Hemodynamic Disorders

By: Dr. SL Rasonable

Edema & Effusion

Edema
Accumulation of fluid in Tissues
Effusion
Fluid in Body Cavities

Due to elevated Hydrostatic Pressure or decreased Colloid Osmotic Pressure

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
Brain Edema
Localized or generalized
Narrowed sulci, distended gyri
Herniation leads to death

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

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)

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
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

ARTERIOLAR VASOCONSTRICTION
• Markedly reduces blood flow
• Reflex neurogenic mechanisms
• Augmented by Endothelin
• Transient effect
PRIMARY HEMOSTASIS
• Primary Hemostatic Plug/ Platelet Plug Formation
• von Willebrand Factor (vWF) & collagen
• Platelet Adherence
• Platelet Activation
• Granule Release
• Alpha Granules:
• P-selectin, Fibrinogen, Factor V, vWF, PF-4, PDGF, TGF-B
• Dense Granules:
• ADP, ATP, iCa, serotonin, epinephrine

• Recruitment
• Platelet Aggregation

SECONDARY HEMOSTASIS

FIBRINOLYSIS
• Plasmin
• Breaks down fibrin and interferes with polymerization
 • 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
ENDOTHELIAL INJURY
• Endothelial activation or dysfunction
• Procoagulant changes
• Antifibrinolytic effects

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
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
HYPERCOAGULABILITY
Inherited
• Factor V Leiden mutation
Acquired
• Hyperestrogenic state
• Cancer
• Smoking
 • Heparin Induced Thrombophilia
• Anti-Phospholipid Antibody Syndrome (APAS)

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
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
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
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
Arterial and Cardiac Thrombosis
Atherosclerosis
Loss of endothelial integrity with Abnormal Blood Flow
Hemostasis, Hemorrhagic Disorders and Thrombosis

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
Types
Pulmonary Embolism
From leg DVTs in 95% of cases
Thrombi from 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 BONE FRACTURE
Trauma or Burns
90% in severe skeletal injuries
<10% have any clinical findings
Fat Embolism Syndrome
Pulmonary insufficiency
Neurologic Symptoms
Anemia-thrombocytopenia
Dyspnea
Tachycardia
Coma after 1 to 3 days onset of symptoms
Air Embolism
Gas bubbles form frothy masses
Obstruct vessel flow
Distal Ischemic Injury
Surgical Complication or Chest Wall Injury
Air >100cc
Decompression Sickness
Sudden decreases in atmospheric pressure
Scuba and deep sea divers
Bends: gas bubbles in muscles and joints
Chokes: edema, hemorrhages, atelectasis or emphysema in lungs
Caisson Disease
Chronic Form of Decompression Sickness

Amniotic Fluid Embolism

Fifth most common cause of maternal mortality
Ominous complication of labor and immediate postpartum period
Tear in the placental membrane or uterine vein rupture
Findings: fetal skin, lanugo hair, fat from vernix caseosa, mucin
Symptoms
Sudden Severe Dyspnea
Cyanosis
Shock
Neurologic impairment
Pulmonary Edema
DIC

INFARCTION
Red Infarct
• Venous occlusions (testicular torsion)
• Loose, spongy tissues
• Tissues with dual circulations (lung, small intestine)
• Tissues previously congested by sluggish venous outflow
• Reestablished flow to a site of arterial occlusion
White Infarct
• Arterial occlusions 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

Factors
Vascular Supply Anatomy
Rate of Occlusion
Slow rate – less likely to cause infarction
Tissue Vulnerability to Hypoxia
Neurons – 3 to 4 min
Myocardial cells – 20 to 30 min
Fibroblasts – hours
Hypoxemia
SHOCK
a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue
perfusion and leads to cellular hypoxia

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
Anaphylactic Shock – IgE-mediated hypersensitivity reaction

Septic Shock
• Inflammatory and Counter-inflammatory responses
• Endothelial activation and injury
• Induction of a procoagulant state
• Metabolic abnormalities
o Hypergylcemia, Insulin resistance
o 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

CLINICAL FEATURES

THANK YOU!

Reference: Kumar, Abbas, Ester. Robbins and Cotran Pathologic Basis of Disease, 9th Ed. (2014)