Hemodynamic Disorders

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Hemodynamic Disorders
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Edema
Hyperemia
Congestion
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Edema
Edema refers to the presence of excess fluid in
the interstitial spaces of the body
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Edema
Local Accumulation hydrothorax,
hydropericardium, hydroperitoneum
(ascites)
Generalized (anasarca)
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Hyperemia
An active process from increased input into a
tissue resulting in local increase in blood
volume in a tissue
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Congestion
An passive process from decreased outflow from a
tissue resulting in local increase in blood
volume in a tissue
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Normal Regulation of Fluid Movement
Starlings law the hydrostatic pressure of the
blood is normally nearly balanced by the oncotic
pressure of plasma proteins
The net result is that there is a continuous
movement of  fluid from the intravascular
compartment into the tissues via the
pre-capillary arteriole, where it is either
transported away by lymphatics, or reabsorbed in
the post-capillary venules
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FLUID TRANSIT ACROSS CAPILLARY WALLS
Hydrostatic pressure
Osmotic pressure
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Edema
Edema is the result of either an increased
hydrostatic pressure or a decreased osmotic
pressure
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Increased Hydrostatic Pressure
Impaired Venous Return
Congestive Heart Failure Constrictive
Pericarditis Ascites-Liver Cirrhosis Venous
Obstruction or compression
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Reduced Osmotic Pressure
Hypoproteinemia
Protein -losing glomerulopathies Liver
Cirrhosis Malnutrition Protein-losing
gastoenteropathies
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Lymphatic Obstruction
Inflammation Neoplastic Post-surgical Post-irradia
tion
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Sodium Retention
Increased salt intake with renal disease Renal
Hypoperfusion Increased Renin-angiotension-aldoste
rone
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Congestive Heart Failure
Impaired Venous Return
Renal NaWater Retention
EDEMA
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Edema
Non-inflammatory edema
Pulmonary edema due to heart failure (increased
hydrostatic pressure and secondary
aldosteronism) Nephrotic syndrome (decreased
oncotic pressure)
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Edema
Inflammatory edema
Direct, irreversible injury - all vessels
(burns) Transient increase in vascular
permeability, i.e., the effect of mediators on
post-capillary venules
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Edema
Local edema - hallmark of acute
inflammation Generalized edema - affects
visceral organs and dependent areas of the trunk
and lower extremities ("pitting edema") Anasarca
- severe generalized edema
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Hyperemia and Congestion
Active (arterial) - augmented supply of blood to
an organ, usually physiologic (exercise) Passive
(venous) - engorgement of an organ by venous
blood, usually the result of left ventricular
heart failure, which leads, in turn, to right
ventricular failure
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Passive Congestion, Acute, Lung
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Pulmonary Edema
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Nutmeg Liver (passive congestion)
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Nutmeg Liver (centrilobular congestion)
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Hemorrhage
Hemorrhage is a discharge of blood from the
vascular compartment to the exterior of the body
or into non-vascular body spaces, most often
caused by trauma congenital defects (Berry
aneurysm) vessel wall defect (atherosclerosis) hyp
ertension coagulopathy
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Hemorrhage
Hematoma - collection of blood within a
tissue (often muscle) Hemopericardium Hemothorax H
emarthrosis Hemoperitoneum
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Hemorrhage
Petechia - pinpoint (capillary) hemorrhagein the
skin or elsewhere, usually inconjunction with a
coagulopathy orvasculitis Purpura - diffuse
superficial hemorrhage in the skin, up to 1 cm in
diameter Ecchymosis (bruise) A superficial
skin hemorrhage 1 cm in size
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Petechial Rash
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Ecchymosis,
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Thrombosis
Thrombosis refers to the formation within a
vascular lumen of a thrombus, defined as an
aggregate of coagulated blood containing
platelets, fibrin, and entrapped cellular
elements. For all practical purposes, the term
"clot" is synonymous.
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Thrombosis
Arterial thrombosis is, by far, the most common
cause of death in Western industrialized
countries. Most often, thrombosis occurs in the
coronary arteries,leading to myocardial
infarction (1 cause of death). However, it may
also occur in the heart or carotid system,
causing stroke (2 cause of death), or peripheral
infarcts.
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Thrombosis, Coronary Artery
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Lines of Zahn
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Thrombosis - Pathogenesis
Three Primary Factors
Endothelial Injury Alterations in blood
flow Increased coagulability of the blood
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Thrombosis
Endothelial Injury
Thrombus
Abnormal Blood Flow
Hypercoagulability
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Endothelial Injury
Most important mechanism caused by
Hypertension Turbulent blood flow Endotoxins Hyper
cholesteremia,homocystine, radiation
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Abnormal Blood Flow
Stasis and Turbulence
Disrupt laminar flow bring platelets in contact
with endothelium
Prevents dilution of activated clotting factors
Retard the inflow of clotting inhibitors
Promote endothelial cell activation
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Hypercoagulability
Relative rare, but is associated with a genetic
defect a lack of anticoagulants
Antithrombin III Protein C Protein S
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Fate of thrombi
Propagation Embolization Dissolution Organizati
on and recanalization
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Propagation
Accumulation of more platelets and fibrin,
becoming larger
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Embolization
Break loose and be transported
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Dissolution
Be removed by the Fibrinolytic System
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Organization and Recanalization
Induce inflammation and fibrosis (organized) and
re-establish vascular flow(recanalize)
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Recanalization
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Recanalization
Coronary Artery
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Thrombosis - Heart
Predisposing factors
Endocarditis Myocardial
infarction Atrial fibrillation
Cardiomyopathy
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Complications of Cardiac Thrombosis
The major complication of thrombi in any location
in the heart is the detachment of fragments and
their transport to distant sites(embolization),
where they lodge and occlude arterial vessels.
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Venous Thrombosis
The deep veins of the leg are the most common
site for thrombosis, primarily due to sluggish
blood flow. This is most often the result of
prolonged immobilization. This condition may
cause swelling of the leg, or may be completely
asymptomatic. The most feared complication is
pulmonary thromboembolism.
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Thrombosis - High risk patient
Tissue damage (surgery, burns) Prolonged
immobilization Myocardial infarction Neoplasms -
solid or hematopoetic Trousseau syndrome
pancreatic adenoCA Prosthetic heart valves DIC
(also increased risk of hemorrhage)
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Thrombosis - High risk patient
Smokers Pregnancy/postpartum Oral
BCPs Hyperlipidemia Sickle cell disease Atrial
fibrillation
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Disseminated intravascular coagulation
Disseminated intravascular coagulation (DIC,
consumption coagulopathy, or microangiopathic
hemolytic anemia) is a serious and often fatal
acquired disorde where platelets and clotting
factors are consumed by massive
intravascular coagulation, often within capillary
beds. Conversely, this leads to
uncontrollable hemorrhage in other areas of the
body.
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Disseminated intravascular coagulation
The central event in the initiation of DIC is the
activation of the intrinsic or extrinsic clotting
cascades within the vascular compartment by
tissue injury, or damage to the endothelium, or
both.
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Disseminated intravascular coagulation
Many venules, capillaries, andarterioles contain
multiple, small, fibrin/platelet thrombi.The
meshwork of fibrin may fragment red blood
cells,forming schistocytes. These altered RBCs
account for the name microangiopathic hemolytic
anemia.Widespread ischemic changes in many organs
occur, leading to multi-organ failure
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Embolism
Embolism is the passage though the venous or
arterial circulations of any material capable of
lodging in a blood vessel and thereby obstructing
the lumen
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Types of Embolism
Thromboembolism (most common) Fat embolism
Amniotic fluid embolism Gas embolism
Cholesterol embolism Septic embolism
Foreign body embolism Bone marrow embolism
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Embolism - Pulmonary
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Embolism - Pulmonary
Bad News
10-15 of death in hospitalized patients 50,000
deaths per year
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Embolism - Pulmonary
Depending on the size and length of the embolic
mass, it may occlude the main pulmonary artery
,impact astride the bifurcation (a saddle
embolus), or pass out into the progressively
smaller branching pulmonary arteries
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saddle embolus
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Clinical Consequences of a Pulmonary Embolus
Most pulmonary emboli (60 to 80) are clinically
silent because they are small.
Sudden death, acute right heart failure (acute
cor pulmonale), or cardiovascular collapse may
occur when more than 60 pulmonary vasculature is
obstructed
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Clinical Consequences of a Pulmonary Embolus
Multiple emboli lead to pulmonary hypertension,
chronic right heart strain (chronic cor
pulmonale), and in time pulmonary vascular
sclerosis with progressively worsening dyspnea.
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Systemic Embolism
This term refers to emboli that travel through
the arterial circulation.
Most arterial emboli (80 to 85) arise from
thrombi within the heart
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Systemic Embolism
In contrast to venous emboli, arterial emboli
follow a much more varied pathway, but they
almost always cause infarction.
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Systemic Embolism
The major sites of lodgment of all systemic
emboli are the lower extremities (70 to 75), the
brain (10), viscera (10), and the upper limbs
(7 to 8).
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Fat Embolism
Minute globules of fat can often be demonstrated
in the circulation following fractures of the
shafts of long bones (which have fatty marrows)
and, rarely, with soft tissue trauma and burns
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Fat Embolism
Traumatic fat embolism can be demonstrated
anatomically in approximately 90 of individuals
who sustain severe skeletal injuries, only about
1 of these individuals manifest clinical signs
or symptoms known as fat embolism syndrome
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Fat Embolism Syndrome
Is characterized by pulmonary insufficiency,
neurologic symptoms, anemia, and
thrombocytopenia. Typically, the symptoms appear
after a latent period of 24 to 72 hours after
injury.
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Fat Embolism Syndrome
There is the sudden onset of tachypnea, dyspnea,
and tachycardia. Neurologic symptoms include
irritability and restlessness, which progress to
delirium or coma. Petechial skin rash is common.
The fat embolism syndrome is fatal in about 10
of cases.
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Air Embolism
Bubbles of air or gas within the circulation
obstruct vascular flow and damage tissues just as
as thrombotic masses The injury is referred to as
barotrauma
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Air Embolism
Air or gas may gain access to the circulation
(1) during delivery or abortion when it is forced
into ruptured uterine venous sinuses by the
powerful contractions of the uterus, (2) during
the performance of a pneumothorax when a large
artery or vein is ruptured or entered
accidentally, (3) when injury to the lung or the
chest wall opens a large vein and permits the
entrance of air during the negative pressure
phase of inspiration.
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Air Embolism
Large quantities of air, about 100 cc, are
required to produce problems.
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Air Embolism
A specialized form of gas embolism known as
decompression sickness occurs in persons exposed
to sudden changes in atmospheric pressure
scuba and deep sea divers
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Air Embolism
When the gas is breathed under high pressure,
increased amounts dissolve in the blood, tissue
fluids, and fat. If the individual decompresses
too rapidly, the gases come out of solution as
minute bubbles.
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Air Embolism
The acute form is commonly known as the bends
or the chokes. The acute obstruction of small
blood vessels in and around the joints and
skeletal muscles causes the patient to double up
in pain a similar process may produce acute
respiratory distress, while involvement of the
cerebral vessels may lead to coma and sometimes
death
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Air Embolism
The chronic form of decompression sickness is
more properly referred to as Caisson Disease.
Here, the presumed persistence of gaseous emboli
leads to multiple foci of ischemic necrosis
throughout the skeletal system
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Amniotic Fluid Embolism
An extreme complication usually of labor and the
immediate postpartum period is a major cause of
maternal mortality
Uncommon, (1 per 50,000 deliveries), but has a
mortality rate of 86.
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Amniotic Fluid Embolism
The clinical presentation is striking suddenly
and without warning, profound respiratory
difficulty with deep cynanosis and cardiovascular
shock appear, followed rapidly in some cases by
clonic-tonic convulsions and profound coma.
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Amniotic Fluid Embolism
The underlying cause is the infusion of amniotic
fluid with all of its contents into the maternal
circulation following a tear in the placental
membranes and rupture of uterine and/or cervical
veins
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Infarction
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Infarction
An infarct is an area of ischemic necrosis within
a tissue or an organ, produced by occlusion of
either its arterial supply or its venous
drainage.
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Infarction
Nearly all infarcts result from thrombotic or
embolic occlusion, but sometimes infarction may
be caused by other mechanisms, such as ballooning
of an atheroma secondary to hemorrhage within a
plaque.
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Infarction
Other uncommon causes include twisting of the
vessels to the ovary or a loop of bowel,
compression of the blood supply of a loop of
bowel in a hernial sac, or trapping of a viscus
under a peritoneal adhesion.
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Infarction
Nearly 99 of infarcts are caused by
thromboembolic events, and almost all are the
result of arterial occlusions. Emboli arising in
the heart or major arteries must impact in
arteries. Similarly, venous thromboemboli lodge
in the pulmonary arterial system and so cause
arterial infarcts.
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Infarction
Although venous thrombosis may cause infarction
of some tissue or organ, more often it merely
induces venous obstruction. Usually, bypass
channels develop, providing some outflow from the
area, which in turn permits some improvement in
the arterial inflow.
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Types of Infarcts
Infarcts are divided on the basis of their color
and the presence or absence of bacterial
contamination. Infarcts are either anemic
(white) or hemorrhagic (red),and either septic or
bland, depending on the presence or absence of
bacterial infection in the area of necrosis.
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White Infarct of the Spleen
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Red or hemorrhagic infarct
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Factors Involved in the Development of an Infarct
Occlusion of an artery or a vein may have little
or no effect on the involved tissue or it may
cause death of the tissue and, indeed, of the
individual.
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Factors Involved in the Development of an Infarct
The major determinants include
the nature of the vascular supply the rate of
development of the occlusion the vulnerability
of the tissue to hypoxia
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Nature of the Vascular Supply
The availability of an alternative or newly
acquired source of blood supply is the most
important factor in determining whether occlusion
of a vessel will cause damage
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Nature of the Vascular Supply
Lungs (pulmonary and bronchial arteries), Liver(
hepatic artery and portal vein), hand or
forearm(radial and ulnar arteries) VS the
kidney and spleen( renal and splenic
end-arteries),
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Rate of Development of the Occlusion
Slowly developing occlusions are less likely to
cause infarction, since they provide an
opportunity for alternative pathways of flow and
anastomotic bypass channels to develop.
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Vulnerability of the Tissue to Hypoxia
Neurons and Myocardial cells are quite sensitive
to anoxia. while fibroblasts within the
myocardium are quite resistant The epithelial
cells of the proximal renal tubules are much more
vulnerable to hypoxia than are the other segments
of the nephron.
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Shock
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Shock
Shock, commonly called circulatory collapse, may
develop following any serious assault on the
bodys homeostasis, such as profuse hemorrhage,
severe trauma, extensive burns, large myocardial
infarction, massive pulmonary embolism, or
bacterial sepsis
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Shock
Shock constitutes widespread hypoperfusion of
tissues due to reduction in the blood volume or
cardiac output, or redistribution of blood,
resulting in an inadequate effective circulating
volume.
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Shock
In addition to the perfusion deficit, there is
insufficient delivery of oxygen and nutrients to
the cells and tissues and inadequate clearance of
metabolites.
The cellular hypoxia induces a shift from aerobic
to anaerobic metabolism, resulting in increased
lactate production and sometimes lactic acidosis
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Shock
While at the outset the hemodynamic and metabolic
derangements are correctable and induce
reversible injury to cells, persistence or
worsening of the shock state leads to
irreversible injury and death of cells and
sometimes the patient
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Shock
Shock is commonly divided into three major types
Cardiogenic shock, caused by failure of the
myocardial pump due to intrinsic myocardial
damage (myocardial infarction), arrhythmias,
extrinsic pressure (cardiac tamponade), or
outflow obstruction (pulmonary embolism)
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Shock
Shock is commonly divided into three major types
Hypovolemic or hemorrhagic shock, due to
inadequate blood or plasma volume caused by
hemorrhage, fluid loss from severe burns, or
trauma (traumatic shock)
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Shock
Shock is commonly divided into three major types
Septic shock, caused by severe bacteremic
infections, most commonly by gram-negative
bacteria (endotoxic shock) but also by
gram-positive organisms and, occasionally, fungi
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Pathogenesis of Septic Shock
Septic shock is currently the most common cause
of death in intensive care units, accounting for
some 100,000 deaths annually in the United
States. It results from the spread of microbes
from severe localized infections (e.g., abscess,
peritonitis, pneumonia) into the bloodstream
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Pathogenesis of Septic Shock
The majority of cases are caused by
endotoxin-producing gram-negative bacilli.
Endotoxins are bacterial wall lipopolysaccharides
(LPS)
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Pathogenesis of Septic Shock
LPS is thought to induce its effects in two ways
directly, by causing injury or altering the
function of cells, but more importantly
indirectly, by initiating the synthesis, release,
or activation of a cascade of mediators derived
from plasma or from cells (monocytes,
macrophages, neutrophils, endothelial cells, and
others
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The mediators that have been implicated in
causing shock include
Cytokines (IL-1, TNF, IL-6, IL-8) Platelet
activating factor Nitric oxide Complement (C5a
and C3a) Prostaglandins Leukotrienes The kinin
system Oxygen metabolites Catecholamines Endorphin
s Myocardial depressant factor
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These mediators, in turn, affect a number of
organ systems, notably the following
the heart, causing myocardial dysfunction the
vascular system, resulting in vasodilation and
hypotension the microcirculation, leading to
endothelial injury and activation as well as
leukocyte aggregation and adhesion the
coagulation system, culminating in disseminated
intravascular coagulation the lungs, leading to
the acute respiratory distress syndrome
(ARDS) the liver, resulting in liver failure the
kidney, causing acute renal failure the central
nervous system, culminating in coma
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