Hemodynamic Disorders

Ma. Minda Luz M. Manuguid, M.D.

Hemodynamic Disorders 
Edema  Hyperemia & Congestion  Hemorrhage  Thrombosis & Embolism  Infarction  Circulatory failure / Shock

Capillary Hemodynamics 
Hydrostatic pressure is the pressure exerted by a fluid

on the walls of its confining space; it is directly proportional to the volume of the fluid; it is an outward force  Osmotic pressure is the pressure exerted by a flow of water across a semipermeable membrane; an µinward¶ pressure attracting fluid; it is directly proportional to the impermeable solute¶s concentration  Hydrostatic & Osmotic pressures are opposing forces 

The net fluid movement between 2 compartments depends on the

algebraic sum of the hydrostatic & osmotic pressures of both.
HPi=10mmHg HPA=35mmHg A OPA=25mmHg OPi= 15mmHg = (HPA ± HPi) ± (OPA ± OPi) = (35 ± 10) ± (25 ± 15) = 25 ± 10 = 15 mm Hg outward = (OPv ± OPi) ± (HPv ± HPi) = (30 ± 15 ) ± (15 ± 10) = 15 ± 5 = 10 mmHg inward OPv= 30 mmHg HPv=15mmHg V

Edema
Edema ² accumulation of fluid in the interstitium or within body cavities
Pathophysiology:

I. Increased hydrostatic pressure II. Decreased Oncotic Pressure III. Sodium Retention IV. Lymphatic obstruction/dysfunction

Pathophysiologic Categories of Edema 
Increased Hydrostatic Pressure

A. Impaired venous return : congestive heart failure; Constrictive pericarditis; Liver cirrhosis; Narrowed / obstructed veins B. Arteriolar dilatation: Heat; Neurohumoral excess / deficit  Reduced Oncotic Pressure Nephrotic syndrome; Liver cirrhosis; Malnutrition; Proteinlosing enteropathies  Sodium Retention: Excessive salt intake; Reduced renal function; Tubular reabsorption, Perfusion, R ± A ± A secretion;  Lymphatic Obstruction/Dysfunction: Inflammatory; Neoplastic; Post-surgical; Post-irradiation ;

Edema 
Hemodynamic  due to imbalance of  Inflammatory  due to increased

Starling¶s forces  specific gravity less than 1.012  low content of proteins/colloids  fluid is a TRANSUDATE

vascular permeability  specific gravity more than 1.020  high content of proteins/colloids  fluid is an EXUDATE

Edema 
Anasarca ² whole body edema; µdropsy¶  Hydrothorax ² increased pleural fluid  Hydropericardium ² increased pericardial fluid ±

may lead to cardiac tamponade  Ascites / Hydroperitoneum ² increased intra-abdominal fluid  Lymphedema ² edema due to lymphatic obstruction  Others : Hydrosalphinx; Hydrops of viscera, etc.

Morphology of Edema 
Gross : increased dimensions (swelling) & weight; turgor; pitting; wet, watery cut surface Microscopic: colorless to pale pink, finely granular material seen in between cells; widened intercellular spaces

Morphology of Edema

Hyperemia
Hyperemia ² increased volume of blood in the affected tissue 
Active hyperemia ² due to arterial / arteriolar dilatation & opening of inactive capillaries--- blood flow --- redness; may be neurogenic e.g. blushing; or chemical / humoral e.g. rubor of inflammation  Passive hyperemia / Congestion ² passive accumulation of blood due to impaired venous drainage; usually accompanied by edema; blue-red color (cyanosis);

- may be acute congestion or chronic (CPC)

Gross Morphology of Hyperemia & Congestion 
increased redness /

cyanosis of the affected area; 
tissues are excessively

wet & bloody; oozing of blood from the cut surface

Histopathology of Hyperemia & Congestion 

Active hyperemia ² swollen arteries & arterioles are full of RBC Congestion / CPC ² dilated veins or venules full of RBC; hemosiderin-laden macrophages; 

Chronic Passive Congestion 
Pathophysiology:  dilated venules/veins full of RBC --->  extravasation into surrounding interstitium ---> breakdown of hemoglobin into hemosiderin ---> engulfment of hemosiderin by macrophages ---> ³ hemosiderin-laden macrophages ´ chronic hypoxia ---> necrosis ---> fibrosis capillary rupture ---> minute hemorrhages ---> ³ hemosiderin-laden scars ´

Chronic Passive Congestion, Lungs 
CPC, Lungs etiology: left ventricular failure morphology: gross: heavy, bloody lobes; cut surfaces oozing blood; micoscopic: septal fibrosisthickened septa; & hemosiderinladen macrophages µheart failure cells¶

Chronic Passive Congestion, Liver 
CPC, Liver

etiology: right ventricular failure; IVC/hepatic vein obstruction morphology : gross - ³nutmeg´ liver microscopic - centrilobular hemorrhagic necrosis ³cardiac´ cirrhosis

Chronic Passive Congestion, Spleen 
CPC, Spleen

etiology : right ventricular failure morphology : gross: congestive splenomegaly microscopic: fibrosis & hemosiderin-laden macrophages³siderofibrotic nodules´ ³Gandy-Gamma bodies´

Hemorrhage
Hemorrhage ± escape of blood into the interstitium through a defect / injury  Petechia ² pinpoint skin hemorrhages  Purpura ² skin hemorrhage up to 1.0 cm. diameter  Ecchymosis ² blotchy confluent skin hemorrhages  Hemothorax ² blood within the pleural cavity  Hemopericardium ² blood w/in the pericardial cavity  Hemoperitoneum ² blood w/in the abdominal cavity

Subcutaneous Hemorrhages

petechiae

purpura

ecchymosis

ecchymosis

hemorrhages

Hemorrhage 
Epistaxis ² bleeding from the nose  Hemoptysis ² coughing out of blood  Hematemesis ² vomiting of blood  Hematochezia ² fresh blood in stools  Melena ² black tarry stoools  Hemarthrosis ² blood within joint spaces

Hemorrhage
Clinical significance:  Volume / amount of blood loss  Rate of blood loss  Site of hemorrhage  Chronic blood loss can lead to Iron deficiency

Hemostasis
hemostasis: the arrest of bleeding from an injured
blood vessel, involving vascular, platelet, & plasma factors  Vasoconstriction  Platelet aggregation & formation of a temporary plug  Plasma coagulation factors activated: extrinsic & intrinsic pathways

The Coagulation Cascade

Fluidity of Blood
Factors that keep blood in a fluid state within blood vessels:  Smoothness of the endothelium  Linear flow of blood ± central column of blood cells, peripheral plasma  Clotting factors in inactive state, dissolved in plasma  Naturally occuring anti-clotting factors e.g. heparin, antithrombin,

Thrombosis & Embolism 
Thrombosis ² formation of an intravascular blood clot in vivo due to one or more of the ff: 
Endothelial injury  Alterations in blood flow: Turbulence or Stasis  Hypercoagulability of blood 

Embolism ² occurrence of an intravascular space-occupying lesion ± solid, liquid, or gas ± in vivo, an embolus is most commonly a broken-off thrombus

Thrombosis
Thrombus ² intravascular blood clot in vivo 
Mural ² attached to the wall of a heart chamber, of the

aorta, iliac a., common carotid a.  Valvular ² on heart valves ± infective endocarditis, thrombotic endocarditis, verrucous endocarditis  Arterial ² most commonly coronary, cerebral, femoral  Venous - ³Phlebothrombosis´- 90% in veins of lower extremities: deep calf, femoral, popliteal, iliac

Thrombosis

Thrombi

Arterial vs Venous 
Usually occlusive, due to  almost always occlusive, due

atherosclerotic damage; less commonly due to acute vasculitis, trauma, RHD, MI, aneurysms 
Gray-white, friable  Tangled strands of fibrin &

to stasis or hypercoagulability states 
Red, moist, many RBC  Less common sites:

platelets; may develop a tail  Lines of Zahn

periprostatic plexus, periuterine & ovarian veins, portal vein, dural sinuses

Arterial & Venous Thrombi

Lines of Zahn

Thrombosis
Fates of a Thrombus: Dissolution by fibrinolytic activity Propagation Organization &/or recanalization Embolization Clinical significance of Thrombosis Obstruction of blood flow Source of emboli--- obstruction of blood flow

Disseminated Intravascular Coagulation 
DIC: ³Disseminated Intravascular

Coagulation´  ³Consumptive Coagulopathy´  ³Defibrination Syndrome´ Development of multiple thrombi in the microcirculation, causing rapid consumption of platelets, prothrombin, fibrinogen, & coagulation factors V, VIII, & X; thus leading to bleeding tendencies

Post-mortem clot 
not attached to the vessel wall  a ³perfect cast´ of the vessel ± the clot follows the exact shape of the blood vessel where it is found  ³currant jelly´ or ³chicken fat´ appearance ± due to stasis and to separation of the serum from the coagulated RBC

Embolism 
Embolus ± any unattached intravascular spaceoccupying mass (solid, liquid, or gas)  99% are thromboemboli  the remaining 1% consists of bone marrow, amniotic fluid, bacterial clusters (septic), fat, tumor, foreign bodies, air bubbles (most frequently Nitrogen), atheromatous debris  may cause sudden death if lodged in coronary or cerebral arteries; or at the MPA bifurcation as a saddle embolus

Pulmonary Embolism
Pulmonary (Venous) Embolism 
most come from deep leg veins;  up to 80% are clinically silent;  death occurs when more than

60% of pulmonary vasculature is occluded;  chronicity can lead to Pulmonary hypertension, cor Pulmonale, pulmonary vascular sclerosis

Venous thrombosis, Pulmonary saddle embolus,& Lung Infarct

Systemic (Arterial) Embolism
Systemic (Arterial) Embolism 60-65% arise from thrombi w/in the LV post-MI; 5-10% from atrial thrombi; 5% from cardiomyopathic lesions; 5-10% from atherosclerotic plaques, aneurysms, prostheses, IE; 10-15% from unknown sources;  almost always causes infarction; 7075% lodge in lower extremities; 10% in the brain, 10% in viscera, & 7-8% in upper extremities;  Paradoxical embolus- broken-off venous thrombus passes through a defect (VSD, ASD, PFO) into the arterial circulation

Fat / Marrow Embolism
Fat / Marrow Embolism  after traumatic injury to

long bones or to soft tissues:  symptoms show 24-72 hrs after injury ± pulmonary & neurologic deficits, anemia, thrombocytopenia, petechiae  mortality = 10%

Amniotic fluid Embolism
Amniotic fluid Embolism ± 
1 in 50,000 deliveries  caused by introduction of amniotic fluid into the circulation - 

  

tear in placental membranes, rupture of uterine/cervical veins in tumultuous labor emboli usually lodge in pulmonary vessels; Lanugo hair, fetal squames, fat, mucin, bile Sx: dyspnea, deep cyanosis, convulsions, coma, DIC, cardiovascular collapse (shock) mortality= 86%

Air Embolism
Air Embolism 
caused by air entering torn vessels (during delivery,

pneumothorax, abortion, trauma) or by air coming out of solution due to abrupt decompression  Significant amount is • 100ml.  Decompression sickness ² acute - ³the bends´; ³the chokes´  Caisson disease ² chronic form ± multiple minute ischemic, then necrotic, foci favoring the heads of the humeri, tibiae, femurs

Infarction 
def: ischemic necrosis due to occlusion of the arterial

supply or of the venous drainage  Coagulative pattern is usual, except in the Brain  nearly 99% caused by thromboembolism, & are arterial occlusions  development depends on : circulation of the patient; type of blood supply; rate of development of the occlusion; & the susceptibility of the affected tissue to hypoxia

Infarct 
Anemic (White) Infarct  Arterial occlusion in solid tissues  Initially hemorrhagic, becomes pale in 24-48 hrs.  Heart, Spleen, Kidneys ± single artery (end-arterial) supply  May be bland or septic  Hemorrhagic (Red) Infarct  Caused by venous occlusion; or in tissues with a double circulation; or in previously congested tissues  Lung, Liver ± dual supply; ovary ± single outlet; small intestines ± rich collaterals

Morphology of Infarction
GROSS  wedge-shaped, the apex being the focus of the occlusion  Poorly defined at first, slightly darker than normal, firmer consistency; Within 24hrs, more defined, color intensifies; Within days, pale infarct becomes yellowwhite & sharply demarcated; red infarct unchanged, leading to hyperemia  Surface of the organ becomes covered by a fibrinous exudate

Morphology of an Infarct
MICROSCOPIC  Ischemic coagulative necrosis (except Brain)  12-18 hrs: hemorrhagic suffusion, inflammatory marginal exudation, fibroblastic reparative response  If sepsis ocurs, the infarct may become an abscess

Hemorrhagic Infarct

Circulatory failure / Shock 
Circulatory collapse  Widespread hypoperfusion of tissues due to reduction

in blood volume or cardiac output, or redistribution of blood, resulting in an inadequate/ineffective circulating volume  Insufficient tissue oxygenation--- hypoxia  Inadequate clearance of metabolites--- accumulation of lactic acid--- acidosis

Types of Shock 
CARDIOGENIC ² due to intrinsic myocardial damage as in   



MI; cardiac tamponade, outflow block, or arrhythmias--- pump failure HYPOVOLEMIC / HEMORRHAGIC ² loss of blood (eg hemorrhage) or plasma (eg severe burns)--- inadequate circulating blood volume SEPTIC / ENDOTOXIC ² severe bacterial infections, usually Gram negative (endotoxins); less common Gram+ or fungi --- profound peripheral vasodilatation NEUROGENIC ² spinal cord injury, anesthetic accidents, severe pain --- massive peripheral vasodilatation ANAPHYLACTIC ² generalized type I hypersensitivity reaction--- massive peripheral vasodilatation

Shock
Cardiogenic Shock cardiac output venous return circulating blood Anaphylactic, Neurogenic Hypovolemic peripheral vasodilatation tissue perfusion Septic shock tissue hypoxia metabolic acidosis

Morphology of Shock 
hypoxic failure of multiple organ systems  Brain ± ischemic encephalopathy ± softening; liquefaction  Liver ± fatty change, central hemorrhagic necrosis  Heart ± subendocardial hemorrhages & necrosis; zonal lesions- hypercontraction of individual myocytes  Kidneys ± acute tubular necrosis  Lungs - ³shock lung´ - diffuse alveolar damage (DAD) --- acute respiratory distress syndrome (ARDS)  Adrenals ± lipid depletion of the zona reticularis & zona fasciculata --- ³stress response´  GIT ± patchy mucosal hemorrhages & necrosis

Morphology of Shock

Diffuse alveolar Damage, Lung

Acute tubular necrosis, Kidney

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