Hemodynamic Disorders

By: Dr. SL Rasonable

 outline
a. Edema and Effusions
b. Exudate vs. Transudate
c. Hyperemia and Congestion
d. Hemostasis, Hemorrhagic Disorders and Thrombosis
e. Embolisms
f. Infarction
g. Shock
Edema & Effusion
Edema & Effusion

• Hydrostatic Pressure
• Push water out

• Colloid Osmotic Pressure

• Pull water in
Edema & Effusion
• Edema
 Accumulation of fluid in
Tissues
• Effusion
 Fluid in Body Cavities
Types
• Due to elevated Hydrostatic Pressure • Inflammatory
or decreased Colloid Osmotic • Exudates
Pressure • Non-Inflammatory
• Transudates
Edema & Effusion
Causes:
• Increased Hydrostatic Pressure
• Focal Impairment in Venous Return
• Local: Deep Venous Thrombosis
• Generalized: Congestive Heart Failure
• Reduced Colloid Osmotic Pressure
• Decreased Albumin
• Nephrotic Syndrome
• Liver Disease
• Protein malnutrition
Edema & Effusion
Causes:
• Salt and Water Retention
• Both increased
Hydrostatic Pressure
and decreased Colloid
Osmotic Pressure
• Renal disorders
• hypoperfusion
Edema & Effusion

Causes:
• Lymphatic Obstruction
• Lymphedema
• Chronic Inflammation with Fibrosis
• Filariasis
• Mastectomy (Breast Removal)
Edema & Effusion
• Subcutaneous Edema
 High hydrostatic pressure
 Distribution is by gravity:
dependent Edema
 Cardiac or Renal disease
• Periorbital
Edema
 Edema of the eyelids
 Severe Renal Disease
• Pulmonary Edema
 Lungs 2 to 3x the normal
weight
 Frothy, blood tinged fluid
 Left Ventricular Failure
 ARDS
 Bacterial Infection
• BrainEdema
 Localized or generalized
 Narrowed sulci, distended gyri
 Herniation leads to death
Hyperemia &
Congestion
Hyperemia & Congestion
• Both from increased Blood Volumes
• Hyperemia
 Active process
 Arteriolar dilatation leads to increased blood flow
 Erythema: Increased Oxygenated Blood at the tissues

• Congestion
 Passive process
 Reduced blood flow from the tissues
 Cardiac Failure – Systemic
 Venous Obstruction – Localized
Hyperemia & Congestion
LUNGS
 Acute Pulmonary Congestion
 Engorged aveolar capillaries
 Alveolar septal edema
 Focal intraalveolar hemorrhage
 Chronic Pulmonary Congestion
 Thickened, fibrotic septa
 Hemosiderin – laden macrophages
(heart failure cells)
Hyperemia & Congestion
LIVER
• Acute Hepatic Congestion
 Distended central vein and
sinusoids
• Chronic Passive Congestion
 Gross: Nutmeg Liver
 Microscopic: centrilobular
hemorrhage, hemosiderin-laden
macrophages and hepatocyte
necrosis
Hemostasis,
Hemorrhagic Disorders
and Thrombosis
Hemostasis, Hemorrhagic Disorders and Thrombosis

• Hemostasis
 process by which blood clots form at sites of vascular
injury
• Hemorrhagic Disorders
 excessive bleeding
• Thrombotic Disorders
 blood clots (often referred to as thrombi) form within intact
blood vessels or within the chambers of the heart
 Hemostasis, Hemorrhagic Disorders and Thrombosis

ARTERIOLAR
VASOCONSTRICTION
• Markedly reduces blood
flow
• Reflex neurogenic
mechanisms
• Augmented by Endothelin
• Transient effect
 Hemostasis, Hemorrhagic Disorders and Thrombosis

PRIMARY HEMOSTASIS
• Primary Hemostatic Plug/
Platelet Plug Formation
• von Willebrand Factor
(vWF) & collagen
• Platelet Adherence
• Platelet Activation
• Granule Release
• Recruitment
• Platelet Aggregation
 Hemostasis, Hemorrhagic Disorders and Thrombosis

PLATELETS

• Alpha Granules:
• P-selectin, Fibrinogen,
Factor V, vWF, PF-4,
PDGF, TGF-B
• Dense Granules:
• ADP, ATP, iCa,
serotonin, epinephrine
Hemostasis, Hemorrhagic Disorders and Thrombosis

SECONDARY
HEMOSTASIS

Fibrin deposition
 Hemostasis, Hemorrhagic Disorders and Thrombosis

SECONDARY HEMOSTASIS
 Hemostasis, Hemorrhagic Disorders and Thrombosis

FIBRINOLYSIS
• Plasmin
• Breaks down fibrin and
interferes with
polymerization
Hemostasis, Hemorrhagic Disorders and Thrombosis
 Hemostasis, Hemorrhagic Disorders and Thrombosis
• Platelet inhibitory effects
• Anticoagulant effects
• Thrombomodulin bind thrombin
• endothelial protein C receptor bind protein C
• vitamin K–dependent protease that requires a cofactor, protein S.
• Activated protein C/protein S complex is a potent inhibitor of
coagulation factors Va and VIIIa
• Heparin-like molecules
• Activate antithrombin
• Inhibit thrombin and IXa, Xa, XIa, XIIa
• Tissue Factor Pathway Inhibitor
• Inhibit VIIa
• Fibrinolytic Effects
THROMBOSIS
 Hemostasis, Hemorrhagic Disorders and Thrombosis

ENDOTHELIAL INJURY
• Endothelial activation or
dysfunction
• Procoagulant changes
• Antifibrinolytic effects
Hemostasis, Hemorrhagic Disorders and Thrombosis
ANORMAL BLOOD
FLOW
• Turbulence – arterial
and cardiac thrombosis
• Stasis – venous thrombi
• Promote endothelial
activation, enhancing
procoagulant activity and
leukocyte adhesion
• Disrupt laminar flow and
bring platelets into contact with
the endothelium
• Prevent washout and dilution
of activated clotting factors by
fresh flowing blood and the
inflow of clotting factor
inhibitors
Hemostasis, Hemorrhagic Disorders and Thrombosis
ANORMAL BLOOD FLOW
• Aneurysms – Aortic and arterial dilatations result
in local stasis
• Acute Myocardial Infarction – Cardiac mural
thrombi
• Rheumatic Mitral Valve Stenosis – Atrial dilation
and fibrillation
• Hyperviscosity – (Polycythemia vera), small
vessel stasis
• Sickle Cell Anemia – deformed RBCs impede
blood flow to small vesselsc
Hemostasis, Hemorrhagic Disorders and Thrombosis

HYPERCOAGULABILITY
Inherited
• Factor V Leiden mutation
Acquired
• Hyperestrogenic state
• Cancer
• Smoking
• Heparin Induced Thrombophilia
• Anti-Phospholipid Antibody Syndrome (APAS)
Hemostasis, Hemorrhagic Disorders and Thrombosis
• Morphology:

• Lines of Zahn
 gross and microscopic laminations
 Pale platelet and fibrin deposits alternating with darker red cell-rich
layers
• Mural Thrombi
 Heart chambers and Aortic lumen
 Arrythmias, DCM, MI, myocarditis
• Arterial Thrombi
 Occlussive
 Coronary, cerebral and femoral arteries
 Friable network of platelets, fibrin, red cells and WBCs
Hemostasis, Hemorrhagic Disorders and Thrombosis
• Morphology:

• Venous Thrombi
 Phlebothrombosis
 Invariably occlusive forming a long luminal cast
 Enmeshed red cells – red, or stasis thrombi
 Firm, focally attached to the vessel wall and has lines of Zahn
 Lower extremity vein
• Post Mortem Clots
 Gelatinous, dark red dependent portion
 Yellow (chicken fat) upper and red lower
 Not attached to the vessel wall
Hemostasis, Hemorrhagic Disorders and Thrombosis

• Morphology:
• Vegetations
 Thrombi in the heart valves
 Fungi or bacteria
 Infective endocarditis
 Non bacterial thrombotic endocarditis
 Sterile vegetations in persons with Hypercoagulable states
 Libman-Sacks endocarditis
 Sterile Verrucous
 Systemic Lupus Erythematosus
Hemostasis, Hemorrhagic Disorders and Thrombosis
FATE OF THE THROMBUS
• Propagation
 Accumulate additional platelets and fibrin
• Embolization
 Thrombi dislodge and travel to other sites
• Dissolution
 Result of Fibrinolysis
• Organization and Recanalization
 Fibrous Lump after vessel wall changes
Hemostasis, Hemorrhagic Disorders and Thrombosis

• Thrombi come to clinical attention when they obstruct arteries or

veins, or give rise to emboli
• Venous Thrombosis (Phlebothrombosis)
 Deep Venous Thrombosis (DVT)
 Edema and pain
 Embolize to the lungs
 Hypercoagulability
 Recent Surgery
 Post Partum Pregnancy
• Arterialand Cardiac Thrombosis
 Atherosclerosis
 Loss of endothelial integrity with Abnormal Blood Flow
Hemostasis, Hemorrhagic Disorders and Thrombosis

• DISSEMINATED INTRAVASCULAR COAGULATION

(CONSUMPTION COAGULOPATHY)
 Not a specific disease
 Systemic activation of thrombin that lead to complicated
conditions
 Organ Dysfunction
 Microvascular thrombi: diffuse circulatory insufficiency
 Activate fibrinolytic mechanisms
 Shock
Embolism
Embolism

• An embolus is a detached intravascular solid, liquid, or

gaseous mass that is carried by the blood from its point
of origin to a distant site, where it often causes tissue
dysfunction or infarction
• Thromboembolism
 Dislodged thrombi
Pulmonary Embolism
• From leg DVTs in 95% of cases
• Thrombifrom larger veins to the Right side of the heart then to the
Pulmonary arteries
• Saddle Embolus – pulmonary artery bifurcation
• Consequences:
 Clinically Silent in 60 to 80%; organization
 Sudden Death, Right Heart Failure (cor pulmonale) or CV collapse in
60% obstruction
 Pulmonary Hemorrhage
 Small end-arteriolar obstruction: Infarction and Hemorrhage
 Multiple Emboli cause Pulmonary Hypertension and Right HF
Systemic Thromboembolism
• 80% from intracardiac mural thrombi
 2/3 from LV wall infarct
 ¼ from LA dilation and fibrillation
• Others:aortic aneurysms, atherosclerotic plaques, valvular
vegetations or venous thrombi
• 10-15% unknown
• Endpoint:
 75% lower extremities
 10% brain
 TISSUE INFARCTION
Fat and Marrow Embolism

• Fat
globules from bone marrow at
pulmonary vessels after LONG Fat Embolism Syndrome
BONE FRACTURE Pulmonary insufficiency
Neurologic Symptoms
• Trauma or Burns Anemia-thrombocytopenia
• 90% Dyspnea
in severe skeletal injuries
Tachycardia
• <10% have any clinical findings Coma after 1 to 3 days onset
of symptoms
Air Embolism
• Gas bubbles form frothy masses
 Obstruct vessel flow
 Distal Ischemic Injury
Bends: gas bubbles in muscles
• Surgical Complication or Chest Wall and joints
Injury Chokes: edema, hemorrhages,
• Air >100cc atelectasis or emphysema in
lungs
• Decompression Sickness
 Sudden decreases in atmospheric
Caisson Disease
Chronic Form of
pressure
 Scuba and deep sea divers Decompression Sickness
Amniotic Fluid Embolism
Symptoms
• Fifth most common cause of maternal • Sudden Severe
mortality Dyspnea
• Ominous complication of labor and • Cyanosis
immediate postpartum period • Shock
• Tear in the placental membrane or uterine • Neurologic
vein rupture impairment
• Findings: fetal skin, lanugo hair, fat from • Pulmonary Edema
vernix caseosa, muci • DIC
 Infarction
An infarct is an area of ischemic necrosis caused by occlusion of either
the arterial supply or the venous drainage
 Red Infarct
• Venous occlusions (testicular
torsion)
• Loose, spongy tissues
• Tissueswith dual circulations (lung,
small intestine)
• Tissuespreviously congested by
sluggish venous outflow
• Reestablished flow to a site of
arterial occlusion
White Infarct

• Arterialocclusions in solid
organs with end-arterial
circulation and tissue density
that limit blood seepage
 Heart, Spleen and Kidney
 Infarction
• Wedge-shaped
 Apex-occluded vessel
 Base-Organ periphery
 Serosal surface can have
fibrinous exudate
• Fresh infarcts are poorly
defined but delineates
better over a few days
• Ischemic Coagulative Necrosis
– dominant histologic
characteristic
• Septic Infarctions
• Infected cardiac valve
vegetations embolize or
microbes seed necrotic tissue
• Converted into an abscess
Infarction
Factors
• Vascular Supply Anatomy
• Rateof Occlusion
 Slow rate – less likely to cause infarction
• TissueVulnerability to Hypoxia
 Neurons – 3 to 4 min
 Myocardial cells – 20 to 30 min
 Fibroblasts – hours
• Hypoxemia
Shock
Shock
•astate in which diminished cardiac output or
reduced effective circulating blood volume
impairs tissue perfusion and leads to cellular
hypoxia
Shock
Cardiogenic Shock
• Low cardiac output due to Myocardial pump
failure
• Intrinsic damage (MI)
• Extrinsic compression (Cardiac Tamponade)
• Ventricular arrythmias
• Outflow Obstruction (PE)
Hypovolemic Shock

• Low cardiac output due to low blood volume

• Massive hemorrhage
• Fluid loss from severe burns
Other Types
• Sepsis
- Systemic Inflammatory Response
Syndrome with a foci of Infection
• Septic Shock – with organ damage
 Massive outpouring of Inflammatory mediators
• Neurogenic Shock – Spinal cord Injury
• AnaphylacticShock – IgE-mediated
hypersensitivity reaction
Septic Shock
• Inflammatory and Counter-inflammatory responses
• Endothelial activation and injury
• Induction of a procoagulant state
• Metabolic abnormalities
 Hypergylcemia, Insulin resistance
 Stressed-induced hormones
• Organ Dysfunction
 Stages of Shock
••An initial nonprogressive phase during which reflex
compensatory mechanisms are activated and perfusion of vital
organs is maintained
•• A progressive stage characterized by tissue hypoperfusion
and onset of worsening circulatory and metabolic imbalances,
including lactic acidosis
••An irreversible stage that sets in after the body has incurred
cellular and tissue injury so severe that even if the
hemodynamic defects are corrected, survival is not possible
Shock
Shock
Reference: Kumar, Abbas, Ester. Robbins and Cotran
Pathologic Basis of Disease, 9th Ed. (2014)
THANK
YOU!