1. Hemodynamic Disorders
Edema
Hyperemia and Congestion
Hemorrhage
Hemostasis and Thrombosis
Embolism
Infarction
Shock
Dr. Krishna Tadepalli, MD, www.mletips.com

2. Embolism
Embolism
 Can be solid ((thrombus), Liquid (Amniotic fluid) or Gas
 Can be solid thrombus), Liquid (Amniotic fluid) or Gas
(Air, Nitrogen) carried by blood flow from the site of
(Air, Nitrogen) carried by blood flow from the site of
origin
origin
 Most commonly  detached thrombus = also called
 Most commonly  detached thrombus = also called
thrombo – embolism
thrombo – embolism
 Rarely  Fat, Air/ Nitrogen, Cholesterol emboli, Tumor
 Rarely  Fat, Air/ Nitrogen, Cholesterol emboli, Tumor
emboli, Foreign bodies
emboli, Foreign bodies
 Consequence  vascular obstruction  Infarction
 Consequence  vascular obstruction  Infarction
 Types  systemic (arterial), Pulmonary
 Types  systemic (arterial), Pulmonary
Dr. Krishna Tadepalli, MD, www.mletips.com

3. Emboli - Types
Systemic
Pulmonary
Systemic
Pulmonary
 Arterial ((exception
 Arterial exception
 Paradoxical ))
 Paradoxical
 Arise in heart
 Arise in heart
 Cause infarctions
 Cause infarctions
lower extremities –
lower extremities –
75%, Brain (15%),
75%, Brain (15%),
Kidney, spleen)
Kidney, spleen)
• Venous
• Venous
• DVT
• DVT
• Emboli cause
• Emboli cause
Pulmonary embolism
Pulmonary embolism
((silent in 50% of pts.).
silent in 50% of pts.).
If 60% of pulmonary
If 60% of pulmonary
circulation is blocked
circulation is blocked
 sudden death due to
 sudden death due to
acute cor -pulmonale
acute cor -pulmonale
(Rt. Heart Failure)
(Rt. Heart Failure)
Dr. Krishna Tadepalli, MD, www.mletips.com

4. Embolism
Pulmonary embolism
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5.  Pulmonary embolism
 Pulmonary embolism
Dr. Krishna Tadepalli, MD, www.mletips.com

6. Fat embolism
Fat embolism
 Causes Most common (90%) with fractures of long
 Causes Most common (90%) with fractures of long
bones, less commonly following soft tissue trauma, Burns
bones, less commonly following soft tissue trauma, Burns
 When ?? 3-5 days after the injury
 When  3-5 days after the injury
 Clinical  Heart =Tachycardia
 Clinical  Heart =Tachycardia
 Lungs Tachypnea,
 Lungs Tachypnea,
 Blood  Petechiae, Anemia
 Blood  Petechiae, Anemia
 Mechanism  Mechanical ((obstruction)
 Mechanism  Mechanical obstruction)
 Biochemical Neutral fats cause platelet & RBC aggregation
 Biochemical Neutral fats cause platelet & RBC aggregation
and destruction
and destruction
 Free fatty acids endothelial injury
 Free fatty acids endothelial injury
 Diagnosis  Frozen sections stained with fat stains ((oil
 Diagnosis  Frozen sections stained with fat stains oil
red –O, Sudan IV)
red –O, Sudan IV)
 Hematological findings (anemia, Petechiae on
 Hematological findings (anemia, Petechiae on
nondependent parts) are very useful
nondependent parts) are very useful
Dr. Krishna Tadepalli, MD, www.mletips.com

7. Fat Embolus
Special stain
ALVEOLI
Dr. Krishna Tadepalli, MD, www.mletips.com

8. Air embolism
Air embolism
 Causes obstetric (pregnancy), chest wall injuries,
 Causes obstetric (pregnancy), chest wall injuries,
sports( scuba diving), occupational (caisson’s)
sports( scuba diving), occupational (caisson’s)
 Clinical  acute  in scuba divers, obstetric, injuries
 Clinical  acute  in scuba divers, obstetric, injuries
 Chronic  caisson’s
 Chronic  caisson’s
 Bends  joint pains, chokes  pulmonary
 Bends  joint pains, chokes  pulmonary
 Mechanism  physical ((circulatory gap), Nitrogen in
 Mechanism  physical circulatory gap), Nitrogen in
scuba divers, caisson’s disease
scuba divers, caisson’s disease
 Lethal dose  100 cc
 Lethal dose  100 cc
 Complications  ischemic necrosis of heads of long
 Complications  ischemic necrosis of heads of long
bones
bones
 Treatment  slow decompression in compression
 Treatment  slow decompression in compression
chambers
chambers
Dr. Krishna Tadepalli, MD, www.mletips.com

9. Amniotic Fluid embolism
Amniotic Fluid embolism
 Causes leak of Amniotic fluid into maternal circulation
 Causes leak of Amniotic fluid into maternal circulation
 Mechanism  thrombogenic  DIC, Mechanical
 Mechanism  thrombogenic  DIC, Mechanical
obstruction
obstruction
 Clinical  uncommon but most important cause of
 Clinical  uncommon but most important cause of
maternal mortality ((30% deaths)
maternal mortality 30% deaths)
 Pulmonary  Dyspnea, Tachypnea, later pulmonary
 Pulmonary  Dyspnea, Tachypnea, later pulmonary
edema and ARDS
edema and ARDS
 CVS Hypotensive shock
 CVS Hypotensive shock
 CNS Seizures, coma
 CNS Seizures, coma
 diagnosis  pulmonary emboli with Lanugo hair, fetal
 diagnosis  pulmonary emboli with Lanugo hair, fetal
squames & Vernix caseosa
squames & Vernix caseosa
 Complications  death due to ARDS, DIC
 Complications  death due to ARDS, DIC
Dr. Krishna Tadepalli, MD, www.mletips.com

10. Amniotic Fluid embolism
Dr. Krishna Tadepalli, MD, www.mletips.com

11. Infarction
Infarction
 Definition = ischemic necrosis of tissue due to occlusion
 Definition = ischemic necrosis of tissue due to occlusion
of arterial ((in most of cases) or venous ((in gonads)
of arterial in most of cases) or venous in gonads)
circulation
circulation
 Most common cause of Death in USA
 Most common cause of Death in USA
 Most commonly  in 99% of cases = arterial occlusion
 Most commonly  in 99% of cases = arterial occlusion
by thrombo-embolism
by thrombo-embolism
 Rarely  venous drainage problem ((in Testis, Ovary)
 Rarely  venous drainage problem in Testis, Ovary)
 Very rarely  vasospasm
 Very rarely  vasospasm
 Morphological Types  Red & White
 Morphological Types  Red & White
 Wedge shaped with base at the periphery of organ
 Wedge shaped with base at the periphery of organ
 Final outcome Coagulative necrosis ((Liquefactive in
 Final outcome Coagulative necrosis Liquefactive in
Brain)
Brain)
 Septic infarction = in pts. With infective Endocarditis
 Septic infarction = in pts. With infective Endocarditis
Dr. Krishna Tadepalli, MD, www.mletips.com

12. Infarctions- Types
Red (Hemorrhagic)
White (Anemic)
Red (Hemorrhagic)
White (Anemic)
 Venous occlusion
 Venous occlusion
 In loose tissues
 In loose tissues
(lung)
(lung)
 Organs with dual
 Organs with dual
blood supply (Lungs,
blood supply (Lungs,
Liver)
Liver)
 Previously congested
 Previously congested
organs
organs
((nutmeg liver)
nutmeg liver)
 Re- perfused tissues
 Re- perfused tissues
• Arterial occlusion
• Arterial occlusion
• Solid organs
• Solid organs
• End arterial supply
• End arterial supply
((Kidney, Spleen,
Kidney, Spleen,
Retina, Heart)
Retina, Heart)
Dr. Krishna Tadepalli, MD, www.mletips.com

13. Hemodynamic Disorders
OBJECTIVES
Edema
Hyperemia and Congestion
Hemorrhage
Hemostasis and Thrombosis
Embolism
Infarction
Shock
Dr. Krishna Tadepalli, MD, www.mletips.com

14. Infarction
Red
&
White
Dr. Krishna Tadepalli, MD, www.mletips.com

15.  Final outcome of Infarction in heart
 Final outcome of Infarction in heart
How old is it ( after the onset of MI)?
Dr. Krishna Tadepalli, MD, www.mletips.com

16. Hemodynamic Disorders, Thromboembolic
Hemodynamic Disorders, Thromboembolic
Disease, and Shock
Disease, and Shock
OBJECTIVES
OBJECTIVES
 Edema
 Edema
 Hyperemia and Congestion
 Hyperemia and Congestion
 Hemorrhage
 Hemorrhage
 Hemostasis and Thrombosis
 Hemostasis and Thrombosis
 Embolism
 Embolism
 Infarction
 Infarction
 Shock
 Shock
Dr. Krishna Tadepalli, MD, www.mletips.com

17. Shock = Cardiovascular collapse
Shock = Cardiovascular collapse
• Final common pathway of many disorders
• Final common pathway of many disorders
((Hemorrhage, Trauma, Burns, MI, PE, Sepsis)
Hemorrhage, Trauma, Burns, MI, PE, Sepsis)
• Main Event  Systemic Hypo perfusion ((due to
• Main Event  Systemic Hypo perfusion due to
↓cardiac output or effective circulatory volume)
↓cardiac output or effective circulatory volume)
•• Types
Types
– Cardiogenic = MI, Ventricular rupture, PE, etc.,
– Cardiogenic = MI, Ventricular rupture, PE, etc.,
– Hypovolemic = Hemorrhage, Fluid loss
– Hypovolemic = Hemorrhage, Fluid loss
– Septic = most important
– Septic = most important
– Others = Neurogenic, Anaphylactic ((Type 1 HSR)
– Others = Neurogenic, Anaphylactic Type 1 HSR)
Dr. Krishna Tadepalli, MD, www.mletips.com

18. Septic Shock = by Gram +ve bacteria
Septic Shock = by Gram +ve bacteria
• MCC of mortality in ICU (in USA)
• MCC of mortality in ICU (in USA)
• Incidence is ↑ ((due to high risk pts., ↑ # of invasive
• Incidence is ↑ due to high risk pts., ↑ # of invasive
procedures & immuno-compromised pts.)
procedures & immuno-compromised pts.)
•• Endotoxic shock  MC sub type of septic shock ((70%
Endotoxic shock  MC sub type of septic shock 70%
of cases),
of cases),
•• Cause  LPS
Cause  LPS
•• Super antigens  bacterial proteins cause polyclonal
Super antigens  bacterial proteins cause polyclonal
activation of T – Lymphocytes
activation of T – Lymphocytes
––
––
Example ––TSS toxin-1 by Staph. Aureus
Example TSS toxin-1 by Staph. Aureus
Cause multi organ failure
Cause multi organ failure
Dr. Krishna Tadepalli, MD, www.mletips.com

19. Septic shock Endotoxic shock
Septic shock Endotoxic shock
•• Causes= LPS (Endotoxin = Lipid core and
Causes= LPS (Endotoxin = Lipid core and
PolySaccharide coat)
PolySaccharide coat)
•• Effects 
Effects 
– Low LPS levels  Activate Macrophages  Local
– Low LPS levels  Activate Macrophages  Local
inflammation  healing
inflammation  healing
– Moderate LPS levels  ↑cytokines  systemic
– Moderate LPS levels  ↑cytokines  systemic
effects
effects
– Higher LPS levels  Septic shock syndrome
– Higher LPS levels  Septic shock syndrome
•• Mechanism  LPS binds with Circulating Protein 
Mechanism  LPS binds with Circulating Protein 
later the complex binds with CD 14 All of them
later the complex binds with CD 14 All of them
finally bind with TLR-4
finally bind with TLR-4
– The interaction on endothelium  ↓anticoagulant
– The interaction on endothelium  ↓anticoagulant
properties
properties
– The interaction on Macrophages  ↑ cytokines
– The interaction on Macrophages  ↑ cytokines
(TNF, IL-1)
(TNF, IL-1)
Dr. Krishna Tadepalli, MD, www.mletips.com

20. Shock
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21. Septic shock syndrome= Multi organ failure
Septic shock syndrome= Multi organ failure
– 1. Hypotension
– 1. Hypotension
– 2. DIC
– 2. DIC
– 3. ARDS
– 3. ARDS
– 4. Loss of Myocardial Contractility
– 4. Loss of Myocardial Contractility
•• Stages
Stages
•• 1. Non – Progressive = compensatory reflex
1. Non – Progressive = compensatory reflex
mechanisms ((Baroreceptors, ADH, Catecholamines)
mechanisms Baroreceptors, ADH, Catecholamines)
•• 2. Progressive = ↓tissue perfusion, Electrolyte
2. Progressive = ↓tissue perfusion, Electrolyte
imbalance ((Acidosis, oliguria, Anaerobic glycolysis)
imbalance Acidosis, oliguria, Anaerobic glycolysis)
•• 3. Irreversible = Tissue injury & Death ((Lysosomal
3. Irreversible = Tissue injury & Death Lysosomal
leakage, ↓ Myocardial contractility, Anuria ))
leakage, ↓ Myocardial contractility, Anuria
Dr. Krishna Tadepalli, MD, www.mletips.com

22. Septic shock syndrome= Multi organ failure
Septic shock syndrome= Multi organ failure
•• Organ damage
Organ damage
Brain  Ischemic encephalopathy
Brain  Ischemic encephalopathy
Heart  Necrosis, Contraction bands
Heart  Necrosis, Contraction bands
Kidney  ATN
Kidney  ATN
Lungs  Shock lungs
Lungs  Shock lungs
GIT  Hemorrhagic Enteropathy
GIT  Hemorrhagic Enteropathy
Liver  Fatty change, Hemorrhagic Necrosis
Liver  Fatty change, Hemorrhagic Necrosis
•• Clinical features useful in diagnosis
Clinical features useful in diagnosis
–– Septicemic shock  skin is warm in early stages
Septicemic shock  skin is warm in early stages
((Vasodilatation
Vasodilatation
–– Hypovolemic or Cardiogenic shock  cool, calmy, cyanotic
Hypovolemic or Cardiogenic shock  cool, calmy, cyanotic
skin ((due to Hypotension)
skin due to Hypotension)
Dr. Krishna Tadepalli, MD, www.mletips.com