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Hemorrhage, Hemostasis and Circulatory Shock

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* C, Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids) results in fibrin polymerization, ... – PowerPoint PPT presentation

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Title: Hemorrhage, Hemostasis and Circulatory Shock


1
Hemorrhage, Hemostasis and Circulatory Shock
2
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

3
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 gt40 of circulating blood volume
  • hypovolemic shock--limit of the body's
    compensation is reached
  • aggressive resuscitation is required to prevent
    death

4
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)

5
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, gt1 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

6
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

7
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

8
Petechiae from strangulation
9
Petechiae
10
Petechiae
11
Petechiae or purpurae
12
Senile or actinic purpura
13
Echymoses or contusions
14
Hematoma--subdural
15
Hematoma
16
Subcapsular hematoma
17
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.
18
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

19
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

20
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

21
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

22
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

23
Hemostatic clot resolution
  • tPA, tissue plasminogen activator, cleaves
    plasminogen to plasmin
  • Plasmin digests fibrin clot
  • Tightly regulated yin-yang of hemostasis

24
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28
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

29
Platelet structure
30
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

31
Platelet aggregation
32
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

33
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-aldoste
    rone 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

34
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

35
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

36
Clinical consequences
  • Hypotension
  • Weak, rapid pulse (tachycardia)
  • Shallow rapid breathing (tachypnea)
  • Cool, damp, cyanotic skin
  • Tissue injuries are due to hypoxia
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