Hemodynamic disturbance DR. USHA.M

HEMODYNAMICS Literally means “Blood movement” is the study of blood flow.

Hemodynamic disturbance Edema Hyperemia & congestion Hemorrhage Thrombosis Infarction Shock

Edema Normal body water distribution:- Two compartments: Intracellular – comprising of two- thirds of total body fluid. Extracellular – comprising of one- third of total body fluid. 1. Interstitial compartment- 75% 2. Intra vascular compartment – 25%

Normal fluid exchange There are two ends for a capillary 1. Arteriolar end 2. Venous end The pressure is high in the arteriolar end then the venous end.Normally the fluid moves out from the vessel in arteriolar end into interstitial tissue. From interstitial tissue same fluid moves back into vessel at venous end.The small amount of fluid which is left in interstitial space is cleared by lymphatics.

Starling forces

Normal fluid pressures 1. Osmotic pressure Is exerted by the chemical constituents of the body fluids Eg. Electrolytes – crystalloid osmotic pressure proteins (albumin)- oncotic osmotic pressure. 2. Hydrostatic pressure Pressure within the blood vessel.

Edema Is accumulation of excessive fluid in the interstitial spaces.

Classification of edema according to distribution of fluid Localized edema involving one organ or part of the body. eg-pleural effusion,ascitis,pericardial effusion ,etc. 2. Generalized edema Involving the entire body- ANSARCA

Pathogenesis of edema:- Increased hydrostatic pressure Increased permeability of the vessel wall Decreased oncotic pressure Sodium retention in the kidneys Obstruction of lymph flow

1. Hydrostatic edema Results from increased intra vascular pressure (hydrostatic pressure).

Causes :- Impaired venous return congestive cardiac failure constrictive pericarditis, ascitis (liver disease) Venous obstruction thrombi, tumor Arteriolar dilatation heat, inflammation

2. Increased vascular permeability Commonest cause is inflammation.Release of inflammatory mediators like histamine, bradykinin, PAF & others leads to increased permeability. Other causes: Injury,

3.Decreased plasma oncotic pressure 1.Decresed synthesis in the liver – end stage liver disease. 2.Incresed loss in urine(nephrotic syndrome) or stool (protein losing enteropathy) 3.Inadequte intake-kwashiokar

Lymphatic obstruction Elephantiasis Edema of the arm following surgical resection of axillary lymph nodes Edema of hand following post irradiation fibrosis.

Ultra filtrate of plasma Edema of inflamed tissue TRANSUDATE & EXUDATE Feature Transudate Exudate Definition Ultra filtrate of plasma Edema of inflamed tissue Endothelial changes No changes  endothelial permeability Character Non inflammatory edema Inflammatory edema

Feature Transudate Exudate Protein Low(<1g/dl) High (>2.5g/dl) Glucose Same as plasma Low(,60mg/dl) Specific gravity Low(1.015) High(>1.018) PH >7.3 <7.3 LDH low High Cells Few Many Example CCF Infections

Renal edema Causes:- 1. Nephorotic syndrome 2. Glomerulonephritis 3. Acute tubular injury

Nephorotic edema Heavy proteinuria hypoproteinemia Activation of renin decreased plasma Angiotensin oncotic pressure Mechanism Retention of Na &water edema

Nephritic edema Glomerulonephritis glomerular lesion I decreased filtration followed by increased absoption of Na & water by tubules Na & water retention edema

Acute tubular injury Toxins , drugs ATN Fails to excrete Na & water edema

Cardiac edema activation of renin angiotensin congestive cardiac failure ↓ cardiac output ↑ central venous renal hypoperfusion Pressure activation of renin angiotensin ↑ capillary hydrostatic aldosterone mechanism pressure Na & water retention edema

Pulmonary edema causes :- Left heart failure ARDS Shock Infections - pneumonia

left ventricular failure ↑ hydroastatic pressure ↑ pressure in pulmonary veins ↑ pressure in pulmonary capillaries interstitial edema pressure on alveolar wall &breaks alveolar linning alveolar edema

Hepatic Oedema hepatic pathology (e.g. cirrhosis) ↓ obstruction of portal venous system increased hydrostatic pressure & ↓albumin synthesis d.t. hepatocyte damge hypoproteinaemia transudate oedema (ascitis).

Ascites

Cerebral edema Causes:- 1. Infection - encephalitis,meningitis 2. Brain infarct, hemorrhage 3. Trauma 4. Tumors

Localised Oedema: acute inflammatory oedema ↑ vascular permeability exudate ↑ hydrostatic pressure of capillaries  hyperaemia ↑ osmotic pressure of interstitial fluid ↑ fluidity of ground substance allergic (hypersensitivity) oedema histamine release  ↑ vascular permeability  exudate (e.g. allergic rhinitis)

Pitting & non pitting edema is clinical terms for subcutaneous edema of leg.

Pitting Oedema

Clinical Features of Oedema Considerable quantities must accumulate before clinically apparent (oedema can be assessed by weighing the patient approx. 5 litres) Generalised Cardiac Oedema gravitational distribution pitting oedema  holds depression for a few minutes Renal Oedema fluid retention generally distributed in C.T.  puffy face/eyelids Serous Cavities e.g. hydrothorax/ascites Brain Oedema swollen; narrow sulci & flattened gyri Pulmonary Oedema exudate prone to infection  e.g. bronchopneumonia rales

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Hemorrhage Indicates extravasation of blood due to rupture of vessel.

Classification based on origin 1. Cardiac- penetrating wound rupture of ventricles in MI 2. Arterial – trauma rupture of aneurysm 3. Capillary – trauma, surgery 4. Venous – trauma, surgery

Petechiae, Pupura, Ecchymoses Refers to the hemorrhage into the skin & mucosae. Petechiae- pinpoint hemorrhage ( < 1mm) Purpura- 1mm- 1cm in diameter Echymoses- >1cm

Petechiae Caused by abnormalities in number or function of platelets or abnormalities in capillary wall (e.g. scurvy)

Purpura The palpable purpura on the foot of this nearly 3-year-old boy are associated with the disease Henoch-Schönlein Purpura. Henoch-Schönlein Purpura involves small vessels, not capillaries. Another common cause of purpura is vasculitis induced by an allergic reaction to drugs.

Ecchymosis The purpura and ecchymosis on the skin of this 12-year-old boy were the presenting symptoms of his acute myelogenous leukemia. The hemoglobin is converted to bilirubin (greenish) and hemosiderin (brown)

Hematoma Is grossly visible accumulation of extravasted blood in tissue. First it is red, then as the blood is deoxygenated it becomes dusky & bluish red.

Body cavity hemorrhage Hemothorax – accumulation of blood in pleural cavity Hemopericardium – in pericardial cavity Hemoperitonium – in peritonial cavity Hemoarthrosis – in intra – articular space Hematocephalus – in ventricles of brain

Hematuria Is appearance of blood in urine. Microscopic – detectable by microscopic examination of urine. Macroscopic – visible to naked eye Hematuria signifies disease of kidney or urinary tract

Hematemesis Is vomiting of blood. Sign of esophageal & gastric hemorrhage like rupture of esophageal varices & peptic ulcer bleeding.

Hematochezia Bleeding through rectem. Sign of diseases in large intestine.

Melena Black colored blood in stools. Indicates bleeding in upper GIT. Blood is partialy digested by HCLof gastric juice & transformed into a black pigment called hematein.This pigmentis not digested in the intestines & is passed in the feces.

Epistaxis & Hemoptysis Epistaxis is bleeding from the nose. Hemoptysis is bleeding from lungs.

Menorrhagia & Metrorrahagia Menorrhagia is heavy menstrual bleeding. Metrorrhagia occurs at any time & is not related to menstrual cycle.

Effects of Hemorrhage Site of hemorrhage Rate of blood loss brain, pericardium, pleural spac Rate of blood loss acute loss of > 20% of blood volume may cause hypotension or hypovolemic shock hemoglobin concentration not altered non-acute volume loss compensated by shift of fluid from extravascular to intravascular compartment hemoglobin concentration decreased

HYPEREMIA & CONGESTION Is increase in volume of blood in a particular tissue. Hyperemia is an “active process” , the increased blood influx results from arteriolar dilatation. Congestion, also known as “passive hyperemia”, results due to stagnation of blood because of venous obstruction.

Normal Figure 4-3 Hyperemia versus congestion. In both cases there is an increased volume and pressure of blood in a given tissue with associated capillary dilation and a potential for fluid extravasation. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM) © 2005 Elsevier

Hyperemia In hyperemia, increased inflow leads to engorgement with oxygenated blood, resulting in erythema. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM) © 2005 Elsevier

Congestion In congestion, diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and resulting in cyanosis. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM) © 2005 Elsevier

Examples:- Hyperemia:- Inflammation Blushing – adrenergic stimulation Exercise – incresed blood flow to the muscle. Congestion:- Obstruction of veins due to thrombi or backward pressure due to heart failure.

Color of hyperemic & congested tissue:- Hyperemic tissue contains increased amounts of oxygenated blood & therefore the tissue appears bright red. Congested tissue contains increased amounts of deoxygenated blood & appears blue. Hyperemic tissue is warm, while congested blood is cold & clammy.

Chronic venous congestion (CVC):- In CVC there is long standing there is accumulation of deoxygenated blood & hence there is damage to the tissue.

Mechanism heart failure left heart failure right heart failure Pressure into pressure into the Pulmonary vein systemic venous system CVC LUNGS CVC LIVER SPLEEN KIDNEY

CVC Lung Causes:- Left heart failure Gross :- The lungs are heavy. Lungs appear brown- BROWN INDURATION OF LUNGS.

CVC Lungs Micro:- Rupture of congested vessel results in edema & hemorrhage. Lysis of RBC’s releases hemosiderin pigment which is taken up by macrophages – HEART FAILURE CELLS.

View of pulmonary congestion and edema View of pulmonary congestion and edema. Often caused by an increase in hydrostatic pressure, a protein poor transudate seeps into interstitial and alveolar spaces. Note the engorged alveolar wall capillaries. If capillaries rupture, RBCs will escape into the alveolar space

Heart failure cells are hemosiderin laden macrophages Heart failure cells are hemosiderin laden macrophages. Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst. Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema. Note the thickening of the alveolar septae. This is caused by chronic pulmonary congestion and edema.

CVC Liver Causes:- Right heart failure Occlusion of inferior vena cava or portal vein. GROSS APPEARANCE:- NUTMEG APPEARANCE – Alternate areas of red & yellow .

CVC Liver Micro:- Periportal zone midzonal Centrilobular

CVC Liver (MICRO) Blood fills up the central vein & sinusoids around it. Followed by centrilobular hepatocytes necrosis. In the long standing cases the necrotic area is replaced by fibrous tissue. The areas with blood appears red & areas with fibrosis appears whitish yellow- NUTMEG APPEARANCE.

Nutmeg liver compared with actual nutmeg. Courtesy of Dr. Ed Friedlander

This view shows a close up of hemorrhagic central necrosis This view shows a close up of hemorrhagic central necrosis. Necrotic cells in the central area have been removed (cell dropout) and been replaced by cellular debris and hemorrhge. There is evidence that the passive congestion and hemorrhage is chronic, as many of the RBCs have been degraded into hemosiderin.

CVC Spleen Causes:- Right heart failure Portal hypertension GROSS:- Spleen is enlarged & congested.

CVC Spleen (micro) Red pulp appears congested. GAMMA GANDY BODIES OR SIDEROFIBROTIC NODULES:- Deposits of hemosiderin & calcium salts on fibrous tissue.

Gamma gandy bodies

CVC Kidney Cause:- Right heart failure Obstruction of renal vein Gross:- Kidney is congested.

CVC Kidney (micro) Glomeruli – shows mesangial proliferation. Tubules – shows degenerative changes (cloudy swelling).

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