The document discusses various types of embolism, infarction, and shock, including definitions, causes, symptoms, and management. It details thromboembolic causes such as those from deep venous thrombosis, fat emboli associated with fractures, gas emboli from decompression sickness, and amniotic fluid emboli during labor. Additionally, the document describes shock types, their clinical presentations, stages, and management strategies, highlighting specific conditions like hypovolemic, cardiogenic, obstructive, and distributive shock.

1. Hemostasis&
Hemodynamic disorders
EMBOLISM, INFARCTION AND SHOCK

2. Embolism
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 A. Definition; Intravascular mass that travels
and occludes downstream vessels; symptoms
depend on the vessel involved.
 B. Thromboembolus is due to a thrombus that
dislodges; most common type of embolus
(>95%).
 C. Atherosclerotic embolus is due to an
atherosclerotic plaque that dislodges.
 1. Characterized by the presence of
cholesterol clefts in the embolus.
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3. Fat embolus
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 D. Fat embolus is associated with bone fractures,
particularly long bones, and soft tissue trauma.
 1. Develops while fracture is still present or
shortly after repair
 2. Characterized by dyspnea (fat, often with
bone marrow elements, is seen in pulmonary
vessels, and petechiae on the skin overlying the
chest
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4. Gas embolus
4
 E. Gas embolus is classically seen in
decompression sickness.
 1. Nitrogen gas precipitates out of blood due
to rapid ascent by a diver.
 2. Presents with joint and muscle pain
('bends') and respiratory symptoms
('chokes’).
 3. Chronic form (Caisson disease) is
characterized by multifocal ischemic
necrosis of bone.
 4. Gas embolus may also occur during
laparoscopic surgery (air is pumped into the
abdomen).
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5.  F. Amniotic fluid embolus enters maternal circulation during labor
or delivery
 1. Presents with shortness of breath, neurologic symptoms, and DIC
(due to the tissue thromboplastin of amniotic fluid).
 2. Characterized by squamous cells and keratin debris, from fetal
skin, in embolus

6. PULMONARY EMBOLISM
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 A. Usually due to thromboembolus; the most
common source is deep venous thrombus
(DVT) of the lower extremity, usually
involving the femoral, iliac, or popliteal veins.
 B. Most often clinically silent because (1) the
lung has a dual blood supply (via pulmonary
and bronchial arteries) and (2) the embolus is
usually small (self-resolves)
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7.  C. Pulmonary infarction occurs if a large- or medium-sized
artery is obstructed in patients with pre-existing
cardiopulmonary compromise; only 10% of PEs cause
infarction.
 1. Presents with shortness of breath, hemoptysis, pleuritic chest
pain, and pleural effusion
 2. V/Q lung scan shows mismatch; perfusion is abnormal.
 3. Spiral CT shows avascular filling defect in the lung.

8.  4. Lower extremity Doppler ultrasound is useful to detect DVT.
 5. D-dimer is elevated.
 6. Gross examination reveals hemorrhagic, wedge-shaped infarct.
 D. Sudden death occurs with a large saddle embolus that blocks both
left and right pulmonary arteries or with significant occlusion of a
large pulmonary artery
 Sudden death is due to electromechanical dissociation (the heart has
electrical activity but no mechanical contraction).
 Pulmonary hypertension may arise with chronic emboli that are
reorganized over time.

9. SYSTEMIC EMBOLISM
 A. Usually due to
thromboembolus.
 B. Most commonly arise in the
left heart.
 C. Travel down systemic
circulation to occlude flow to
organs, most commonly the
lower extremities.
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10. INFARCTION
 A. An infarct is an area of ischemic necrosis caused by
occlusion of the vascular supply to the affected tissue;
 1. classical examples are pulmonary infarction, myocardial
infarction, cerebral infarction, bowel infarction, and ischemic
necrosis of distal extremities (gangrene) that causes
substantial morbidity in the diabetic population.

11. Most common causes
 B. Most common causes are;
 1. Arterial thrombosis or arterial embolism underlies the vast majority of
infarctions.
 Local vasospasms,
 bleeding into an atheroma plaque and
 extrinsic vessel compression such as by a tumor,
 a dissecting aortic aneurysm or
 edema within confined space (anterior compartment syndrome).

12.  2.Other rare causes of tissue
infarction include vessel
twisting (e.g., in testicular
torsion or bowel volvulus).
 Hint; a volvulus is when a loop
of intestine twists around itself
and the mesentery that supports
it, resulting in
a bowel obstruction.
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13. 13
 traumatic vascular rupture, and entrapment
in a hernia sac.
 A hernia is the abnormal exit of tissue or an
organ, such as the bowel, through the wall
of the cavity in which it normally resides
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14. venous thrombosis
 3. Although venous thrombosis can cause infarction,
 I. The more common outcome is simply congestion;
typically, bypass channels rapidly open to provide sufficient
outflow to restore the arterial inflow.
 II. Infarcts caused by venous thrombosis thus usually occur
only in organs with a single efferent vein (e.g., testis or
ovary).

15. Capillary obstruction
 Capillary obstruction can cause infarction.
 Vasculitis of the capillaries may narrow the lumen causing
ischemia and infarction of the affected area.
 DIC
 Frost bites
 Fat embolism

16. Factors That Influence Infarct Development
 A. The effects of vascular occlusion range from inconsequential to
tissue necrosis leading to organ dysfunction and sometimes death.
 B. The range of outcomes is influenced by
 (1) the anatomy of the vascular supply
 (2) the time over which the occlusion develops
 (3) Tissue vulnerability to ischemia
 (4) the blood oxygen content.

17.  Anatomy of the vascular supply; the presence or
absence of an alternative blood supplies is the most
important factor in determining whether the occlusion
of a vessel causes damage.
 II. Organs that have end-arterial circulation are more
vulnerable to tissue necrosis as the thrombus occludes
the arteries.
 Rate of occlusion; slowly developing occlusions are
less likely to cause infarction because they allow time
for the development of collateral blood supplies.

18.  The organs that have dual circulations are more persistent to the
infarctions (e.g., lungs, liver, hand and forearm.)
 Tissue vulnerability to ischemia;
 Neurons are highly susceptible to ischemic injury; whereas, skeletal
muscle is relatively more persistent.
 Myocardial cells, although hardier than neurons, still die after only 20 to
30 minutes of ischemia.
 Hypoxemia. Understandably, abnormally low blood O2 content
(regardless of cause) increases both the likelihood and extent of
infarction.

19. MORPHOLOGY
 Infarcts are classified on the basis of their color (reflecting the amount
of hemorrhage) and the presence or absence of microbial infection.
 Thus, infarcts may be either red (hemorrhagic) or white (anemic) and
may be either septic or bland.
 Red Infarcts occur (1) with venous occlusions (such as in ovarian
torsion); (2) in loose tissues (e.g., lung) where blood can collect in
infarcted zones; (3) in tissues with dual circulations such as lung and
small intestine, where partial, inadequate perfusion by collateral
arterial supplies is typical;

20.  (4) in previously congested tissues (as a
consequence of sluggish venous outflow); and
(5) when flow is reestablished after infarction
has occurred (e.g., after angioplasty of an
arterial obstruction).
 White infarcts occur with arterial occlusions in
solid organs with end-arterial circulations (e.g.,
heart, spleen, and kidney), and as the occlusion
occurs blood seeps into the affected area.
 Secondary infection leads to an abscess
formation (Abscess - Proteolytic enzymes from
neutrophils liquefy tissue).

21. 21
 Infarcts tend to be wedge-
shaped
 Occluded vessel at the apex
 Periphery of the organ
forming the base.
 If the base is a serosal
surface, there is often
overlying fibrinous
exudate.
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22.  Acute infarcts are poorly defined and
slightly hemorrhagic
 With the time the margins are better
defined by a narrow rim of congestion
due to inflammation.
 In most tissues, the main histologic
finding associated with infarcts is
ischemic coagulative necrosis.
 In the brain;
 Infarcted are undergoes rapid
liquefactive necrosis.

23. Septic Infarcts
 Septic infarcts occur when infected cardiac valve
vegetations embolize, or when microbes seed
necrotic tissue.
 In these cases the infarct is converted into an
abscess, with a correspondingly greater
inflammatory response and healing by organization
and fibrosis.

24. Shock
 shock occurs when the body’s organs does not
get adequate oxygen and blood supply leading
to hypoxia.
 Life threatening condition
 Reversible if treated early
 Can quickly become irreversible and cause
multi-organ failure and death.

25. Clinical presentations
 Hypotension; low Bp (<90/60 mm Hg)
 Tachycardia; rapid HR( > 100 beats/min)
 Tachypnea; rapid breathing rate ( >25 breaths/min)
 Oliguria; low urine output ( < 400 ml/24 hrs)
 Changes in mental state; agitation, confusion, unresponsiveness,
etc.
 Skin changes; cool, clammy, pale with reduced peripheral
perfusion.

26.  Mean arterial pressure (MAP) is a good indicator of tissue
perfusion rather than systolic blood pressure.
 MAP is the average arterial pressure throughout one cardiac
cycle.
 MAP is influenced by cardiac output and systemic vascular
resistance
 Hence MAP; cardiac output X systemic vascular resistance

27.  Actual MAP; 2x diastolic + systolic/3.
 Normal MAP; 65 mm Hg----100 mm Hg.
 Stages of shock:
 1. pre-shock or initial nonprogressive stage
 A. early compensated shock.
 B. symptoms are absent or mild.

28.  2. Shock or progressive stage
 A. compensatory mechanisms are overwhelmed.
 Symptoms of organ dysfunction begin to appear
 worsening circulatory and metabolic derangement, including
acidosis.
 3. End-organ dysfunction
 A. An irreversible stage in which cellular and tissue injury is so
severe
 B. ultimately can lead to death.

29. Management
 Depends on the severity and cause of shock.
 Goal of treatment is to decrease the mortality and treat the
underlying causes.
 Fluid replacement and blood transfusions if it is needed.
 Medications to increase blood pressure, such as, metaraminol.
 Emergency surgery
 Iv antibiotics for septic shock
 IV steroids and allergy medications for anaphylactic shock

30. Types of shock
I. Hypovolemic shock
II. Cardiogenic shock
III. Obstructive shock
IV. Distributive shock

31. Hypovolemic shock
 Results from low cardiac output due to loss of blood or plasma
volume.
 It can be hemorrhagic or non-hemorrhagic.
 Hemorrhagic is decrease of blood volume due to blood loss of
blood.
 Examples are trauma, interstitial bleeding, intra-operative and post-
operative bleeding.
 non-hemorrhagic is decrease of blood volume due to loss of fluids.
 Burns, sodium and water loss from GIT, skin and kidney are
classical examples.

33. Cardiogenic shock
 Results from low cardiac output as a result of myocardial pump failure.
 Causes of cardiogenic shock are
 1. cardiomyopathies; problems with heart muscle,
 A. myocardial infarction and ischemia.
 B. myocarditis
 2. Arrythmia; problems with heart rate or rhythm,
 A. atrial and ventricular tachyarrhythmia.
 B. atrial or ventricular bradyarrhythmia.

34. mechanical causes are;
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1. valve insufficient or
defects like mitral valve
stenosis.
 Aortic dissection of
aneurysm
 Ventricular septal
defect
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35. Aortic dissection
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 Aortic dissection is an acute process in
which a tear in the internal face of the aorta
leads to dissection through the laminas and
formation of a new lumen (false lumen) and
acute hypotension.
 Most common cause is uncontrolled
hypertension.
 the most common complication of aortic
dissection is death due to severe internal
bleeding.
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36. Obstructive Shock
 Results from obstruction to cardiac outflow or filling
 This can result from pulmonary embolism, severe pulmonary
hypertension, and
 Cardiac tamponade which is when the fluid sac around your heart
fills with too much blood or other fluid and puts pressure on your
heart.
 Tension pneumothorax; a severe condition that results when air is
trapped in the pleural space under positive pressure, displacing
mediastinal structures and compromising cardiopulmonary function.

38. Distributive Shock
 Distributive shock, also known as vasodilatory shock.
 Systemic vasodilation leads to decreased blood flow to the brain,
heart, and kidneys causing damage to vital organs.
 They are three main types of distributive shock;
 1. septic shock.
 2. anaphylactic shock.
 Neurogenic shock.

39. Septic Shock
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 Septic shock is triggered by microbial
infections and is associated with severe
systemic inflammatory response syndrome
(SIRS).
 The common pathogenic mechanism is a
massive production of inflammatory
mediators from innate and adaptive immune
cells that produce arterial vasodilation,
vascular leakage, and venous blood pooling.
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40.  These cardiovascular abnormalities result in tissue
hypoperfusion, cellular hypoxia, and metabolic
derangements that lead to organ dysfunction.
 if severe and persistent, organ failure and death
 Septic shock is most frequently triggered by gram -
positive bacterial infections, followed by gram-negative
bacteria and fungi.
 More common in ICU and immunosuppressed patients.

41. Pathogenesis of septic shock

42. Anaphylactic shock
 Results from severe allergic reactions.
 Allergen enters the blood stream and results in an
exaggerated inflammatory response.
 This includes massive release of histamine that
triggers systemic vasodilation, bronchiolar
constriction and tongue swelling.

44. Neurogenic shock
 Results from severe brain or spinal cord injury that
compromise the sympathetic nervous system.
 Occurs with spinal cord injury above the level of T6.
 Results in unopposed parasympathetic response and lead to
decrease in vascular resistance and vasodilation.
 Presentations
 Hypotension
 Bradyarrhythmia
 Temperature dysregulation