Hemodynamic disturbances

Dr. Dhamyaa Al-Rahal

Congestion
Hyperemia

 Increase in volume of blood in tissue or part of body Divided into - active hyperemia - passive hyperemia Active congestion arterial + arteriolar dilatation flow of blood into capillaries redness Examples - exercise - febrile states - inflammation (local)

Arterial and arteriolar dilatation is brought about by 1. Neurogenic mechanisms ( Sympathetic ) 2. Release of vasoactive substances 3- Hormones.

Passive (venous) congestion

The result of impaired venous drainage Divided into - localized -generalized (systemic) Systemic venous congestion: Heart failure (inability to expel received blood) in stroke volume arteriolar tone (sympathetic stimulation) damming of blood in atria damming in systemic veins venous blood accumulation Veins become engorged Increased blood volume (?mechanism: renal)

 Lt sided heart failure

pulmonary congestion (systemic venous circulation spared) systemic congestion (lungs spared.)

Rt sided heart failure

Combined Rt and Lt sided heart failure generalized congestion (systemic + pulmonary)

Rt heart failure
Causes 1.chronic lung diseases (COAD - chronic obstructive airway diseases ) : chronic bronchitis/ emphysema) , which interfere with blood flow 2.Pulmonary valve diseases (stenosis and/or incompetance ). 3. Lt sided heart failure

Localized venous congestion

A. Pulmonary venous congestion
Occurs in 1. Left sided heart (ventricular) failure - coronary artery disease - systemic arterial hypertension. 2. Mitral valve stenosis Chronic pulmonary venous congestion Rt ventricular failure Pulmonary arterial hypertension

systemic venous congestion.

Locaized venous congestion B. venous outflow obstruction : Causes : 1. Venous thrombosis of major vein e.g. thrombosis of lower limb veins (femoral ,popleteal) congestion + swelling of lower limb 2. Cirrhosis of the liver portal hypertension - congestive splenomegaly - ascites i.e collection of transudate in the peritoneal cavity - esophageal varices/ hemorrhoids 3. Mechanical compression of veins - strangulated hernia - tumor - volvulus small intestine (twisting of loop of bowel). - torsion of vascular pedicle of ovary/testis

CVC liver
main changes are around central veins of the hepatic lobules (centrilobular regions) Microscopic features - central vein/central ends of sinusoids appear distended/packed with RBCs - hepatic cells in center of lobules undergo degeneration/necrosis , due to anoxia or pressure effect. - hepatic cells at periphery of lobule are normal/fatty change. Thus each lobule presents a dark brown center (congestion), and a light yellow periphery (fatty degeneration). Nutmeg liver

Vascular anatomy of liver

Gross appearance - liver enlarged/firm - cut surface mottled dark/pale: simulating cut surface of a nutmeg nutmeg liver

If the congestion is unrelieved, there will be necrosis of central zones with replacement by fibrosis (cardiac cirrhosis X ).

Chronic venous (passive) congestion liver

CVC liver

CVC spleen
- enlarged/firm in consistency - tense thickened capsule.

Microscopically - venous sinuses distended with RBCs - lymphoid follicles atrophied. - large number of macrophages loaded with hemosiderin. - fibrous trabeculae increased in thickness.

CVC kidney
Grossly - Slightly enlarged, - Firm in consistency - Dark red in color - The cut surface presents dark red dots/dark red streaks Microscopically - glomerular capillaries distended with RBCs

CVC lung
Grossly
Lungs are heavy/dark red/firm

Microscopically
- alveolar capillaries/venules: dilated/packed with RBCs. - venous congestion transudate in alveolar spaces capillaries ruptur--- intra-alveolar hemorrhage. - Macrophages move in to engulf RBCs + hemosiderin granules heart failure cells - hemosiderin deposition in interstitium - hemosiderin is fibrogenic brown induration

Venous congestion lung

CVC lung

Edema
Pathological accumulation of excess fluid in tissue
spaces, serous cavities, or pulmonary alveoli.

Normally water 60% of body wt. 2/3 intracellular

intercellular (interstitial)

1/3extracellular

intravascular fluid (blood plasma) 5% total body water.

Nature of accumulated fluid

a. Transudate: - serous (thin)/protein-poor - encountered in heart failure/nephrotic syndrome - SG < 1.020 (protein concentration <2.5g/dl) - related to hydrostatic pressure within intravascuar (IV ) compartment. b. Exudate: differs from transudate - protein-rich - encountered with inflammation. - resulting from vascular permeability escape of intravascular proteins (albumin) - having SG > 1.020 (protein conc. > 2.5 g/dl). Types of exudate: purulent, fibrinous, hemorrhagic , eosinophilic

Edema 1. Localized 2. Generalized (systemic) Anasarca: severe, generalized edema, including profound subcutaneous tissue accumulations. Ascites: collection of (edema) fluid in the peritoneal cavity. Hydrothorax: collection of fluid in pleural cavity (pleural effusion) Pericardial effusion: collection of fluid within pericardial cavity. Finger pressure over edematous subcutaneous tissue displace interstitial fluid pitted depression (pitting edema).

Ascites (severe form)

Rt sided heart failure secondary to lung disease (note cyanosis)

A case of liver cirrhosis

Pitting edema Ankle region

Mechanisms and causes of edema

mean blood hydrostatic pressure at arteriolar ends of capillaries 30 mm Hg colloid osmotic pressure of plasma (oncotic pressure) 25 mm Hg net difference of the two forces escape fluids from IV compartment into interstitial compartment. fluids move from IV compartment to interstitial compartment at arteriolar end of microcirculation largely under influence of blood hydrostatic pressure.

Forces determine exchange of fluids across capillary bed

Hydrostatic pressure low Hydrostatic pressure high

 Mean blood hydrostatic pressure at venous end of capillaries is lower than arteriolar end (12 mm Hg)

Net difference of the two forces

tissue fluids return back to vessels

fluids return to intravascular compartment at venular end of the microcirculation mainly because of the osmotic (oncotic) pressure of blood.
Small quantities of tissue fluids (contain large molecules) drain along lymphatic vessels venous circulation. []

Pathological accumulation of tissue fluids may result from: 1. hydrostatic pressure

2. colloid osmotic pressure of plasma (oncotic

pressure)

3. Lymphatic obstruction
4. Sodium retention 5. capillary permeability (inflammation)

Mechanisms of edema formation

2&3

1. 2. 3. 4.

hydrostatic pressure: heart failure, venous obstruction vascular permeability: acute inflammation, allergy oncotic pressure: hypoproteinemia Interference with lymphatic drainage: obstruction, congenital absence

 Generalized Localized Generalised: due to 1.Rt sided or combined Rt & Lt sided heart failure. 2. Constrictive pericarditis.

I. Increased capillary hydrostatic pressure

Rt ventricular failure
Rt. ventricular failure/combined Rt + Lt ventricular failure: Heart fails to pump received blood from Rt atrium. Accumulation/damming of blood reflected back into systemic veins increase in systemic venous pressure generalized CVC (congestive cardiac failure) edema formation (cardiac edema)

Contribution of kidney in cardiac edema

Diminution in cardiac output Reduced renal blood flow juxta -glomerular apparatus rennin/angiotensin/aldosterone system excessive tubular re-absorption of Na+ secretion ADH water reabsorption

intravascular compartment expansion

edema

Localized increase in hydrostatic pressure

Partial/complete obstruction of a large venous trunk local venous pressure beyond obstruction.

capillary pressure.
Decreased oxygen/nutrition capillary endothelial cells permeability localized edema.

Examples of localized edema

1. Portal hypertension (cirrhosis) ascites

2. Pressure of gravid uterus limbs.

edema lower

( iliac veins) 3. Acute LV failure acute pulmonary edema (Lt atrial pressure pulmonary veins Pul.edema) 4. Thrombosis of major veins 5. Incompetence of venous valves in varicose veins.

Ascites (severe form) A case of liver cirrhosis

Pulmonary edema mic

a case of Lt heart failure

II. Decrease in colloid osmotic pressure of plasma (hypoproteinemia)

Total plasma protein < 2 . 5 g% ( 6.4-8 g% ) or Albumin fraction < 1 . 5 g % ( 4-5.5 g% )

osmotic (oncotic) pressure of blood

excess of fluid passes into tissue spaces/serous cavities

generalized form of edema

Examples
1. Nephrotic syndrome - amyloidosis - diabetes - rapidly progressive GN. - minimal change GN 2. Diffuse liver disease: cirrhosis
3. Malnutrition e.g. famine edema/Kwashiorkor (sever protein-calorie malnutrition). 4. Protein losing gastro-enteropathy.

Kwashiorkor

Note edema of the feet in the child on the Lt

III. Obstruction of lymphatic vessels

Interference with lymphatic drainage

retention of tissue fluids

localized (non pitting) edema of affected part of body.

Causes of lymphedema
A. Congenital absence of lymphatic vessels
B. Parasitic: filarial worm C. Tumor invasion. D. Post-radiation. E. Post-surgical. elephantiasis

Lymphedema

 IV. Sodium and water retention

generally contributory aggravating factor salt retention may be a primary cause Salt retention may occur with any acute reduction of renal function
Increased salt retention + obligate water retention expansion of intravascular fluid volume hydrostatic pressure/colloid osmotic pressure edema

V. Increased capillary permeability (exudation)

A. Loclized B. Generalized ; In allergic conditions 1- Articaria 2- Angioneurotic edema.

Localized increase in cap permeability

inflammatory lesions
damaged capillary endothelium

permeability

free escape of plasma fluid/proteins into T. spaces oncotic pressure of tissue drawing of more water from the blood

localized swelling (inflammatory edema)

Clinical manifestations/significance of edema

Subcutaneous edema of cardiac or renal failure - drawing attention and pointing to the underlying disease - impair wound healing or clearance of infection. Edema of the lung - severe dyspnea/anoxia/death - favorable environment for bacterial infection. Edema of the brain - can be rapidly fatal - increase in the intracranial pressure

brain substance may be herniated

Edema of the larynx may cause suffocation

Acute laryngeal edema

Thrombosis
formation of a solid or semi-solid mass from the constituents of the blood within the vascular system during life. The mass itself is called a thrombus.

Causes of thrombosis
Three major factors predispose to thrombosis (Virchows triad)
1. 2. Endothelial injury Changes in blood flow

3.

Changes in composition of blood

Virchow triad in thrombosis

Injury to vascular endothelium

A. Mechanical injury 1. Pressure on vessel 2. Rupture of vessel 3. Torsion of vessel B. Degeneration of vascular endothelium at sites of 1. Atherosclerosis 2. Aneurysm e.g. aortic aneurysm 3. Myocardial infarction. C. Inflammatory processes 1. Phlebitis. 2. Arteritis. 3. Inflammatory valve diseases as rheumatic & infective endocarditis valvular vegetations.

Infective endocarditis aortic valve

II. Slowing/stasis/turbulence of blood flow

atria (auricles) in association with valvular diseases atrial fibrillation aneurysms

varicose veins.

III. Changes in composition of blood

a. Platelets: quantitative/qualitative changes after surgical operation - increase in number - become stickier - become more fragile (lysis) release thrombogenic factors b. Fibrinogen/plasma coagulation factors - increase during pregnancy& following delivery.
c. Red blood cells - polycythemia: red blood cells blood viscosity slowing in blood flow - marasmus (severe dehydration): viscosity

Appearance and composition of thrombi

depends on speed of blood flow 1. in rapidly flowing blood (artery): mainly of aggregated platelets/some fibrin firm/pale (pale thrombus). 2. in stagnant blood: complete occlusion of blood vessel: consists of network of fibrin/trapped red cells-leucocytes platelets red thrombus soft/dark red/gelatinous 3. Between these two extremes: mixed thrombi - form in slowly flowing blood usually veins - consist of alternating layers of platelet aggregates & network of fibrin entrapping red and white cells - laminated appearance (lines of zahn)

Composition of thrombus

Thrombi classified on basis of presence or absence of pyogenic bacteria into

1. Septic thrombi e.g. those complicating bacterial endocarditis 2. Aseptic thrombi (bland)

Venous thrombosis
two types of vein thrombosis . Thrombophlebitis a. Septic thrombophlebitis b. Aseptic thrombophlebitis 2. Phlebothrombosis a. chronic heart failure/confined to bed for long time DVT-deep venous thrombosis. b. after abdominal operations changes in the composition of blood + venous stasis

Arterial thrombosis
Develops - over sites of atherosclerosis - Aneurysm, - polyarteritis nodosa/ thromboangiitis obliterans Arterial thrombi may cessation of the arterial blood supply to part affected ischemic damage

superadded thrombosis

Narrowing of arterial lumen by atheroma

Complete obstruction by
superadded thrombosis

Coronary atherosclerosis + superadded thrombosis

Cardiac thrombosis
1. Mural thrombosis - over the endocardial surface of infracted heart wall
2. Vegetations over diseased valves 3. Thrombosis of auricular appendages 4. Agonal thrombosis composed mainly of fibrin, which separated out from the sluggishly moving blood just before death.

Outcomes of thrombosis ( Fate )

1. Propagation.

2.

Embolism

3. Lysis and removal (by fibrinolytic action)

4.

Organization and recanalization

Potential outcomes of venous thrombosis

coronary thrombosis organization and re-canalization

 Comparison of thrombus with a blood clot Thrombus: Found intravascular, has a shape, composed of platelets, RBC,WBC & fibrin. Lines of Zahn are present. Blood clot : Found extravascular or intravascular( postmortem ), lacks shap, composed of fibrin, ,RBCs,& WBCs (lack platelets), Lines of Zahn are absent

Hemorrhage

Extravasation of blood due to vessel rupture, may be external or internal.

Hematoma :accumulation of blood within a tissue. Petechiae: small 1-2 mm haemorrhagic spots of the skin,
mucous memb., or serosal surfaces, associated with local increase in intravascular pressure, thrombocytopenia, defective platelet function-uremia, clotting factors deficiency.

Purpura : larger than petechiae >3 mm, caused by the

same conditions as in petechiae & also can be seen in trauma, inflammation of vessels & increased vascular weakness (fragility)-amyloidosis.

 Ecchymosis ( Bruises ) : larger 1-2 cm

subcutaneous hematomas caused by trauma. The condition is intensified( even in trivial trauma) in the presence of the previous mentioned conditions in petechiae or ecchymosis.The sequential color changes from red-blue to bluegreen & then yellow brown are due to conversion of Hb to bilirubin & then to hemosiderin. Hemothorax, hemopericardium, hemoperitoneum & hemarthrosis: large accumulation of blood within the pleural cavity pericardial cavity, peritoneum & joint spaces respectively.

End