Hemodynamics And Fluid Disorders

Front 1

what are the states of health of normal cells?

Back 1

a) Intact circulation- encompasses the integrity of the vessel wall, endothelial lining as well as intravascular pressure and osmolarity --> delivers oxygen and removes waste
B) Normal fluid exchange
C) Role of kidney and hormones in normal maintenance

Front 2

How much of the body weight is fluid in newborns compared to adults?

Back 2

Newborns- 83% is fluid
Adults- 60% is water

Front 3

What is the normal fluid distribution in the body?

Back 3

Intracellular fluid- 40%
Interstitial fluid- 10%
Intravascular fluid- 5%
Dense CT and bone fluid- 4%
Transcellular fluid- 1%

Front 4

Fluid of the circulatory system delivers and removes what?

Back 4

O2, nutrients, water, salts, hormones, CO2, metabolites, Waste, Heat

Front 5

What is cardiac output?

Back 5

the volume of blood pumped out by the heart per/minute.

= heart rate X stroke volume

stroke volume = amount of blood pumped out per minute (~70 ml)
heart rate= beats/min

During vigorous exercise the CO may increase 7 fold (35L per minute)

Front 6

Types of disorders of fluid and hemodynamics

Back 6

1) distrbances of water and electrolyte balance = edema
2) disturbances in volume of circulating blood = hypermia, hemorrhage and shock
3) disturbances of obstructive nature to vessels = thrombosis, embolism and infarction

Front 7

What is edema?

Back 7

The abnormal accumulation of fluid in the intersitital compartment of body cavity

Front 8

Fluid exchange between capillaries and tissue

Back 8

- capillaries are lined by endothelial cells w/ pores between them
- plasma fluid and small nutrient molecules exit capillaries and enter the interstial fluid in a process known as bulk flow
-BLOOD and PLAMS PROTEINS are TOO LARGE to pass through these pores under normal blood pressure

Front 9

factors controlling fluid and nutrient transport

Back 9

1)blood hydrostatic pressure- depends on blood pressure- it is the interstitial fluid hydrostatic pressure
2) Blood osmotic pressure- depends on plasma proteins
3) Kidneys- conserve or excrete water. if there is an excess of water then blood volume will increase and water will then be excreted to lower blood volume and maintain a normal blood volume. the kidneys also control metabolic waste, minerals and electrolytes.
4) endocrine factors-
--- ADH- conserves water and blood volume
--- ACTH- stimulates adrenal cortical hormones
** extra fluid in the interstitial compartment is removed by the lymphatic vessels.**

Front 10

factors that lead to abnormal fluid hemodynamics

Back 10

- increase blood volume or pressure (inc. hydrostatic pressure)
- decreased protein content (decreased osmotic pressure)
-increase of endothelial gaps (inflammation)
-retention of sodium and water (compromised renal function)
-obstruction of lymphatic drainage (will effect the net movement of WATER across the vascular wall)

Front 11

Types of Edema

Back 11

localized (venous congestion)
generalized (congestive heart failure)
inflammatory (infection)
non-inflammatory )in heart failure and renal failure)

** edema results when the rate of fluid formation within the intersitital compartment exceeds the rate of drainage by the venous and lymphatic systems.

Front 12

pathophysiologic catagories of edema

Back 12

- Increased venous pressure- impaired venous return, venous obstruction, constricitve pericarditis, arteriolar dilation
-reduced plasma osmotic pressure- protein losing glomerulnophropathies, liver cirrhosis, malnutrition
-lymphatic obstruction- inflammatory, neoplastic, post-surgical, post-irradiation
- sodium retention- excessive salt intake w/ renal diffiency, increased renal tubular reabsorption of sodium
-inflammation- acute inflammation

Front 13

differences in exudate and transudate

Back 13

exudate- high specifi gravity, high protein content
transudate- low specific gravity, low protein content

Front 14

Edema clinical subtypes

Back 14

Anasarca- diffuse swelling of all tissue
hydroperitoneum- collection of excessive fluid into the peritonial cavity
hydrothorax- collection of fluid in the pleural cavity
hydropericardium- collection of fluis in the pericardial sac

Front 15

Causes of localized edema?

Back 15

1)impaired venous drainage
-thrombosis --> stasis (standing still or sluggish circulation) --> increased hydrostatic pressure --> edema
2) lymphatic obstruction
- lymph node resection or fibrosis of the lymphatics --> impaired lymphatic drainage --> accumulation of fluid in the interstitial spaces --> edema
3) inflammation
-3 causes
1) inflammatory mediators cause vasodilation and inc. hydrostatic pressure
2) inc. intierstitial fluid osmotic pressure due to break down of tissue into small molecules
3) obstruction of draining lymphatics

Front 16

Causes of generalized edema

Back 16

1) congestive heart failure
- left side failure= pulmonary edema ** increased capillary pressure, fluid spillage into the alveolar spaces **
- right side failure = pitting edema, liver, kidney, spleen ** liver edema - increased back pressure and microcirculatory involvement. renal edema- salt and water retention, hypovolumic complication and dysregulation of hemodynamics **
2) renal diseases
- kidney failure--> reduced plasma osmotic pressure--> damage to glomeruli and blood proteins spilled into urine--> dec. osmotic pressure and inc. interstitial tissue fluid gain --> inc. salt and water retention --> **MAINLY MANIFESTED IN LOOSE TISSUE PRIMARILY IN THE FACE AND AROUND EYES**
3) liver cirrhosis
4) starvation
5) pregnancy
6) hypothyroidism

** generalized edema has a good prognosis IF in the visceral orgagans or subcutaneous tissue, and a POOR prognosis IF in the brain or lungs

Front 17

disorders of disturbances in circulating blood volume.

Back 17

-hypermia
-hemorrhage
-shock

Front 18

What is hyperemia?

Back 18

an active process resulting from increased blood flow due to arterial dilation.
Causes:
1) sympathetic neurogenic impluses with dilation
2) release of chemical mediators causing arteriolar dilation
3) hyperemia is seen in early stages of inflammation

Front 19

what is congestion?

Back 19

a passive process caused by increase in blood volume of the vascular bed due to impaired venous drainage
causes:
1) CHF
2) venous congestion/ occlusion
implication:
- short duration: no sig. pathology
- long duration: tissue appears deep blue (cyanosis)

congestion effecting the lungs:
- lungs are heavier then normal and more wet. increased hydrostatic pressure and vascular permeability which causes fluid to accumulate and edema to occur.

congestion in the liver-
- liver is heavier and bigger than normal and appears darker. called nutmeg liver

Front 20

what is hemorrhage?

Back 20

escape of the blood from a vessel which can be external or within a tissue
Causes:
- trauma
-disease of the vessel wall
- hypertension
- disorders of clotting and coagulation

Front 21

Hemorrhage Diatheses

Back 21

pathology related to platelet disorders:
- thrombocytopenia--> low platelet count
- thrombocytopathy--> abnormal platelet function

pathology related to clotting factors:
- hemophilia A (factor VIII deficiency)
- hemophilia B (factor IX deficiency)

Front 22

clinical patterns of hemorrhage

Back 22

-petechia: 1-2 mm blood spots seen on skin or mucosa. seen in coagulopathies (thrombocytopenia, thrombocytopathy and clotting defiencies)
-purpura: 3-5 mm or larger hemorrhagic areas. seen in vascular inflammation
-ecchymosis: several cm subcutaneous hematomas. large blotchy bruises. seen in surgical traumas, accidents, and bites
-hematoma: large blood clot w/in the tissue, body cavity, spaces. seen in surgery and trauma. clinical consequences vary

Front 23

types of disturbances of a obstructive nature?

Back 23

-thromboembolism

Front 24

Thrombosis?

Back 24

formation of a clot in uninjured tissue., living tissue or heart
involves 3 components:
-vascular wall
-platelets
-coagulation cascades

embolism: detached intravascular mass carried by the blood to a site distant from its point of origin

Front 25

fate of thrombus?

Back 25

1) propagation; accumulation of platelets and fibrin leading to vessel obstruction
2) embolization: fragemtn breaks off and travels with circulation as an embolus
3) dissolution: thrombus may be removed

Front 26

thrombus etiology?

Back 26

- injury to endothelium
- stasis or tubrulence of blood flow
-hypercoagulation

Front 27

arterial thrombus vs. venous thrombus

Back 27

arterial: occurs in vessels with rapif flow, exhibits laminations, grossly white , dry and fibrile, begins as a mural thrombus (attached to a wall) with continued flow more elements become attached and form a tail which then fills the lumen and occludes the vessel

venous: occludes a vessel with slow flow, attaches to the wall and has layers of fibrinogen, red, geatinous masses twists back on itself, usually occludes vessel. may calcify and become a phlebolith

Front 28

embloism etiology

Back 28

99% arise from thrombus
1% arise from other sources aich as air, fat, gas, amniotic fluid

** pulmonary thromboembolism is the most common fatal embolism.** 95% of these begin as DVT in the legs

Front 29

what is an infarction?

Back 29

a localized area of necrosis in a living tissue or organ.
Causes:
- occlusion of an artery which leads to impairment of the blood supply --> tissue death

factors:
-general status of the blood and cardovascular system
-anatomic pattern of the arterial blood supply
-rate of occlusion
-ability of cells to regenerate

Front 30

red hemorrhagic infarct

Back 30

occurs:
1) w/ venous occlusion
2) in loose tissue
3) in tissues w/ duel circulation
4) in tissues that were previously congested

Front 31

white infarct

Back 31

occurs:
1) w/ arterial occlusion in solid organs w/ end- arterial circulation as the solid nature of the tissue limits the hemorrhage.

Front 32

infarct clinical significance

Back 32

- over 1/2 of all deaths are caused by CVD
- most CVD deaths are dues to myocardical infarcts
- cerebral infarction
-renal infarction

Front 33

developmental (berry aneurysm)

Back 33

- occurs in the cerebral vessels in the form of small, spherical dilations of the circle of willis.
when reptured they can cause intracerebral hemorrhage, infarction or death.