Hemodynamic disturbance

Hemodynamic disturbance

DR. USHA.M

HEMODYNAMICS

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

Hemodynamic disturbance

1. Edema

2. Hyperemia & congestion

3. Hemorrhage

4. Thrombosis

5. Infarction

6. Shock

Edema Normal body water distribution:-

Two compartments:

1. Intracellular – comprising of two- thirds of total body fluid.

2. 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 capillary1. Arteriolar end2. Venous endThe 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 pressures1. Osmotic pressureIs exerted by the chemical constituents of the

body fluids Eg. Electrolytes – crystalloid osmotic

pressure proteins (albumin)- oncotic osmotic

pressure.2. Hydrostatic pressurePressure within the blood vessel.

Edema

Is accumulation of excessive fluid in the interstitial spaces.

Classification of edema according to distribution of fluid

1. 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:-

1. Increased hydrostatic pressure

2. Increased permeability of the vessel wall

3. Decreased oncotic pressure

4. Sodium retention in the kidneys

5. Obstruction of lymph flow

1. Hydrostatic edema

Results from increased intra vascular pressure (hydrostatic pressure).

Causes :-1. Impaired venous return congestive cardiac failure constrictive pericarditis, ascitis (liver disease)2. Venous obstruction thrombi, tumor3. 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

Sodium RetentionSodium Retention

Excessive salt intake with renal Excessive salt intake with renal insufficiencyinsufficiency

Increased tubular Increased tubular reabsorptionreabsorption of of sodiumsodium

Renal Renal hypoperfusionhypoperfusion

Increased Increased reninrenin--angiotensinangiotensin--aldosteronealdosterone secretionsecretion

Lymphatic obstruction

Elephantiasis Edema of the arm following surgical

resection of axillary lymph nodes Edema of hand following post irradiation

fibrosis.

Feature Transudate Exudate

Definition Ultra filtrate of plasma

Edema of inflamed tissue

Endothelial changes

No changes endothelial permeability

Character Non inflammatory edema

Inflammatory edema

TRANSUDATE & EXUDATE

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

Volume Repletion ReactionVolume Repletion Reaction

Goldman: Cecil Textbook of Medicine, 22nd ed.

Renal edema

Causes:-

1. Nephorotic syndrome

2. Glomerulonephritis

3. Acute tubular injury

Nephorotic edema Heavy proteinuria hypoproteinemia

Activation of renin decreased plasmaAngiotensin oncotic pressureMechanism

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 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 :-

1. Left heart failure

2. ARDS

3. Shock

4. 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

Pitting EdemaPitting Edema

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

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

Purpura

Ecchymosis

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.

1. Microscopic – detectable by microscopic examination of urine.

2. 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 & HemoptysisEpistaxis & 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

– 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.

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)

© 2005 Elsevier

Normal

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)

© 2005 Elsevier

Hyperemia

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)

© 2005 Elsevier

Congestion

Examples:-

Hyperemia:-

1. Inflammation

2. Blushing – adrenergic stimulation

3. 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.

CVC Liver

Causes:-

1. Right heart failure

2. 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.

CVC Spleen

Causes:-

1. Right heart failure

2. 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:-

1. Right heart failure

2. Obstruction of renal vein

Gross:-

Kidney is congested.

CVC Kidney (micro)

Glomeruli – shows mesangial proliferation.

Tubules – shows degenerative changes (cloudy swelling).