Vascular congestion results from..

impaired outflow

increased hydrostatic pressure causes vasodilation 

What are the causes of vascular congestion?

Local: isolated venous obstruction

Systemic: cardiac failure 

Color of tissue in vascular congestion?

Blue (cyanotic)

deoxyhemoglobin

example of systemic cyanosis

Blue baby syndrome (heart issues)

Compare hyperemia to vascular congestion

it is an active process

cause is vasodilation caused by inflammation

color of tissue is red vs blue in congestion

Complications of vascular congestion?

Definition of Hemorrhage

extravasation of blood because of vessel rupture

hemorrhage associated with...

-chronic congestion

-hemorrhage diathesis

----increased fragility of vessels

------platelet deficiency or abnormal function

-----abnormalilites in clotting factors

-vascular injury

What is a petichiae hemorrhage

*1-2 mm hemorrhages into skin, mucous membranes, or serosal surface

* associated with: increased intravascular pressure , low platelet counts, defective platelet function,  & clotting factor deficiencies.

What is pupura hemorrhage?

>3 mm

Causes: same as petichiae, trauma, vasculitis, increases vascular fragility. 

What is ecchymoses hemorrhage?

>10-20 cm

*trauma , hemorrhage

Accumulation of blood in body cavity types...

hemorthorax

hemophericardium

hemoperitoneum

hemoarthrosis

*rate and volume of blood loss

*site of bleeding 

*loss of iron 

Two main functions of hemostasis

1. maintian blood in fluid state 

2. respond to vascular injury with formation of hemostatic plug

1.Inappropriate activation of normal hemostatic processes in uninjured vasculature

2.Thrombotic occlusion of a blood vessel after minor injury 

What are the influences in thrombus formation.

1. endothelial injury

2. stasis or turbulence of blood flow

3.blood hypercoagulability

1. injury to heart endothelium

2.ulcerated atherosclerotic plaque

3. trauma

4.vasculitis

1.Disrupts laminar flow, brings platelets into contact with endothelium

2.Prevent dilution of activated coagulation factors by fresh flowing blood

3.Retard influx of clotting factor inhibitors permit buildup to clots

4.Promote continued endothelial cell activation

clinical settings leading to turbulence or stasis..

1.Ulcerated atherosclerotic plaque

2.Aneurysm

3.Myocardial infarction

4.Mitral valve stenosis

5.Hyperviscosity syndromes

6.Sickle cell anemia 

hydrostatic pressure 

pressure exerted on a membrane by fluid contained by that   membrane

osmotic pressure

Osmosis: high solvent to low solvent, goes from low solute to high solute 

Net filtration rate

Osmotic pressure - Hydrostatic Pressure

Edema

Palpable swelling produced by and increase in interstitial fluid volume

increase hydrostatic pressure

decrease osmotic pressure

lymphatic obstruction

sodium retention

increased vascular permeability 

Overall cause of increased hydrostatic pressure 

poor venous circulation and resultant fluid accumulation 

two forms of increased hydrostatic pressure

Localized- emboli, external pressure, lower extremity inactivity.

Systemic- congestive heart failure, constrictive pericarditis, ascites (fluid in the peritoneal cavity)

protein concentration in blood is lower than in interstitial tissue

most influential protein: Albumin

Decreased synthesis

liver disease (cirrhosis) 

malnutrition 

Increased Excretion 

Nephrotic Syndrome 

Consequences of reduced plasma osmotic pressure

fluid leaves the plasma and causes reduced intravascular volume

renal hypoperfusion occurs

Hypovolemia with an ineffective hyperaldosteronism

and can lead to further adema

 How does the body handle reduced intravascular volume 

Reninangiotensin system 

What is sodium and water retention 

excessive salt intake with renal insufficiency 

increased tubular reabsorption 

renal hypoperfusion

increased renin-angiotensin-aldosterone secretion 

causes of sodium and water retention

increased hydrostatic pressure

diminished vascular colloid osmotic pressure

causes of lymphatic obstruction

impaired lymphatic drainage

usually localized

causes:

  inflammatory

  neoplastic

  postsurgical 

  post irradiation 

'definition of embolism and examples:

Detached intravascular mass that is carried by blood to a site distant from point of origin

-Dislodged thrombus

-Fat (bone marrow)

-Air (gas) 

most common form of embolus

thromboembolism

causes of pulmonary embolism

Age

Burns

Heart failure or atrial fibrillation

Long term immobility

Obesity

Pregnancy

Recent surgery 

systemic thromboembolism 

 thrombus that forms in the heart

arotic aneurysm

swelling of the aorta 

thrombi on ulcerated atherosclerotic plaques

fragmentation of vavular vegetation 

destinations of systemic thromboembolism

lower extremities (75%)

brain (10%)

definition of infarction

Area of ischemic necrosis caused by occlusion of either arterial supply or venous drainage in tissue 

infarction results from

Thrombotic or embolitic events

Arterial occlusions (really bad)

what are the stages in acute myocardial infarction

ischemia- blood flow and oxygen demand are out of balance

injury-prolonged ischemia damages heart tissue

infarction- damage is irreversible, death of myocardial cells, scar tissue replaces dead tissue

Factors that influence development of an infarction

Nature of the vascular supply

Rate of development of occlusion

Vulnerability of a tissue to hypoxia

Oxygen content of blood 

Shock

group of signs and sympotoms and usually a consequance of previous problem. 

-systemic hypoperfusion

hypotension

impaired tissue perfusion

cellular hypoxia 

categories of shock

cardiogenic

hypovolemic

distrubitive

low cardiac output due to myocardial pump failure

MI (most common cause)

ventricular arrythmias

cardiac tamponade

-compression of the heart

pulmonary embolism

compensatory mechanisms of cardiogenic shock

increase heart rate

stregnthen myocardial contractions

promote sodium and water retention

compensatory mechanisms in cardiogenic shock are ineffective because it leads to....

increase myocardial workload, reducing pumping ability of the heart

blood backs up

pulmonary edema

mechanism of hypovolemic shock

low cardiac output due to inadequate blood or plasma volume (decrease preload)

clinical examples of hypovolemic shock

hemorrhage (most common cause)

fluid loss (vomiting, diarrhea, burns, trauma)

ascites (fluid build up in abdomen)

hemothorax

mechanism of distributive shock

vasodilation causes state of hypovolemia

neurogenic

septic

anaphylactic

mechanism of neurogenic shock

loss of sympathic vasoconstriction tone in the vascular smooth muscle and reduced autonomic function

results in blood pooling in the venous system  

causes of neurogenic shock

spinal anesthesia

spinal cord injury

vasomotor center depresssion  

inflammatory response due to bacterial endotoxns

macrophages secret TNF and interleukins

responsible for PAF, prostaglandins, leukotrienes, thromboxane A2, kinins, complement

vasodilation, increased capillary permeability

loss of fluids to the interstitium  

gram neg bacteria (most common)

gram- positive septmia

Fungal sepsis

catecholamines

epinephrine and norepinephrine  

stimulation of sympathetic nervous system causes release of catecholamines from adrenal medulla  

increase heart rate

increase force of contractions

1. liver converts glycogen to glucose and releases glucose to blood

(to create energy)

2.Dilation of bronchioles

why? (To take in more oxygen)

3.Changes in blood flow patterns leading to decreased digestive system activity and reduced urine output

why?(induces parasymapthetic system which slows down heart rate...sympathetic takes over which increases heart rate and shuts off parasympathetic)

4.increased metabolic rate

why?(more energy and heat)

Angiotension II effects

*stabilization of systeminc blood pressure and extracelllular fluid volume

*vasoconstrictor of smooth muscle (arterioles)

*stimuates reabsorbtion of sodium and water

-direction action on renal tubules

-aldosterone release from adrenal cortex

*stimulates hypothalamus to release antidiuretic hormone  

Effects of ADH

insertion of aquaporins into the collecting ducts causing reabsorbtion of water as the filtrate passes through the collection duct water is conserved

compensatory stages of non progessive stage

-tachycardia, bounding pulse due to sympathetic stimulation

-restless and irrability related to cerebral hypoxia

-tachypnea to compensate for hypoxia

-reduced urine output secondary to vasoconstriction

-cool, pale skin (vasoconstrction); warm, dry skin in septic shock (vasodilation)

progressive stage tissure hypofusion/hypoxia leads to

circulatory and metabolic imbalances

acidosis (depresses myocardial function)

systemic tissue hypoxia

systemic tissue hypoxia

promotes release of endothelial mediation

vasodilatin leading to venous pooling

increased capillary permeability

sluggish blood flow, risk of DIC

signs and sympotoms of progressive stage

hypertension as compensatory mechanisms starts to fail

reduced stroke volume

weak, rapid, thready pulse caused by decreased cardiac output

shallow respirations

reducsed urine output

cold, clammy skin (vasoconstriction)

cyanosis (hypoxia)

Ireversible (refractory) stage

cell injury is wide spread

reduced perfusion damages cell membranes

multple system organ failure

Irreversible stage signs and symptoms

-unconciousness and loss of reflexes (reduced cerebreal perfusion, acid base imaleances elecrotlyte abnormalities)

-rapidly falling blood pressure

-weak pulse (redcued cardiac output)

-slow, shallow respirations (respirations center depression)

anurua (renal failure)