CHAPTER 4: HEMODYNAMIC DISORDERS, * Ecchymoses

THROMBOEMBOLIC DISEASE AND SHOCK HEMODYNAMIC * hemothorax,hemopericardium, hemoperitoneum, or

DISORDERS hemarthrosis
-Edema
-Congestion HEMOSTASIS AND THROMBOSIS
-Shock * Antithrombotic Properties
EDEMA * Antiplatelet effects
Pathophysiologic Categories of Edema * Anticoagulant effects
- INCREASED HYDROSTATIC PRESSURE * Fibrinolytic effects
* Impaired venous return
* Congestive heart failure
* Constrictive pericarditis * Prothrombotic Properties
* Ascites (liver cirrhosis) * Platelet effects
* Venous obstruction or compression * Procoagulant effects
* Thrombosis * Antifibrinolytic effects
* External pressure (e.g., mass)
* Lower extremity inactivity with prolonged dependency PLATELET ADHESION AND AGGREGATION
* Arteriolar dilation PLATELETS THROMBOSIS
* Heat THROMBOSIS
* Neurohumoral dysregulation * Endothelial injury
- REDUCED PLASMA OSMOTIC PRESSURE * Alterations in Normal Blood Flow
(HYPOPROTEINEMIA) * Stasis and Turbulence
* Protein-losing glomerulopathies (nephrotic syndrome) * Promote endothelial activation
* Liver cirrhosis (ascites) * Disrupt laminar flow and bring platelets into contact with
* Malnutrition the endothelium[26]
* Protein-losing gastroenteropathy EDEMA * Prevent washout and dilution of activated clotting factors
- LYMPHATIC OBSTRUCTION by fresh flowing blood and the inflow of clotting factor
* Inflammatory inhibitors
* Neoplastic * Hypercoagulability
* Postsurgical HYPERCOAGULABLE STATES
* Postirradiation PRIMARY (GENETIC)
- SODIUM RETENTION * Common
* Excessive salt intake with renal insufficiency * Factor V mutation (G1691A mutation; factor V Leiden)
* Increased tubular reabsorption of sodium * Prothrombin mutation (G20210A variant)
* Renal hypoperfusion * 5,10-Methylenetetrahydrofolate reductase (homozygous
* Increased renin-angiotensin-aldosterone secretion C677T mutation)
- INFLAMMATION * Increased levels of factors VIII, IX, XI, or fibrinogen
* Acute inflammation * Rare
* Chronic inflammation * Antithrombin III deficiency
* Angiogenesis * Protein C deficiency
* Protein S deficiency
* Very Rare
EDEMA * Fibrinolysis defects
* Increased hydrostatic pressure * Homozygous homocystinuria (deficiency of cystathione β-
* Congestive heart failure synthetase)
* Deep venous thrombosis SECONDARY (ACQUIRED)
* Reduced Plasma Osmotic Pressure * High Risk for Thrombosis
* Nephrotic syndrome * Prolonged bedrest or immobilization
* Sodium and Water Retention * Myocardial infarction
* Lymphatic Obstruction * Atrial fibrillation
* Tissue injury (surgery, fracture, burn)
Morphologically: * Cancer
* clearing and separation of the extracellular matrix and * Prosthetic cardiac valves
subtle cell swelling * Disseminated intravascular coagulation
* Subcutaneous edema * Heparin-induced thrombocytopenia
* Dependent Edema * Antiphospholipid antibody syndrome
* Pitting Edema * Lower Risk for Thrombosis
* Periorbital Edema * Cardiomyopathy
* Pulmonary Edema * Nephrotic syndrome
* Brain Edema * Hyperestrogenic states (pregnancy and postpartum)
* Oral contraceptive use
* Sickle cell anemia
HYPEREMIA AND CONGESTION * Smoking
Hyperemia
* Active process; arteriolar dilation leads to increase blood Fate of the Thrombus
flow * Propagation
Congestion * Embolization
* passive process resulting from reduced outflow of blood * Dissolution
from a tissue * Organization and recanalization
HEMORRHAGE
* extravasation of blood into the extravascular space Clinical Consequences
* Hypovolemic shock * Venous Thrombosis (Phlebothrombosis)
COMPLICATIONS: * Arterial and Cardiac Thrombosis
* Hematoma * Atherosclerosis
* Petechiae
* Purpura
DISSEMINATED INTRAVASCULAR COAGULATION (DIC) Kidney Infarct
EMBOLISM Factors That Influence Development of an Infarct
* detached intravascular solid, liquid, or gaseous mass that is * the nature of the vascular supply
carried by the blood to a site distant from its point of origin * the rate at which an occlusion develops
* dislodged thrombus * vulnerability to hypoxia
* the oxygen content of the blood
PULMONARY EMBOLISM
* Sudden death, right heart failure (cor pulmonale), or SHOCK
cardiovascular collapse * final common pathway for several potentially lethal clinical
* Embolic obstruction of medium-sized arteries with events, including severe hemorrhage, extensive trauma or
subsequent vascular rupture burns, large myocardial infarction, massive pulmonary
* Embolic obstruction of small end-arteriolar pulmonary embolism, and microbial sepsis
branches * systemic hypotension due either to reduced cardiac output
* Multiple emboli or to reduced effective circulating blood volume
CONSEQUENCES OF SHOCK
SYSTEMIC THROMBOEMBOLISM * impaired tissue perfusion and cellular hypoxia
* emboli in the arterial circulation * prolonged shock eventually leads to irreversible tissue
* intracardiac mural thrombi injury that often proves fatal.
* Left ventricular wall infarcts
* left atrial dilation and fibrillation Three general categories
* aortic aneurysms, Cardiogenic shock
* thrombi on ulcerated atherosclerotic plaques, or * results from low cardiac output due to myocardial pump
fragmentation of a valvular vegetation failure
Hypovolemic shock
* results from low cardiac output due to the loss of blood or
plasma volume
Septic shock
SYSTEMIC THROMBOEMBOLISM * results from vasodilation and peripheral pooling of blood
* Major sites for arteriolar embolization:
* Lower extremities CARDIOGENIC SHOCK
* the brain * Myocardial infarction
* with the intestines, kidneys, spleen, and upper extremities * Ventricular rupture
* Arrhythmia
FAT AND MARROW EMBOLISM AIR EMBOLISM * Cardiac tamponade
* decompression sickness * Pulmonary embolism
* occurs when individuals experience sudden decreases in
atmospheric pressure HYPOVOLEMIC SHOCK
* the bends * Fluid loss (e.g., hemorrhage,
* Chokes * Vomiting
* caisson disease * diarrhea
* burns
AMNIOTIC FLUID EMBOLISM * trauma
* sudden severe dyspnea,
* cyanosis, and shock SEPTIC SHOCK
* neurologic impairment ranging from headache to seizures * Overwhelming microbial infections (bacterial and fungal)
and coma * Superantigens (toxic shock syndrome)
* infusion of amniotic fluid or fetal tissue into the maternal
circulation via a tear in the placental membranes or rupture PATHOGENESIS OF SEPTIC SHOCK
of uterine veins * severe hemodynamic and hemostatic derangements
* systemic vasodilation and pooling of blood in the periphery
Infarction leads to tissue hypoperfusion
* an area of ischemic necrosis caused by occlusion of either * accompanied by widespread endothelial cell activation and
the arterial supply or the venous drainage injury, often leading to a hypercoagulablestate
Pulmonary infarction -ischemic necrosis of the extremities SEPTIC SHOCK
(gangrene) * Inflammatory mediators
* local vasospasm, hemorrhage into an atheromatous plaque, * Endothelial cell activation and injury
or extrinsic vessel compression * Metabolic abnormalities
* include torsion of a vessel traumatic rupture, or vascular * Immune suppression
compromise by edema or by entrapment in a hernia sac * Organ dysfunction

Morphology of Infarct STAGES OF SHOCK

Red infarct * Initial nonprogressive phase
* venous occlusions ( ovary) * Progressive stage
* in loose tissues (lung) * Irreversible stage
* blood can collect in the infarcted zone
* in tissues with dual circulations (lung and small intestine) Clinical Consequences of Shock
* in tissues previously congested by sluggish venous outflow Hypovolemic and Cardiogenic shock
* when flow is re-established to a site of previous arterial * hypotension; a weak, rapid pulse; tachypnea; and cool,
occlusion and necrosis (following angioplasty of an arterial clammy, cyanotic skin
obstruction) Septic shock
* the skin may initially be warm and flushed because of
White infarct peripheral vasodilation
* occur with arterial occlusions in solid organs with end-
arterial circulation
* heart, spleen, and kidney