6. embolism; hemodynamic disordrs

Hemodynamic Disorders

Edema Hyperemia and Congestion HemorrhageHemostasis and ThrombosisEmbolismInfarction Shock

Dr. Krishna Tadepalli, MD, www.mletips.com

Embolism Can be solid ( thrombus), Liquid (Amniotic fluid) or Gas

(Air, Nitrogen) carried by blood flow from the site of origin

Most commonly detached thrombus = also called thrombo – embolism

Rarely Fat, Air/ Nitrogen, Cholesterol emboli, Tumor emboli, Foreign bodies

Consequence vascular obstruction Infarction Types systemic (arterial), Pulmonary

Embolism Can be solid ( thrombus), Liquid (Amniotic fluid) or Gas

(Air, Nitrogen) carried by blood flow from the site of origin

Most commonly detached thrombus = also called thrombo – embolism

Rarely Fat, Air/ Nitrogen, Cholesterol emboli, Tumor emboli, Foreign bodies

Consequence vascular obstruction Infarction Types systemic (arterial), Pulmonary


Emboli - Types

Systemic Arterial

( exception Paradoxical )

Arise in heart Cause

infarctions lower extremities – 75%, Brain (15%), Kidney, spleen)

Systemic Arterial

( exception Paradoxical )

Arise in heart Cause

infarctions lower extremities – 75%, Brain (15%), Kidney, spleen)

Pulmonary• Venous

• DVT• Emboli cause

Pulmonary embolism ( silent in 50% of pts.). If 60% of pulmonary circulation is blocked sudden death due to acute cor -pulmonale (Rt. Heart Failure)

Pulmonary• Venous

• DVT• Emboli cause

Pulmonary embolism ( silent in 50% of pts.). If 60% of pulmonary circulation is blocked sudden death due to acute cor -pulmonale (Rt. Heart Failure)


Embolism

Pulmonary embolism


Pulmonary embolism Pulmonary embolism


Fat embolism Causes Most common (90%) with fractures of

long bones, less commonly following soft tissue trauma, Burns

When ? 3-5 days after the injury Clinical Heart =Tachycardia

Lungs Tachypnea, Blood Petechiae, Anemia

Mechanism Mechanical ( obstruction) Biochemical Neutral fats cause platelet & RBC

aggregation and destruction Free fatty acids endothelial injury

Diagnosis Frozen sections stained with fat stains ( oil red –O, Sudan IV) Hematological findings (anemia, Petechiae on

nondependent parts) are very useful

Fat embolism Causes Most common (90%) with fractures of

long bones, less commonly following soft tissue trauma, Burns

When ? 3-5 days after the injury Clinical Heart =Tachycardia

Lungs Tachypnea, Blood Petechiae, Anemia

Mechanism Mechanical ( obstruction) Biochemical Neutral fats cause platelet & RBC

aggregation and destruction Free fatty acids endothelial injury

Diagnosis Frozen sections stained with fat stains ( oil red –O, Sudan IV) Hematological findings (anemia, Petechiae on

nondependent parts) are very useful


ALVEOLI

Fat Embolus

Special stain


Air embolism Causes obstetric (pregnancy), chest wall

injuries, sports( scuba diving), occupational (caisson’s)

Clinical acute in scuba divers, obstetric, injuries Chronic caisson’s Bends joint pains, chokes pulmonary

Mechanism physical ( circulatory gap), Nitrogen in scuba divers, caisson’s disease

Lethal dose 100 cc

Complications ischemic necrosis of heads of long bones

Treatment slow decompression in compression chambers

Air embolism Causes obstetric (pregnancy), chest wall

injuries, sports( scuba diving), occupational (caisson’s)

Clinical acute in scuba divers, obstetric, injuries Chronic caisson’s Bends joint pains, chokes pulmonary

Mechanism physical ( circulatory gap), Nitrogen in scuba divers, caisson’s disease

Lethal dose 100 cc

Complications ischemic necrosis of heads of long bones

Treatment slow decompression in compression chambers


Amniotic Fluid embolism Causes leak of Amniotic fluid into maternal

circulation Mechanism thrombogenic DIC,

Mechanical obstruction Clinical uncommon but most important

cause of maternal mortality ( 30% deaths) Pulmonary Dyspnea, Tachypnea, later

pulmonary edema and ARDS CVS Hypotensive shock CNS Seizures, coma

diagnosis pulmonary emboli with Lanugo hair, fetal squames & Vernix caseosa

Complications death due to ARDS, DIC

Amniotic Fluid embolism Causes leak of Amniotic fluid into maternal

circulation Mechanism thrombogenic DIC,

Mechanical obstruction Clinical uncommon but most important

cause of maternal mortality ( 30% deaths) Pulmonary Dyspnea, Tachypnea, later

pulmonary edema and ARDS CVS Hypotensive shock CNS Seizures, coma

diagnosis pulmonary emboli with Lanugo hair, fetal squames & Vernix caseosa

Complications death due to ARDS, DIC


Amniotic Fluid embolism


Infarction Definition = ischemic necrosis of tissue due to occlusion

of arterial ( in most of cases) or venous ( in gonads) circulation

Most common cause of Death in USA Most commonly in 99% of cases = arterial occlusion

by thrombo-embolism Rarely venous drainage problem ( in Testis, Ovary) Very rarely vasospasm

Morphological Types Red & White Wedge shaped with base at the periphery of organ

Final outcome Coagulative necrosis ( Liquefactive in Brain)

Septic infarction = in pts. With infective Endocarditis

Infarction Definition = ischemic necrosis of tissue due to occlusion

of arterial ( in most of cases) or venous ( in gonads) circulation

Most common cause of Death in USA Most commonly in 99% of cases = arterial occlusion

by thrombo-embolism Rarely venous drainage problem ( in Testis, Ovary) Very rarely vasospasm

Morphological Types Red & White Wedge shaped with base at the periphery of organ

Final outcome Coagulative necrosis ( Liquefactive in Brain)

Septic infarction = in pts. With infective Endocarditis


Infarctions- Types

Red (Hemorrhagic)

Venous occlusion In loose tissues

(lung) Organs with dual

blood supply (Lungs, Liver)

Previously congested organs ( nutmeg liver)

Re- perfused tissues

Red (Hemorrhagic)

Venous occlusion In loose tissues

(lung) Organs with dual

blood supply (Lungs, Liver)

Previously congested organs ( nutmeg liver)

Re- perfused tissues

White (Anemic)• Arterial occlusion• Solid organs• End arterial supply

( Kidney, Spleen, Retina, Heart)

White (Anemic)• Arterial occlusion• Solid organs• End arterial supply

( Kidney, Spleen, Retina, Heart)


Hemodynamic Disorders

OBJECTIVESEdema Hyperemia and Congestion HemorrhageHemostasis and ThrombosisEmbolismInfarction Shock


Infarction

Red & White


Final outcome of Infarction in heart Final outcome of Infarction in heart

How old is it ( after the onset of MI)?


Hemodynamic Disorders, Thromboembolic Disease, and

ShockOBJECTIVES Edema Hyperemia and Congestion Hemorrhage Hemostasis and Thrombosis Embolism Infarction Shock

Hemodynamic Disorders, Thromboembolic Disease, and

ShockOBJECTIVES Edema Hyperemia and Congestion Hemorrhage Hemostasis and Thrombosis Embolism Infarction Shock


Shock = Cardiovascular collapse• Final common pathway of many disorders

( Hemorrhage, Trauma, Burns, MI, PE, Sepsis)

• Main Event Systemic Hypo perfusion ( due to ↓cardiac output or effective circulatory volume)

• Types– Cardiogenic = MI, Ventricular rupture, PE, etc.,

– Hypovolemic = Hemorrhage, Fluid loss

– Septic = most important

– Others = Neurogenic, Anaphylactic ( Type 1 HSR)

Shock = Cardiovascular collapse• Final common pathway of many disorders

( Hemorrhage, Trauma, Burns, MI, PE, Sepsis)

• Main Event Systemic Hypo perfusion ( due to ↓cardiac output or effective circulatory volume)

• Types– Cardiogenic = MI, Ventricular rupture, PE, etc.,

– Hypovolemic = Hemorrhage, Fluid loss

– Septic = most important

– Others = Neurogenic, Anaphylactic ( Type 1 HSR)


Septic Shock = by Gram +ve bacteria• MCC of mortality in ICU (in USA)• Incidence is ↑ ( due to high risk pts., ↑ # of invasive

procedures & immuno-compromised pts.)

• Endotoxic shock MC sub type of septic shock ( 70% of cases),

• Cause LPS

• Super antigens bacterial proteins cause polyclonal activation of T – Lymphocytes– Example – TSS toxin-1 by Staph. Aureus

– Cause multi organ failure

Septic Shock = by Gram +ve bacteria• MCC of mortality in ICU (in USA)• Incidence is ↑ ( due to high risk pts., ↑ # of invasive

procedures & immuno-compromised pts.)

• Endotoxic shock MC sub type of septic shock ( 70% of cases),

• Cause LPS

• Super antigens bacterial proteins cause polyclonal activation of T – Lymphocytes– Example – TSS toxin-1 by Staph. Aureus

– Cause multi organ failure


Septic shock Endotoxic shock• Causes= LPS (Endotoxin = Lipid core and

PolySaccharide coat)• Effects

– Low LPS levels Activate Macrophages Local inflammation healing

– Moderate LPS levels ↑cytokines systemic effects

– Higher LPS levels Septic shock syndrome• Mechanism LPS binds with Circulating Protein

later the complex binds with CD 14 All of them finally bind with TLR-4 – The interaction on endothelium ↓anticoagulant

properties– The interaction on Macrophages ↑ cytokines

(TNF, IL-1)

Septic shock Endotoxic shock• Causes= LPS (Endotoxin = Lipid core and

PolySaccharide coat)• Effects

– Low LPS levels Activate Macrophages Local inflammation healing

– Moderate LPS levels ↑cytokines systemic effects

– Higher LPS levels Septic shock syndrome• Mechanism LPS binds with Circulating Protein

later the complex binds with CD 14 All of them finally bind with TLR-4 – The interaction on endothelium ↓anticoagulant

properties– The interaction on Macrophages ↑ cytokines

(TNF, IL-1)


Shock


Septic shock syndrome= Multi organ failure

– 1. Hypotension

– 2. DIC

– 3. ARDS

– 4. Loss of Myocardial Contractility

• Stages • 1. Non – Progressive = compensatory reflex

mechanisms ( Baroreceptors, ADH, Catecholamines)

• 2. Progressive = ↓tissue perfusion, Electrolyte imbalance ( Acidosis, oliguria, Anaerobic glycolysis)

• 3. Irreversible = Tissue injury & Death ( Lysosomal leakage, ↓ Myocardial contractility, Anuria )


– 1. Hypotension

– 2. DIC

– 3. ARDS

– 4. Loss of Myocardial Contractility

• Stages • 1. Non – Progressive = compensatory reflex

mechanisms ( Baroreceptors, ADH, Catecholamines)

• 2. Progressive = ↓tissue perfusion, Electrolyte imbalance ( Acidosis, oliguria, Anaerobic glycolysis)

• 3. Irreversible = Tissue injury & Death ( Lysosomal leakage, ↓ Myocardial contractility, Anuria )



• Organ damageBrain Ischemic encephalopathy

Heart Necrosis, Contraction bands

Kidney ATN

Lungs Shock lungs

GIT Hemorrhagic Enteropathy

Liver Fatty change, Hemorrhagic Necrosis

• Clinical features useful in diagnosis– Septicemic shock skin is warm in early stages

( Vasodilatation

– Hypovolemic or Cardiogenic shock cool, calmy, cyanotic skin ( due to Hypotension)


• Organ damageBrain Ischemic encephalopathy

Heart Necrosis, Contraction bands

Kidney ATN

Lungs Shock lungs

GIT Hemorrhagic Enteropathy

Liver Fatty change, Hemorrhagic Necrosis

• Clinical features useful in diagnosis– Septicemic shock skin is warm in early stages

( Vasodilatation

– Hypovolemic or Cardiogenic shock cool, calmy, cyanotic skin ( due to Hypotension)


Health & Medicine

6. embolism; hemodynamic disordrs