Hemodynamic Disorders

Hemodynamic
Disorders
Thromboembolic
Disease
Shock
Overview
Edema (increased fluid in the ECF)
Hyperemia (INCREASED flow)
Congestion (INCREASED backup)
Hemorrhage (extravasation)
Hemostasis (keeping blood as a fluid)
Thrombosis (clotting blood)
Embolism (downstream travel of a clot)
Infarction (death of tissues w/o blood)
Shock (circulatory failure/collapse)
WATER
60% of body
2/3 of body water is INTRA-cellular
The rest is INTERSTITIAL
Only 5% is INTRA-vascular

EDEMA is SHIFT to the INTERSTITIAL SPACE
HYDRO-
-THORAX, -PERICARDIUM, -PERITONUM,(ASCITES)
( EFFUSIONS),
ANASARCA(total body edema)


Fluid Homeostasis
Starlings Law
Homeostasis is
maintained by the
opposing effects of:
Vascular Hydrostatic
Pressure
and
Plasma Colloid
Osmotic Pressure
EDEMA
Increased hydrostatic pressure:
Impaired venous return
Congestive heart failure (poor right ventricular function)
Constrictive pericarditis
Ascites (peritoneal dropsy; e.g. from liver cirrhosis)
Venous obstruction or compression (thrombosis, external pressure,
dependency of lower limbs)

Arteriolar dilation (heat; neurohumoral dysregulation)

Reduced plasma osmotic pressure (hypoproteinemia)
Nephrotic syndrome (protein-losing glomerulopathies)
Liver cirrhosis (ascites)
Malnutrition
Protein-losing gastroenteropathy
Increased fluid in the interstitial tissue spaces or body
cavities.
Lymphatic obstruction
Interstitial fluids are removed via lymphatic drainage, to thoracic duct
and left subclavian vein
Inflammation, neoplasm, surgery, irradiation

Sodium retention (water follows sodium)
Excess salt intake with renal insufficiency
Increased tubular reabsorption of sodium (renal hypoperfusion--
increased renin-angiotensin-aldosterone secretion)
Inflammation (acute, chronic, angiogenesis)


CHF EDEMA
INCREASED VENOUS PRESSURE DUE TO
FAILURE

DECREASED RENAL PERFUSION,
triggering of RENIN-ANGIOTENSION-
ALDOSTERONE complex, resulting
ultimately in SODIUM RETENTION
HEPATIC ASCITES
PORTAL HYPERTENSION
HYPOALBUMINEMIA
RENAL EDEMA
SODIUM RETENTION


PROTEIN LOSING GLOMERULOPATHIES
(NEPHROTIC SYNDROME)
Transudate vs Exudate
Transudate
results from disturbance of Starling forces
specific gravity < 1.012
protein content < 3 g/dl,
Exudate
results from damage to the capillary wall
specific gravity > 1.012
protein content > 3 g/dl,

GENERALIZED EDEMA
HEART
LIVER
KIDNEY
Dependent Edema is a prominent feature of Congestive
Heart Failure; in legs if standing or sacrum in sleeping
patient

Periorbital edema is often the initial manifestation of
Nephrotic Syndrome, while late cases will lead to
generalized edema.
Pulmonary Edema
is most frequently seen in Congestive Heart
Failure
May also be present in renal failure, adult
respiratory distress syndrome (ARDS), pulmonary
infections and hypersensitivity reactions
Pulmonary Edema
The Lungs are typically
2-3 times normal
weight
Cross sectioning causes
an outpouring of
frothy,
sometimes blood-
tinged fluid
It may interfere
with pulmonary
function
Pulmonary edema
Brain Edema
Trauma, Abscess, Neoplasm, Infection (Encephalitis due
to say West Nile Virus), etc
The surface of the brain with cerebral edema demonstrates
widened gyri with a flattened surface. The sulci are
narrowed
Brain Edema
Clinical Correlation
The big problem is:
There is no place for the
fluid to go!
Herniation into the
foramen magnum will
kill
SHOCK
Definition: CARDIOVASCULAR COLLAPSE
Common pathophysiologic features:
INADEQUATE CARDIAC OUTPUT and/or
INADEQUATE BLOOD VOLUME
Pathogenesis
Cardiac
Septic
Hypovolemic



GENERAL RESULTS
INADEQUATE TISSUE PERFUSION
CELLULAR HYPOXIA
UN-corrected, a FATAL outcome
TYPES of SHOCK
CARDIOGENIC: (Acute, Chronic Heart Failure)
HYPOVOLEMIC: (Hemorrhage or Leakage)
SEPTIC: (ENDOTOXIC shock, #1 killer in ICU)

NEUROGENIC: (loss of vascular tone)
ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased
vascular permeability)

CARDIOGENIC shock
MI
VENTRICULAR RUPTURE
ARRHYTHMIA
CARDIAC TAMPONADE
PULMONARY EMBOLISM (acute RIGHT heart
failure or cor pulmonale)
HYPOVOLEMIC shock
HEMORRHAGE, Vasc. compartmentH2O
VOMITING, Vasc. compartmentH2O
DIARRHEA, Vasc. compartmentH2O
BURNS, Vasc. compartmentH2O
SEPTIC shock
OVERWHELMING INFECTION
ENDOTOXINS, i.e., LPS (Usually Gm-)
Degraded bacterial cell wall products
Also called LPS, because they are Lipo-Poly-Saccharides
Attach to a cell surface antigen known as CD-14

Gm+
FUNGAL
SUPERANTIGENS, (Superantigens are polyclonal T-lymphocyte activators
that induce systemic inflammatory cytokine cascades similar to those occurring
downstream in septic shock, toxic shock antigents by staph are the prime
example.)
Effects of Lipopolysaccharide
LPS = lipopolysaccharide
TNF = tumor necrosis factor
IL = interleukin
NO = nitric oxide
PAF = platelet-activating factor
SEPTIC shock events
(linear sequence)
SYSTEMIC VASODILATION (hypotension)
MYOCARDIAL CONTRACTILITY
DIFFUSE ENDOTHELIAL ACTIVATION
LEUKOCYTE ADHESION
ALVEOLAR DAMAGE (ARDS)
DIC
VITAL ORGAN FAILURE CNS




NON-PROGRESSIVE
COMPENSATORY MECHANISMS
CATECHOLAMINES
VITAL ORGANS PERFUSED
PROGRESSIVE
HYPOPERFUSION
EARLY VITAL ORGAN FAILURE
OLIGURIA
ACIDOSIS
IRREVERSIBLE
HEMODYNAMIC CORRECTIONS of no use

CLINICAL STAGES of shock
Morphologic Features of Shock
Brain: ischemic encephalopathy
lung :DAD (Diffuse Alveolar Damage,)
Heart: subendocardial hemorrhages and
necrosis
Kidneys: acute tubular necrosis or diffuse
cortical necrosis
Gastrointestinal tract: patchy hemorrhages and
necrosis
Liver: fatty change or central hemorrhagic
necrosis
DIC
MULTIPLE ORGAN FAILURE

CLINICAL PROGRESSION
of SYMPTOMS(linear sequence)
Hypotension
Tachycardia
Tachypnea
Warm skin Cool skin Cyanosis
Renal insufficiency
Obtundance
Death

Embolism
Embolism refers to the transport of an
intravascular solid, liquid or gaseous mass in the
blood to a site distal to its point of origin.
Thromboembolism refers to the transport of a
thrombus; The thrombus becomes a
thromboembolus.
At least 90% of all emboli are thromboemboli.
Emboli eventually cause some kind of
downstream vascular obstruction and this is their
clinical significance.
Embolism is a cause of sudden death.

Types of Embolism

Thromboembolism (most common)
Fat embolism
Amniotic fluid embolism
Gas embolism
Cholesterol embolism
Septic embolism
Foreign body embolism
Bone marrow embolism

SOURCES AND EFFECTS OF
VENOUS EMBOLI
SOURCES OF ARTERIAL
EMBOLI
PULMONARY THROMBOEMBOLISM
The commonest type of thromboembolism
A common complication in hospitalized patients, especially in post
operative and chronic bedridden settings.
The most common source is the deep leg veins.
Large thromboemboli can obstruct the bifurcation of the main pulmonary
artery (saddle embolus) causing sudden death.
Small PTE obstruct distal (small) arteries and are often clinically silent.
Medium-sized PTE may also cause death or cardiovascular collapse.
Progressive obstruction of the distal pulmonary bed by small TE may lead to
pulmonary arterial hypertension.
Most non-fatal TE do not cause pulmonary infarcts because of the dual lung
circulation; Infarcts are more likely to occur when there is a co-morbidity
such as heart failure or COPD.
THROMBOEMBOLUS BLOCKING PULMONARY ARTERY
R Ventricle Embolus from Leg Vein
SYSTEMIC (ARTERIAL) THROMBOEMBOLISM
Refers to TE traveling in the systemic arterial circulation.
About 80% arise from intracardiac mural thrombi.
About 2/3s are associated with left ventricular infarcts.
The remainder arise from ulcerated atherosclerotic plaques with or
without attached mural thrombi, including from mural thrombi lining
aortic aneurysms.
A relatively small number arise from thrombotic lesions on cardiac valves
(vegetations).
Arterial thromboemboli impact in downstream arterial beds, such as
cerebral, splenic, renal, intestinal or distal limb beds - causing infarcts in
most cases.
The most common sites are the lower extremity (75%) and the brain
(10%).

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
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


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.
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.


Fat Embolus to Lung
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
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.
Large quantities of air, about 100 cc, are required to produce problems.

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
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.
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 severe pain; a similar process may produce acute
respiratory distress, while involvement of the cerebral vessels may lead to
coma and sometimes death
The chronic form of decompression sickness is more properly referred to
Caisson Disease. Here, the presumed persistence of gaseous emboli leads
to multiple foci of ischemic necrosis throughout the skeletal system

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%.
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.
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

HEMORRHAGE
EXTRAVASATION beyond vessel
HEMORRHAGIC DIATHESIS
HEMATOMA (implies MASS effect)
DISSECTION
PETECHIAE (1-2mm) (PLATELETS)
PURPURA <1cm
ECCHYMOSES >1cm (BRUISE)
HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS
ACUTE, CHRONIC

EVOLUTION of HEMORRHAGE
ACUTE CHRONIC
PURPLE GREEN BROWN
HGB BILIRUBIN HEMOSIDERIN


Hemorrhage
Ruptured vessels, usually from trauma or infection or
atherosclerosis
Can lose 20% of blood volume (more if slow lose) with little effect
on health
Great blood loss >> hypovolemic shock (hemorrhagic shock)

Hemorrhagic diathesis: tendency to bleed with minor injury

Hematoma: localized pool of blood outside vessels (e.g. bruise)
If severe: death from blood loss (e.g. dissecting aortic aneurysm)

Hemorrhage (Haemorrhage)
Rupture of Blood Vessels
Term Description Main Cause(s)
Purpura
(2-10mm)
Focal hemorrhage
(submucosal, etc.)
Vessel fragility
Petechiae
(1-2 mm)
Focal hemorrhage
(submucosal, etc.)
Increased pressure, small
vessel disease platelet
no.&function defects.
Ecchymosis
Widespread surface
petechiae
Same as above
Purpura
Colonic Petechiae
Telangiectasia
(Blood in Vessels)
Thrombocytopenia
Idiopathic Thrombocytopenic Purpura