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Home , Hyperaemia, Hypovolemia

Circulatory disturbances

17. 18. 19. Hemostasis, Main pathological categories

• Circulatory disturbances • Regressive changes • Proliferative changes • Inflammations • Tumors • Developmental anomalies Topics

• Local hyperaemia • Local oligaemia (ischaemia) • Hemostasis, shock • Hemorrhage • Thrombosis • Embolism • • Heart • Network of vessels – Blood distribution – – Blood collection – • Microcirculation – between blood and extravascular tissue – exchange of nutrient and waste products • Lymphatics – draining fluid into the blood vascular system Normal circulation

• Heart (mechanical energy) • Valves (cardiac, aortic, venous) • Elastic walls of blood vessels • Pressure differentials • Volume of the blood • Distribution of the blood • Hydrodynamic factors Regulation

• Hydrodynamic factors + • Neurohormonal regulation • Vasomotion control maintaining harmonized calibre changes in the vessels

• Terminal circulatory bed Terminal circulatory bed • Section between the and venules – Most important part – Maintaining the normal function of tissues – Microcirculation – Nutrient, oxygen supply & waste removal – Cross sectional area is 1300 × the Ø of the aorta, but normally contain 5% of the blood • Major place of circulatory disturbances The terminal circulatory system Role of the

• Function: – To maintain blood in a fluid state – Anti-thrombotic and pro-fibrinolytic – Upon injury opposite effect

• Critical participant: – Fluid distribution, inflammation, immunity – , hemostasis Circulatory disturbances

Alterations in blood flow and

• Local: • General: – Hyperemia – collapse • In the – shock – Active hyperemia – Slowdown of the arterial flow • In the : – Local venous congestion – Systemic venous congestion – Ischaemia Hyperemia due to increased b. f. Normal composition of the blood No leakage No extravasation

Physiological: – Muscles – Digestion Normal – Irritation to CNS Hyperemia due to decreased b. f.

• Following active h. • contracted • Decreased influx in the terminal bed • Vasoconstrictor paralysis • Prehemostasis Normal • Increased vascular permeability Prehemostasis

• Plasma leakage • Extravasation – RBCs – WBCs • In case of inflammation • Strong stimuli – mechanical, thermal, chemical or toxic Pathology • On the body surfaces of alive animals

• Increased blood flow – Bright red, slightly swollen, warm area • Decreased blood flow – Bluish red, swollen, colder • Distended blood vessels appear – Vascular injection

Local congestion

• Passive process • Blood accumulates and slows down in the venous circulation – prehemostasis, hemostasis • Vein is obstructed or compressed – Torsion of the intestine – Strangulation of the – Thrombosis Normal

Pathology • Organs – Dark red, bluish red, cyanotic – Swollen – Large amount of blood on the cut surface • Mucosal membranes (skin) – Dark red, bluish red, swollen – Edemic submucosa – Wrinkled – Serous fluid in the lumen of the

Torsion of one uterine horn, cat Strangulation, small intestine, horse

Infarceratio – venous infarct

• Infarceratio haemorrhagica • Long lasting or final obstruction of a vein – No nutrient or oxygen supply – Plasma and RBCs in the tissues – of large area (similar to hemorrhagic infarct) Slow occlusion

• Collaterals enlarge • Remodel • Drainage is maintained • Liver cirrhosis – Compressed portal veins – Veins of – „medusa head”

Systemic venous congestion • Not only the terminal circulatory bed is affected • Causes – Acute or chronic heart failure – Paralysis of the vasomotor center – Shock • Appearance – In all the organs

Pathology

• Liver – First centrolobular, than general – Chronic case: nutmeg liver • Spleen – Hyperemic septic splenitis ! • Kidneys (medulla only) • Lung (plus ) • Intestines – Dark from the serous membranes

The chronic case

MIRISTICA FRAGRANS Congestive induration

• Chronic congestion • Parenchyma is destroyed • Replaced by collagen fibrous connective tissue • Pathology: – Firm, moist content is less on the cut surface Pangásos induratio, máj Ischaemia

• Local inadequate blood supply – General: anemia, • Physiological – Digestion, uneven distribution of blood • Pathological – Compression – Obturation – Vasoneurotic disturbance • Consequences Ischaemia • Ischaemia compressiva – Tympany (horse, cow, rabbit, etc.) – Tumors • Ischaemia obturativa – , embolus • Vasoneurotic ischaemia – Angiospasm (CNS, cold, chemical subs.) • Collateral ischaemia

Consequences of the ischaemia • Depends on – degree and type of narrowing, time, type of tissue, collaterals (lung, liver) • Collapsus / shock

• Necrosis - Infarct: – Infarctus haemorrhagicus – Infarctus ischaemicus Infarct • Definition – Necrosis of circumscribed area of a tissue due to acute ischemia • The vessels are obturated • The circulation of tissue – End arteries –No anastomotic channel – Anastomotic arteries –Kidneys

Ischemic infarct • End arteries – Area becomes bloodless, necrotic – Appearence: • Pale grey, dry • Margin of infarct is reddish –The collateral vessels are full with RBCs – Location • Kidneys, heart, spleen, brain Pathology of the infarct • Formation of the infarct – Pale, swollen, no sharp edges – Histochemical methods are needed • Fresh infarct – Cone shaped, pale, enlarged, sharp edged, cut surface is still moist (!) • Evolved infarct – Cut surface dry, homogenous, crumbled – Dark red, hyperaemic rim • Older or chronic infarct – Surrounded by demarcation zone, scar

Ischeemic infarcts, kidney, swine, cross section

Colonic mucosal necrosis, horse Ischemic infarct, heart

Hemorrhagic infarct

• Double circulation – In the necrotic area the vessels are filled with RBCs • Red (darker), dry

– Location • Lungs, kidney, spleen, liver

Haemorrhagic infarct, testicle, dog Haemorrhagic infarcts, spleen, dog Haemorrhagic infarcts, kidney

Conquences of an infarct • Nature of vascular supply – Double (lungs, liver) or end-arterial (kidney, spleen) • Rate of occlusion development – If it is slow, collateral blood supply may develop • Vulnerability to – Neurons (3–4 min) – Myocardial cells (20–30 min) – Fibroblasts (hours) • Oxigen conent of the blood Conquences of an infarct

• Death – Insufficient –Heart –Lung • Survival – Reactive inflammation – Repair – Organisatio – connective tissue

Anaemic infarcts, kidney

Infarct – arterial occlusion

Infarceration – venal occlusion Hemostasis • arrest of • finely regulated physiologic response – to vascular damage to prevent blood loss – without affecting fluidity and flow of blood in normal undamaged vasculature • interactions – between endothel, platelets and coagulation factors • disruption of the delicate balance – hemorrhage, thrombosis Events of the hemostasis 1. Primary – Transient , platelet aggregation to form platelet plug 2. Secondary – Coagulation to form a meshwork of fibrin • intrinsic (XII activation) • extrinsic (TF – VII activation) – common pathway activation of X, FIBRIN formation 3. Thrombus dissolution – thrombus retraction by plasmin, fibrinolysis 4. Tissue repair at the dameged site Disturbances of microcirculation

• Prehemostasis –blood flow slows down • Hemostasis – stop of the blood flow – In the terminal bed – Leakage – Reversible • Posthemostasis – start of the blood flow

• Peristasis – slow bloodflow

Inducing effects

• Cellular changes – Stabile suspension – labile suspension – Thrombocytes, RBCs, WBCs • Viscosity – Plasma leakage, higher density • Chemical factors – Intercellular bridges, hypercoagulobility • Rheological factors Resistance

Capillary Stasis Shock

• General circulatory disturbance • Peripheral circulatory failure – Clinical term – Blood is in the terminal circulatory bed

• Mild case: collapse – Mild disorder for a short time Shock • Definition – cardiovascular collapse – A syndrome resulting from a disproportion between and volume of the circulatory system (1:6) – Profound circulatory failure resulting in life-threatening hypoperfusion of vital organs Types of shock • Cardiogenic – Acute or chronic heart failure • Hypovolemic – Blood loss • Reduced circulating blood volume – Fluid loss • secondary to vomiting, diarrhea, burn • Blood maldistribution – Neurogenic • vasodilatation - paralysis of the vasomotor centre – Anaphylactic - type I hypersensitivity reaction – Septic (endotoxin)

Caused by Gr- lipopolisacharid (LPS); (Gr+, fungi as well without LPS) and cytokins, vasactive mediators – LPS blocks the production of anticoagulnt substances by the endothelial cells – Activates complement cascade (C3a, C5a anafilatoxins!!) – Activates intrinsic coagulation (XII faktor) – TNFα, és IL-1 production by activated macrophages promote extrinsic coagulation on endothelial cells by TF expression – PAF – thrombocyte aggregation Phases of shock, pathogenesis 1. non-progressive – compensation – • Sympathic effect, (nor)epinefrin – Increase cardiac output, increased peripherial resistance (vasoconstriction) • ADH (hypotalamus – neurohypophysis) • renin-angiotensin-aldosteron system – ACE – blockers!!! Phases of shock, pathogenesis

2. progressive – inadequate compensation

– anaerob glycolysis in the cells (lack of O2)

– lactate, local hypoxia, increased CO2– sudden arteriolar relaxation and dilation 3. irreversible – severe metabolic acidosis – Insufficient blood supply of the vital organs (brain, kidneys), DIC Pathology • Hemorrhages – under the serosal membranes, on the mucosal membranes, in some organs • Congestion in the abdominal organs (intestines) • Transsudate in the abdominal cavity, liver and lung edema • Acute dilatation of the heart • Ischemia in the kidney () • Hyalin-thrombus in the small blood vessels • Subacute case – degeneration in liver, kidney, heartmuscle

Liver edema

„Shock-gut”, pig, E.coli enterosorption