Chapter

three

hemodynamic derangements

hemodynamic derangements

Section 1 Hyperemia and congestion
Disorder of the volume of blood in local tissue

Section 2 Hemorrhage
Destroy of the integrity of the vessel

Section 3 Thromobosis
Disorder of the quality

Section 4 Embolism

Section 1 Hyperemia and congestion
Both terms mean increased volume of blood in the affected tissue and organ. Hyperemia (active hyperemia), occurs when arterial and arteriolar dilatation produces an increased inflow of blood into capillary beds, with opening of inactive capillaries. Congestion (passive hyperemia), results from impaired venous drainage with passive distention of distal veins, venules and capillaries, also called venous hyperemia.

Congestion may be localized as with venous obstruction, or being pressed, or systemic as with heart failure. In left ventricular failure, the lungs are mainly affected; in rightsided failure, systemic organs are affected, sparing the lungs.

Congestion of capillary beds is closely related to the development of edema, so that congestion and edema commonly occur together.

Morphology
 Grossly:  The

affected tissue of organs turn swelling and with a deep red color. In skin or mucosa, the affected part is red-blue color with lower temperature owing to deoxgenation of impounded red cells—cyanosis.  In chronic congestion, the tissue and organ will turn hard—cirrhosis

Nephritic anemia

Normal kidney

Nephritic congestion

Morphology histologically
congestive edema: the fluid transudated from the vessel because of the high pressure. Hemorrhage: Injury of the tissue: degeneration and necrosis because of hypoxia. Cirrhosis: fibrous proliferation following the injury of the parenchymal cell.
long term congestion called chronic passive congestion, most often affects the lung, liver and spleen.

Important organs congestion
chronic pulmonary congestion: congestion and edema seen main with left ventricular failure Normal structure Dilation and congestion of capillary

Fibrosis of alveolar septa

Sketch map of alveolar septal capillary congestion

Microscopic : chronic pulmonary congestion
Dilatation and congestion of alveolar septal capillary, alveolar spaces contain transudation

Heart failure cell

Prussian blue 10 × 10

H.E 10 × 10

Microscopic

chronic lung congestion
Dilation and congestion of alveolar septal capillary, alveolar spaces contain transudation and edema liquid

Heart failure cell

H.E 10 × 20 the septa have become thickened and fibrotic, and the alveolar spaces contain hemosiderin

H.E 10 × 20

Pulmonary congestion
 Grossly,

the lung turns brown and hard or rubbery —— pulmonary brown duration.  Microscopically, there are several features: septal capillary dilation and congestion; hemorrhage in alveolar; hemosiderin laden macrophages (heart failure cells) ; septal fibrosis and hemosiderin deposition.

Hepatic congestion
 In

right heart failure  Grossly, the congestive liver turned swollen and rubbery on the section surface, red strips alternated with yellow strips—— nutmeg liver.  Microscopically, the central veinule and adjacent sinusoids distended and congested; the associated hepatocytes atrophy or necrosis. (red) The peri-portal hepatocytes fatty degeneration. (yellow)  The disease kept development: liver cirrhosis, usually cardiac liver cirrhosis.

Nutmeg Liver

Yellow stripes alternated with red stripes on the section surface of the liver

microscopic

chronic liver congestion (nutmeg liver)

the central vein and sinusoids are distended with blood
central hepatocytes degeneration ; the periportal hepatocytes, better oxygenated because of their proximity to hepatic arterioles, experience less severe hypoxia and may only develop fatty change. Yellow stripes alternated with red stripes on the section surface of the liver, (nutmeg liver).

H.E 10 × 20

microscopic

chronic liver congestion (nutmeg liver)

the central vein and sinusoids are distended with blood

H.E 4 × 10

In severe and longstanding hepatic congestion (most commonly associated with severe heart failure), there may even be grossly evident hepatic fibrosis (“cardiac cirrhosis”).

Congestive hepatic cirrhosis

Section 3

Thromobosis

• Thrombosis is a pathologic process, which represents the formation of a blood clot (thrombus) within a living cardiovascular system. 1. It is located within the vessel or the heart. 2. It is formed in a living body. 3. It remains attached to the vessel or the heart at the site of its formation.

Pathogenesis
Three major influences predispose to thrombus formation

 endothelial injury;  alterations in normal blood flow;  blood hypercoagulability

 Endothelial injury is the dominant and most frequent influence, It is particularly important in thrombus formation in the heart and arterial circulation, whatever the cause of injury to endothelium, it is a potent thrombogenic influence.

Regardless of the cause of endothelial damage, the end results include exposure of subendothelial collagen (and other platelet activators), adherence of platelets, release of tissue factor, and local depletion of prostacyclin and plasminogen activator (PA).

 Stasis and turbulence ① disrupt laminar flow and bring platelets into contact with the endothelium; ② prevent dilution of activated clotting factors by fresh-flowing blood and hepatic clearance of the activated coagulation factors; ③ retard the inflow of clotting factor inhibitors and permit the build-up of thrombi; ④ turbulence may cause dysfunction or damage to the endothelium, favoring platelet and fibrin deposition while at the same time reducing the local release of prostacyclin and tissue type plasminogen activator (tPA) to promote endothelial cell activation, predisposing to thrombosis, leukocyte adhesion, and a variety of other endothelial cell effects.

 Hypercoagulability is an uncommon and poorly understood cause of thrombosis; it is loosely defined as any alteration of the coagulation pathways that predisposed to thrombosis, and can be divided into primary (genetic) and secondary (acquired) disorders. The pathogenesis of thrombotic diathesis in a number of common clinical setting is more complicated and multifactorial.

Morphology and forming process of thrombi
Pale thrombus------- (head)------plt.+Wbc+ fibrin vegetation, Arterial thrombus mixed thrombus------(body)------plt.+Rbc.+Wbc+ fibrin Venous thrombus, globular thrombus in aneurysms, propagating thrombus laminations thrombus Red thrombus-------(tail)----Rbc+fibrin Venous thrombus Hyaline thrombus-----fibrinous DIC(microthrombus)

Mixed thrombus Mixed thrombus

Microscopic

thrombosis in nephritic arteriola

Thrombosis on arteriolar intima

H.E

10 × 10

H.E

10 × 20

Disseminated intravascular coagulation (DIC)
A variety of disorders ranging from obstetric complications to advanced malignancy may be complicated by DIC, the sudden or insidious onset of widespread fibrin thrombi in the microcirculation,and appear hemorrhage in organs due to consume coagulatic factors.

H. E

10 × 10

microscopic
hyaline thrombus in glomerulus

H. E 10 × 20

Goldner

10 × 40

Occlusive Thrombus
Thrombus block the vescular lumen

Mural Thrombus
When arterial thrombi arise in heart chambers or in the aortic lumen, they are usually applied to the wall of the underlying structure and are termed mural thrombi.

Mural thrombus in atria

Fate of the thrombosis
Dissolution and resorption Organization and recanalization Calcifications (phlebolith) Propagation and Embolization

Clinical correlation
(1) obstruction of arteries and veins (2) sources of emboli (3) heart valves malformation (4) hemorrhage

Coronary artery thrombi forming and the blocking of artery lumen

Coronary artery thrombi forming with hemorrhage microscopic
H.E 4 × 10

Vegetation

thrombi may form on heart valves

vegetation

H.E

4 × 10

Section 4

EMBOLISM

An abnormal insoluble substance moved with the blood flow and blocked the lumen of some small blood vessels, known as embolism and that abnormal substances is known as embolus. The kinds of embolus An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.

The pathways of embolism
The emboli moved in the same direction with the blood flow. (1) Venous embolus may cause pulmonary embolization and infarction (2) Arteria embolus can embolize the important organs of body, such as coronary, cerebal, liver and kidney vessles. (3) Portal veinous embolus may cause hepatic .+Wbc+ fibrin embolization. (4) Venous embolus from right heart to left heart cause arteria system embolism, known as crosses embolism. (5) Large venous embolism may cause small venous known as retrograde emblism.

brain

lower extremity

Embolism in important organs
1.thromboembolism Pulmonary thromboembolism
thromboemboli originate from deep leg veins above the level of the knee. They are carried through progressively larger channels and usually pass through the right heart into the pulmonary vasculature Most pulmonary emboli (60% to 80%) are clinically silent because they are small. With time they undergo organization and become incorporated into the vascular wall; in some cases organization of the thromboembolus leaves behind a delicate, bridging fibrous web.

microscopic Thrombus block the small vescular lumen in myocardial stroma
H.E 10 × 20

pulmonary embolization by thrombus

pulmonary embolization by thrombus

straddle pulmonary embolization by thrombus

Microscopic

pulmonary embolization by thrombus

H.E

4 × 10

H.E

4 × 10

The causes of the sudden death 1. mechanical obstruction : acute right heart failure (cor pulmonale), or cardiovascular collapse occur when 60% or more of the pulmonary circulation is obstructed with emboli (that is a large embolus or multiple, simultaneous, small emboli). 2. nerval role;nerve hyperexcited stimulate pulmonary ,brochial and Coronary arteries constrict cause pulmonary hypertension with right heart failure 3. chemical mediator role;TXA2 and 5-HT cause pulmonary ,brochial and Coronary arteries constrict ,so that cause acute bleed of lung ,mycardia ischemia and respiratory failure and heart failure

(2). Systemic Thromboembolism
Systemic thromboembolism refers to emboli traveling within the arterial circulation. Most arise from intracardiac with ulcerated atherosclerotic plaques or aortic aneurysms, or from fragmentation of a valvular vegetation (infective endocarditis) and paradoxical embolism from venous thrombi that gain access to the left side of the circulation through a right-to-left congenital cardiac anomaly. The major sites of arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, and spleen involved to a lesser extent.

The consequences of systemic emboli depend on the extent of collateral vascular supply in the affected tissue, the tissue’s vulnerability to ischemia, and the caliber of the vessel occluded; Embolic occlusion of the femoral artery is disastrous inasmuch as it cause infarction (gangrene) of the lower extremity, but it is not necessarily life-threatening. In contrast, a much smaller embolus that occludes the middle cerebral artery may lead to death in days, or even hours.

2.Gas embolism
Gas bubbles within the circulation can obstruct vascular flow (and cause distal ischemic injury) almost as readily as thrombotic masses.

(1).Air embolism
Air may gain access to the circulation (1) during delivery or abortion when it is forced into ruptured uterine venous sinuses by the powerful contractions of the uterus, (2) during the performance of a pneumothorax when a large artery or vein is ruptured or entered accidentally, and (3) when injury to the lung or the chest wall opens a large vein and permits the entrance of air during the negative phase of inspirations. Generally in excess of 100 ml of air is required to produce a clinical effect,or sudden death; the bubbles act like physical obstructions and may coalesce to form frothy masses sufficiently large to occlude major vessels.

(2). decompression sickness:
A particular form of gas embolism called caisson disease or decompression sickness occurs when individuals are exposed to sudden changes in atmospheric pressure. Scuba and deep sea divers, underwater construction workers, and individuals in unpressurized aircraft in rapid ascent are all at risk. When air is breathed at high pressure (e.g., during a deep sea dive), increased amounts of gas (particularly nitrogen) become dissolved in the blood and tissues. If the diver then ascends (depressurizes) too rapidly, the nitrogen expands in the tissues, and bubbles out of solution in the blood to form gas emboli.

The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called the bends. Gas emboli may also induce focal ischemia in a number of tissues, including brain and heart. In the lungs, edema, hemorrhages, and focal atelectasis or emphysema may appear, leading to respiratory distress, the so-called chokes. Treatment of gas embolism consists of placing the individual in a compression chamber where the barometric pressure may be raised, thus forcing the gas bubbles back into solution. It is then hoped that subsequent slow decompression will permit gradual resorption and exhalation of the gases so that obstructive bubbles do not reform.

3.Amniotic fluid embolism
Amniotic fluid embolism is a grave but fortunately uncommon complication of labor and the immediate postpartum period (1 per 50,000 deliveries). The underlying cause is the infusion of amniotic fluid(and all of its contents) into the materal circulation via a tear in the placental membranes and rupture of uterine veins.

Amniotic fluid embolis m

The classic findings are therefore the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tracts.

H.E

10 × 10

The onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma.

Pulmonary edema typically develops, and in about half the cases excessive bleeding from the uterns and birth canal,along with (in half the patients)disseminated intravascular coagulation.due to realse of thrombogenic substances from amniotic fluid. The protein in amniotic fluid may cause especially sensitive chock It is suspected that some humoral factor (possibly prostaglandins) in aumniolic fluid causing pulmonary vasoconstruction and impaired cardiac contractility is responsible for the respiratory and cardiac decompensation.

4.Fat embolism
Microscopic fat globules may be found in the circulation after fracture of long bone (which have fatty marrows) or rarely , in the setting of soft tissue trauma and burns. It should be emphasized that whereas traumatic fat embolism can be demonstrated anatomically in some 90% of individuals with severe skeletal injures, only about 1% of such patients show any clinical findings. Fat embolism syndrome is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia and is fatal in about 10% of cases. Typically the symptoms appear 1 to 3 days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia. Neurologic symptoms include irritability and restlessness, with progression to delirium or coma.

Fat embolism in lung Alveolar septal capillaries and small arteries are full of red stained fat microglobule Sudan 5 × 10

Section 5

Infarction

infarct is an area of ischemic necrosis caused by occlusion of either
the arterial supply or the venous drainage in a particular tissue. Nearly 99% of all infarcts result from thrombotic or embolic events, and almost all result from arterial occlusion. infarction may

also be caused by other mechanisms, such as local vasospasm, swelling of an atheroma secondary to hemorrhage within a plaque, or extrinsic compression of a vessel, for example, by tumor. Other uncommon causes include twisting of the vessels (e.g., in testicular torsion or bowel volvulus), compression of the blood supply by edema or by entrapment in a hernial sac, and traumatic rupture of the blood supply.

Factors that Influence infarct
(1) the nature of the vascular supply;
lungs have a dual pulmonary and bronchial artery blood supply, obstruction of small pulmonary arterioles does not cause infarction in a healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, is relatively resistant to infarction. Infarction or gangrene of the hand or forearm is almost never encountered, because of the double arterial supply through the radial and ulnar arteries, with their numerous interconnection. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction.

(2) the rate of development of the occlusion;
Slowly developing occlusions are less likely to cause infarction because they provide time for the development of alternative pathways of flow and arteriolar anastomoses .

(3) the vulnerability of a given tissue to hypoxia;
Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells, although hardier than neurons, are also quite sensitive and die after only 20 to 30 minutes of ischemia. In contrast, fibroblasts within myocardium remain viable after many hours of ischemia.The epithelial cells of the proximal renal tubules are much more vulnerable to hypoxia than are the other segments of the nephron.

(4) the blood oxygen content.
Partial flow obstruction of a small vessel in an anemic or cyanotic patient might lead to tissue infarction, whereas it would be without effect under conditions of normal oxygen tension.

Types of infarcts
White infarcts (anemic ) White or pale infarcts occur with arterial occlusions. or in solid organs (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds.

Microscopic All infarcts tend to be wedge shaped, with the occluded vessel at the apex and the periphery of the organ forming the base; when the base is a serosal surface, there is often an overlying fibrinous exudate. The lateral margins may be irregular, reflecting the pattern of vascular supply from adjacent vessels.. Different range of infarction caused by different artery branch blocking in kidney

Sketch map of kidney infarction

Nephritic anemic infarction

Nephritic anemic infarction

inflammatory response Necrotic region

Infarct area

H.E

10 × 10

H.E

10 × 10

Spleen anemic infarction

myocardial infarction
macroscopic

microscopic

H.E 10 × 10

Myocardial infarction

H.E

10 × 20

Cerebral infarction
The brain is an exception to these generalizations; like other causes of necrosis, ischemic tissue injury in the central nervous system results in liquefactive necrosis.

Red infarcts (hemorrhagic ) (1) with venous occlusions(such as in ovarian torsion); (2) in loose tissues(such as lung) that allow blood to collect in the infarcted zone; (3) in tissues with dual circulations such as lung and small intestine, permitting flow of blood from the unobstructed vascular channel into the necrotic area (obviously such perfusion is not sufficient to rescue the ischemic tissues); (4) in tissues that were previously congested because of sluggish venous outflow; (5) when flow is reestablished to a site of previous arterial occlusion and necrosis (e.g., fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion).

Pulmonary hemorrhagic infarction wedge shaped, with the occluded vessel at the apex and the periphery of the organ forming the base

Pulmonary hemorrhagic infarction

usually does not cause pulmonary infarction because of blood flow into the area from an intact bronchial circulation and other anastomoses. When combined with left heart failure, because of the increased pressure of pulmonary vein and pulmonary congestion,

the blood flow of bronchial circulation can not overcome the resistance of pulmonary vein, so the infarction happened.

Intestinal hemorrhagic infarction
The necrotic intestinal canal is deep purple, the peristalsis disappears and hemorrhage in the intestinal lumen

Septic infarctions
In these cases. the infarct is converted into an abscess, with a correspondingly greater inflammatory response.

The structure of necrotic tissue disappeared , infiltration of inflammatory cells with hemorrhage

H.E

10 × 10

Clinical signification of infarction
Infarction of tissues, is a common cause of clinical illness. Myocardial infarction is by far the predominant cause of fatal coronary heart disease. Cerebral infarct (encephalomalacia) is also the most frequent type of central nervous system disease. Pulmonary infarction is an extremely common complication in a variety of clinical settings. Renal infarction does not have the paramount importance. Ischemic necrosis (gangrene) of the lower extremities is a major concern in diabetics.

summary
integrality
rupture of blood vessel hemorrhage

permeability↑
artery vein little hyperemia

edema

much

Blood volume

congestion

ischemia
thrombosis embolization

Characters of blood

infarction

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