Fluid and Hemodynamic Part i 6-29-10

FLUID ANDHEMODYNAMIC DERANGEMENTS

SOCORRO CRUZ – YANEZ MD, FPSP

Course objectives •Understand and define terms

•Demonstrate knowledge and understanding of etiopathogenesis and pathophysiology of disorder

•Recognize , describe its morphologic features

• Identify presenting clinical features and providing correlation and explanation

•List outcomes , complications

Learning activities

• Lectures ( Part 1 – Mon and 2- Thurs )

• Laboratory : ( Tues and Thurs )• Guided projection of glass slides • Gross • Microscopic slides

• Evaluation• Formative : SRS• Summative : ( Long exam and

practical exam )

FLUID AND HEMODYNAMIC DERANGEMENTS :

Edema Hyperemia / congestion Hemorrhage Thrombosis / DIC Embolism Infarction Shock

Normal fluid hemeostatic

balance

Normal distribution of body Normal distribution of body

waterwater

2/3

BODY WATER(60% of lean body

weight)

INTRACELLULAR EXTRA-

CELLULAR

1/3

INTERSTITIAL

95%

INTRAVASCULAR5%

• The exchange of fluid is between the vascular and interstitial compartments

• The exchange occur at the capillary level

• No net gain or loss of fluid

• Lymphatic drainage plays a part in maintaining this equilibrium

“THE NORMAL SITUATION”

Normal Fluid Homeostasis •Normal fluid homeostasis is

maintenance within physiologic ranges by :

o endothelial / vessel wall integrity

o intravascular pressure

o plasma osmolarity

TWO TYPES OF FORCES DRIVE THE NORMAL FLUID EXCHANGE

• Hydrostatic pressure o Affected by : cardiac output, vessel wall

elasticity, vascular tone, and blood volume.

• Oncotic or osmotic pressureo Maintained by protein level in the bloodo Serum Albumin level

Normal Microcirculation

Capillary Arterial VenousHydrostatic Pressure + 36 + 16Oncotic Pressure - 26 - 26Net filtration Pressure + 10 mmHg - 9 mm Hg

(leak-out) (Reabsorb)

“The abnormal situation”- Excessive accumulation of fluid in the interstitium and

body cavities EDEMA

EDEMA : definition

Increase accumulation of fluid in the interstitium and body cavities

TYPES OF EDEMA :

A. Inflammatory edema increased vascular permeability

B. Non- inflammatory edema changes in hemodynamic

forces

INFLAMMATORY VERSUS NON-INFLAMMATORY EDEMA

INFLAMMATORY

• Protein-rich fluid because of altered permeability of endothelial cells

• Fibrin-rich fluid• Inflammatory cells

typical• Specific gravity > 1.020• Usually a localized

process

NON-INFLAMMATORY

• Lower protein content no alteration in endothelial permeability

• No fibrin in fluid• No inflammatory cells in

fluid• Specific gravity < 1.012• Often a generalized

process

(These differences can be used in analyzing fluid from tissue cavities.)

D.TRANSUDATE

E. EXUDATE

S.G < 1.012 > 1.020

PROTEIN Low High

CELLCONTENT

few cells high cells

PATHOGE-NESIS

Hydrostatic imbalance

inc vascular permeability

TYPES OF EDEMA cont..

C. Localized• Hydropericardiu

m• hydrothorax• hydroperitoneu

m ( ascitis )

HYDROTHORAX

LOCALIZED SUB EPIDERMAL BULLAE

TYPES OF EDEMA cont..

D. Generalizedaka : Anasarca

• CHF• NS• Malnutrition

ANASARCOUS - HYDROPS FETALIS

Pathophysiologic categories of edema

1. Increased hydrostatic pressure

2. Reduced plasma osmotic pressure

3. Lymphatic obstruction4. Sodium retention5. Inflammation

Edema : Increased HP

1. Impaired venous return/Inc venous pressure

CHF Constrictive pericarditis Liver cirrhosis Venous obstruction / compression

2. Arteriolar dilatation Heat Neurohumoral regulation

CAPILLARY LUMEN(BLOOD)

INTERSTITIAL SPACE

ARTERIOLAR END

VENULEEND

INCREASED MOVEMENT OF FLUIDINTO INTERSTITIUM DUE TOINCREASED HYDROSTATIC PRESSURE

MOVEMENT OF FLUIDBACK INTO BLOODBASED ON DIFFERENTIALOSMOTIC PRESSURE

EXCESS FLUID REMOVEDBY LYMPHATIC DRAINAGE

MECHANISMS OF EDEMA – INCREASED HYDROSTATIC PRESSURE

NOTE: The lymphatic system attempts to compensate by increasing drainage.

Pathogenesis of edema in CHF

Inc plasma volume transudation EDEMA

Pathogenesis of edema in cirrhosis

Edema : Decreased OP

Nephrotic syndromeLiver cirrhosisMalnutritionProtein losing enteropathy

CAPILLARY LUMEN(BLOOD)

INTERSTITIAL SPACE

ARTERIOLAR END

VENULAREND

MOVEMENT OF FLUIDINTO INTERSTITIUMBASED ON DIFFERENTIALHYDROSTATIC PRESSURE

DECREASED MOVEMENT OF FLUID INTO BLOOD DUE TO DECREASED OSMOTIC PRESSURE

EXCESS FLUID REMOVEDBY LYMPHATIC DRAINAGE

MECHANISMS OF EDEMA – DECREASED OSMOTIC PRESSURE IN

BLOOD

NOTE: The lymphatic system attempts to compensate by increasing drainage.

Pathogenesis of Nephrotic Syndrome

Edema : Lymphatic obstruction Tumor

infiltrationInflammatory

scarring ex. filariasisPostsurgical

complicationPostradiation

complication

FILARIASIS

Edema : Na / H2O retention

Acute renal failure Increase salt intake Increased tubular reabsorption

Edema : Inflammation

Acute inflammation Chronic inflammation Angiogenesis

LOCALIZED SUBEPIDERMAL BULLAE

LARYNGEAL EDEMA

Edema : morphology

1. GROSS : increase weight organomegaly moist , wet , glistening subcutaneous edema -

dependent / pitting

DEPENDENT PITTING EDEMA

PITTING EDEMA

URINARY BLADDER – MUCOSAL EDEMA

Edema : morphology

2. Histologic loosening / separation of

extracellular matrix accumulation of poor

staining extracellular material ( water )

PULMONARY EDEMA

Assoc Ds : LV failure , renal failure , ARDS,

infections S/S : dyspnea , PND, orthopnea Morphology :

= distended alveoli with pink, proteinaceous fluid

= septal congestion

NORMAL LUNG PULMUNARY EDEMA

PULMONARY EDEMA

Pulmonary edema

PULMONARY EDEMA

NORMAL LUNG

AIR SAC

ALVEOLAR WALL

CONGESTED SEPTAL VESSELS

PULMONARY EDEMA

PULMONARY EDEMA

CEREBRAL EDEMA

Assoc Ds : brain tumors, infection, HPN , injury S/S : stupor , coma death CX : herniation Morphology : enlargement , swelling , narrowing of sulci, distension of gyri

CEREBRAL EDEMA

CEREBRAL EDEMA

WIDENED GYRI

FLATTENED SULCI

CEREBRAL EDEMA

TONSILLAR HERNIATION

EDEMA : CLINICAL SIGNIFICANCE

Edema of vital organs a. Lungs respiratory

insuff/ failure b. Brain increase ICP

brain herniation

HYPEREMIA AND CONGESTION

Definition : local increased volume of blood in an affected organ or tissue

Hyperemia and Congestion

Hyperemia ( Active Hyperemia )increase blood flow to capillaries

secondary to arterial / arteriolar dilatation

Ex : blushing Congestion ( passive hyperemia ) Retention of blood secondary to

impaired venous drainage Ex : CHF

PATHOGENESIS

MORPHOLOGY

ACTIVE HYPER-EMIA

Art dilatation 2 o SNS stim /vasoactive subs

Bright red discolorationEx. Blushing , exercise, inflam

PASSIVE HYPER- EMIA /

CONGES-TION

Impaired outflow Venous obstruction

Blue – red discoloration ( cyanotic )

TYPES OF CONGESTION

1.Acute congestion – passive hyperemia 2. Chronic congestion- long standing congestion

Acute pulm congestion : Morphology

Heavy , dark red, violaceous

Septal capillary engorged and thickened with blood

Assoc septal edema, alveolar hge and edema

PULMONARY CONGESTION

SEPTAL CAPILLARY CONGESTION

Chronic Passive Congestion of Lung : Morphology

Thickened , fibrotic alveolar septal wall

Alveolar congestion/ septal Hge

Heart failure cells Long standing : pulm HPN

HEART FAILURE CELLS

CPC OF THE LUNG

ACUTE HEPATIC CONGESTION

Central venous congestionCentral hepatocytic necrosis and hgesSparing of periportal hepatocytes

NORMAL HEPATOCYTE LOBULE

CENTRILOBULAR

MID-ZONAL

PERI-PORTAL

CENTRAL CONGESTION

SPARRING OF PERI-PORTAL AREA

ACUTE HEPATIC CONGESTION

CPC OF LIVER

“ Nutmeg “ liver Centrilobular necrosis , hemosiderin

macrophages Long standing

complication : cardiac cirrhosis

NORMAL LIVER

NUTMEG SPICE NUTMEG LIVER

CPC OF THE LIVER - NUTMEG LIVER

CPC OF THE LIVER

CENTRAL VEIN

CENTRAL HEPATOCYTIC CONGESTION

LIVER CELL NECROSIS

HEMOSIDERIN MACROPHAGES

CONGESTIVE SPLENOMEGALY

HEMORRHAGE

DEFINITION : Extravasation of RBCsecondary to blood vessel rupture

HEMORRHAGE : TYPES

1. AS TO SITE : Hemothorax Hemopericardium Hemoperitoneum Hemarthrosis

HEMOPERICARDIUM

HEMOTHORAX

HEMORRHAGES : TYPES

2. AS TO SIZE :a. Petechiae - 1-2 mm b. Purpura - > 3 mm c. Ecchymosis - > 1-2 cm d. Hematoma - large

pools of blood

PETECHIAE

PURPURIC HGES

ECCHYMOTIC HEMORRHAGES

ECCHYMOSIS

SUB-UNGAL HEMORRHAGES

SUBDURAL HEMATOMA

INTRACEREBRAL HEMATOMA

Subcapsular hematoma - liver

hematoma

HGE : PATHOGENESIS

1. Trauma, laceration2. Atherosclerosis3. Inflammatory4. Neoplastic erosion of

blood vessel5. Hgic diathesis

HEMORRHAGE : CLINICAL SIGNIFICANCE

1. Significant blood loss hgic / hypovolemic shock

2. Bleeding into vital organs like brain, lung and pericardium (cardiac tamponade )

3. External blood loss iron def anemia

4. Internal blood loss jaundice

GOOD DAY!

UNILATERAL EDEMA

Fluid and Hemodynamic Part i 6-29-10

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