavier than normal and has a nutmeg-like appearance. Sections show centrilobular hemorrhage, hemosiderin-laden macrophages, and hepatocyte loss of variable degrees. What is the diagnosis?
Chronic passive congestion, liver
Components of Virchow triad (abnormalities that lead to thrombus formation)
endothelial injury
stasis
hypercoagulability
It is a major contributor to the development of arterial thrombi
turbulence of endothelial injury
It is a major contributor to the development of arterial thrombi
turbulence or
endothelial injury
It is a major contributor to the development of venous thrombi
stasis
Any alteration of the coagulation pathway that predisposes to thrombosis; can be primary (e.g. Factor V Leiden, Protein C and S deficiency) or secondary (e.g. Cancer, atrial fibrillation, and prolonged immobilization)
hypercoagulability
Factor V Leiden
hypercoagulability
a. primary
b. secondary
a.
cancer
hypercoagulability
a. primary
b. secondary
b.
protein c deficiency
hypercoagulability
a. primary
b. secondary
a.
atrial fibrillation
hypercoagulability
a. primary
b. secondary
b.
S deficiency
hypercoagulability
a. primary
b. secondary
a
prolonged immobilization
hypercoagulability
a. primary
b. secondary
b
Laminations composed of pale platelet and fibrin deposits alternating with darker red cell-rich layers; signify formation of thrombus in flowing blood; present in antemortem thrombosis
lines of zahn
Most common site of arterial thrombosis
coronary > cerebral
Most common site of venous thrombosis
Superficial or deep veins of the leg
the most common sources of venous emboli
thrombi in deep leg veins are the most common sources of venous emboli
(Thrombi in superficial leg veins rarely embolize)
Thrombi accumulate additional platelets and fibrin
Propagation
Thrombi dislodge and travel to other sites in the vasculature
Embolization
Rapid shrinkage and total disappearance of recent thrombi
Dissolution
Thrombi becomes incorporated in the vessel wall with formation of new capillary channels that restore blood flow
Organization and recanalization
Most common and most dreaded sequela of deep venous thrombosis
Pulmonary embolism
Embolus occluding the bifurcation of the pulmonary trunk; associated with sudden death due to acute right-sided heart failure
Saddle embolus
65/F, known case of DVT, came from a 17-hour flight, developed respiratory distress with right ventricular wall dysfunction on 2D-Echo. What is the diagnosis?
Pulmonary embolism
45/F, known case of thyrotoxic heart disease and chronic atrial fibrillation, developed sudden left-sided weakness and loss of sensation. What is the type of embolism observed in the patient?
Systemic thromboembolism (from mural thrombus)
38/M, known case of Non-Hodgkin lymphoma, developed sudden right-sided weakness. Patient has had a recent admission for a month, and has a history of a cardiac pathology that the cardiologist deemed benign. What is the phenomenon observed in the patient?
Paradoxical embolism (Cardiac pathology is PFO patent foramen ovale)
refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale,[1] or arteriovenous shunts in the lungs.
paradoxical embolism
32/M, involved in a motorcycle accident, and sustained a mid-shaft right femoral fracture, without any blunt or penetrating head and chest trauma. Patient developed progressive respiratory distress, and died. Autopsy shows fat globules in pulmonary vasculature. What is the diagnosis?
fat embolism
25 G1P1(1001) developed respiratory distress, seizures, and refractory bleeding post-partum, and died. Autopsy shows fetal skin and lanugo in pulmonary vasculature. What is the diagnosis?
Amniotic fluid embolism
30/M, diver, developed respiratory distress and joint pain after rapid ascent. Work-up showed gas bubbles in pulmonary vasculature and joints. What is the diagnosis?
Air embolism (Decompression sickness)
also called generalized barotrauma or the bends, refers to injuries caused by a rapid decrease in the pressure that surrounds you, of either air or water. It occurs most commonly in scuba or deep-sea divers, although it also can occur during high-altitude or unpressurized air travel.
decompression sickness
Infarcts that tend to occur in loose tissues and in those with dual circulations, previously congested tissues, or when flow is reestablished after an infarction (i.e. after angioplasty of obstructed artery);
Red (hemorrhagic) infarct
examples: Pulmonary and Bowel infarcts
Red (hemorrhagic) infarct
Infarcts that tend to occur in solid organs with end-arterial circulations
White (anemic) infarct
examples: Myocardial and Splenic infarcts
White (anemic) infarct
55/M, known case of massive MI, developed ventricular fibrillation, and died. What kind of shock did the patient suffer from?
Cardiogenic shock
65/M, with ruptured abdominal aortic aneurysm, died. What kind of shock did the patient suffer from?
Hypovolemic shock
23/M, college student and dormer, developed cough and colds for 2 days, followed by remittent high-grade fever, with dusky ecchymoses on the lower extremities. At ER, patient was stuporous with BP = 50 palpatory. What is the diagnosis, and the kind of shock did the patient suffer from?
Meningococcemia; Septic shock
25/F, suffered from a bee sting, developed generalized wheals, periorbital edema, and respiratory distress. At ER, BP = 70/50. What kind of shock did the patient suffer from?
Anaphylactic shock
28/F, suffered from a blunt trauma of the back after a vehicular accident, was hypotensive for several days, and was started on vasopressors for management. What kind of shock did the patient suffer from?
Neurogenic shock
