Hemorrhage, Hemostasis

and Circulatory Shock

Hemorrhage
Extravasation of blood due to ruptured
vessels
From hemo = blood, rrhagia = to burst forth

Hemorrhage may be external or internal

Hemorrhage may be obvious (gross) or
hidden (occult)
This is whole blood with RBCs, not just
edemic transudates or exudates

How much blood loss?

Class I: up to 15% of blood volume
typically no change in vital signs
routine blood donation amounts to ~10%

Class I: 15-30% of total blood volume

tachycardia (rapid heart beat) with a narrowing of the difference
between the systolic and diastolic blood pressures
compensatory peripheral vasoconstriction; cool, pale skin;
altered mental status, dizzy or confused
fluid resuscitation with saline or Lactated Ringer's solution

Class III: 30-40% of circulating blood volume

blood pressure drops, heart rate increases, peripheral perfusion
worsens, mental status worsens
fluid resuscitation and/or blood transfusion

Class IV: >40% of circulating blood volume

hypovolemic shock--limit of the body's compensation is reached
aggressive resuscitation is required to prevent death

Indications of internal hemorrhage

Deep
Anemiafewer circulating RBCs
Increased indirect bilirubin (unconjugated,
albumin-bound)

Surface
Hemorrhage under the skin or mucous
membranes looks red (oxygenated Hb) or
purple (deoxygenated Hb)

Enclosed bleeding by size and shape

Petechiae are flat, tiny, 1- to 2-mm, multifocal
locally increased intravascular pressure, coagulation (platelet)
defects, the trauma of sudden hypoxia (strangulation)
from Italian, petecchie = flea bites (puh-teek-ee-uh)
petechia (s.); petechiae (pl.); petechial (adj)

Purpura are flat, small, 1 mm, multifocal

Term used to describe platelet-related bleeding disorders that
result in bruised skin and/or mucous membranes
from Latin, purple

Ecchymoses, contusions (bruises) are smooth and

noticeably large, >1 cm, focal
trauma, vascular inflammation
chymose = juicy

Hematoma are emergent, lumpy, hardened, focal

Clotted blood collected near the skin surface or internally at
serosal surfaces or aneurysms

Colors of bruising
Initial hemorrhage of RBCs into tissue is
cleared by macrophages, which process Hb

Oxyhemoglobin and Deoxyhemoglobin

Deoxyhemoglobin and Biliverdin
Biliverdin and Bilirubin
Bilirubin and Hemosiderin
Hemosiderin

When iron and porphyrins are completely

cleared, tissue resumes normal color

Distribution of hemorrhage(s)
Multifocal indicates problem affecting vessels or platelets
thrombocytopenia or thrombocytopathy
reduced number or function of platelets preventing coagulation

inherited coagulation defectshemorrhagic diathesis

anticoagulants inhibit production of vitamin K-dependent coagulation
proteins
end stage hepatic disease.
With approximately 80% loss of functional hepatic tissue, production of
coagulation factors can become inadequate.

disseminated intravascular coagulation (DIC)

coagulation out of control

vasculitis
immune mediated--precipitation of Ag-Ab complexes, which are chemotactic
for neutrophils, resulting in vascular damage
infections of endothelium

Focal distribution
single or a few focal hemorrhages are typical of trauma
regional neoplasm, thrombosis, or microbial invasion
problems with protein clotting factors

Petechiae from strangulation

Petechiae

Petechiae

Petechiae or purpurae

Senile or actinic purpura

Echymoses or contusions

Hematoma--subdural

Hematoma

Subcapsular hematoma

Hemopericardium
This is hemopericardium as demonstrated
by the dark blood in the pericardial sac
opened at autopsy. Penetrating trauma or
massive blunt force trauma to the chest
(often from the steering wheel) causes a
rupture of the myocardium and/or coronary
arteries with bleeding into the pericardial
cavity. The extensive collection of blood in
this closed space leads to cardiac
tamponade. A pericardiocentesis, with
needle inserted into the pericardial cavity,
can be a diagnostic procedure.

Gastrointestinal hemorrhage
When rate is slow, blood is digested or lost
in feces
In upper GI, blood turns black and tarry as it is
digested and is called melena
Melena is symptomatic of peptic ulcers, ruptured
esophageal varices, cancers

In lower GI, blood remains red and is excreted

with feces
Fecal occult blood test; now fecal immunochemical
test
FOBT used dye adsorbed on paper to detect Fenton
reaction catalyzed by heme iron
FIT uses Ab against globin portion of hemoglobin

Hemorrhage into cavities

Pleural hemorrhagehemothorax
Build-up of pressure prevents lung expansion
Prevents gas exchange
May lead to lung collapse

Instigates coughing or hiccups, which exacerbates

bleeding

Pericardial hemorrhagehemopericardium
Build-up of external pressure inhibits filling
Cardiac tamponade = compression

Intracranial hemorrhage
Always bad because of the rigid cranium
CSF pressure increases rapidly if bleeding rate is
greater than rate of fluid resorption

Hemodynamics
Maintenance of blood volume
Maintenance of blood pressure
Mainenance of clot-free flow
plasmin

Development of clot in response to

vascular damagehemostasis
thrombin-fibrin

Mechanism of hemostasis
Reflex sympathetic noradrenergic
vasoconstrictor system activated locally
Damaged vascular endothelium releases
endothelin
10 times more potent than angiotensin II

Platelets contact collagenprimary hemostasis

Adhere: GpIb receptor tethered to collagen via vWF
Secrete: ADP, TxA2, Ca++, growth and clotting
factors
Aggregate: Ca++ bridges with surface phosphoserine

Coagulation cascadesecondary hemostasis

Stimulated by tissue factor (factor III)
Platelets, fibrin, net of captured RBCs and WBCs

Primary hemostatic clot formation

Platelets are activated by contact with
Extra Cellular Matrix
Circulating von Willebrand Factor tethers
platelet glycoprotein receptors to ECM
collagen
Thrombin is released to cleave fibrinogen
creating fibrin nets that capture more
platelets as well as RBCs and WBCs
Platelets contract with microtubular
contractile proteins, consolidating plug

Hemostatic clot resolution

tPA, tissue plasminogen activator, cleaves
plasminogen to plasmin
Plasmin digests fibrin clot
Tightly regulated yin-yang of hemostasis

Platelet structure
Anuclear cell fragments synthesized in marrow
Surface glycoprotein Ib and IIa/IIIb receptors
Internal alpha granules containing
Factors V and VIII and IV
Fibrinogen, fibronectin, thromboxaneA2
PDGF, TGF-b

Internal dense granules containing

ATP, ADP and Ca++
Histamine, serotonin, epinephrine

Internal canaliculiopen canals

Contractile cytoskeletal fibers

Platelet structure

Platelet actions
Adhesion to extracellular matrix
GpIb links to collagen via vWF
GpIIb/IIIa links platelets via fibrinogen

Secretion from granules into canaliculi and

exterior
Transition of phosphlipids to outer lamina
Aggregation
Primary hemostatic plug

Contraction
Secondary hemostatic plug

Platelet aggregation

Clotting v. thrombosis
THROMBUS: Blood that has solidified
within the vascular lumens or cardiac
chambers
CLOT: Blood that has solidified anywhere
else
THROMBOEMBOLISM: Portion of
thrombus that travels through the
vasculature to form a plug elsewhere
EMBOLISM: vascular plug, not always
from a thrombus

Consequences of acute hemorrhage

Loss of blood beyond a certain volume will cause
systemic hypotension
rapid compensation by the baroreceptor response leads to
peripheral vasoconstriction
fluids shift from the interstitial into the IV compartment
slower response from the renin-angiotensin-aldosterone system
results in vasoconstriction and retention of sodium and water by
the kidney
antidiuretic hormone (ADH) also kicks in, acts on nephron to
promote water resorption

Loss of blood beyond the body's ability to compensate

will cause systemic hypotension, reduced cardiac filling,
reduced tissue perfusion, loss of erythrocytes and their
Hb, hypoxemia, and a further cascade of events called
shock

Hypovolemic, cardiogenic shock

Causes

Blood loss
Dehydration
Reduced cardiac output
Deranged peripheral vasomotor control

Consequenses
Inadequate perfusion
Hypoxia, lactic acidosis

Recovery dependent on duration and

severity

Stages of Shock
Early Stage
Compensatory mechanisms maintain perfusion of
vital organs
Include increased heart rate and increased peripheral
resistance

Progressive Stage
Compensatory systems no longer adequate with
tissue hypoperfusion
Onset of circulatory and metabolic imbalance,
especially metabolic acidosis from lactic acidemia

Irreversible Stage
Organ damage and metabolic disturbances
Survival not possible

Clinical consequences

Hypotension
Weak, rapid pulse (tachycardia)
Shallow rapid breathing (tachypnea)
Cool, damp, cyanotic skin
Tissue injuries are due to hypoxia