Hemodynamic Disorders

Ma. Minda Luz M. Manuguid, M.D.

Hemodynamic Disorders

 Edema
 Hyperemia & Congestion
 Hemorrhage
 Thrombosis & Embolism
 Infarction
 Circulatory failure / Shock
Capillary Hemodynamics
 Hydrostatic pressure is the pressure exerted by a fluid
on the walls of its confining space;
it is directly proportional to the volume of the fluid; it is
an outward force
 Osmotic pressure is the pressure exerted by a flow of
water across a semipermeable membrane; an ‘inward’
pressure attracting fluid; it is directly proportional to the
impermeable solute’s concentration
 Hydrostatic & Osmotic pressures are opposing forces
  The net fluid movement between 2 compartments depends on the
algebraic sum of the hydrostatic & osmotic pressures of both.

HPi=10mmHg
HPA=35mmHg HPv=15mmHg

A V

OPA=25mmHg OPv= 30 mmHg

OPi= 15mmHg

= (HPA – HPi) – (OPA – OPi) = (OPv – OPi) – (HPv – HPi)

= (35 – 10) – (25 – 15) = (30 – 15 ) – (15 – 10)
= 25 – 10 = 15 – 5
= 15 mm Hg outward = 10 mmHg inward
 Edema
Edema – accumulation of fluid in the
interstitium or within body cavities
Pathophysiology:
I. Increased hydrostatic pressure
II. Decreased Oncotic Pressure
III. Sodium Retention
IV. Lymphatic obstruction/dysfunction
Pathophysiologic Categories of Edema
 Increased Hydrostatic Pressure
A. Impaired venous return : congestive heart failure;
Constrictive pericarditis; Liver cirrhosis; Narrowed
/ obstructed veins
B. Arteriolar dilatation: Heat; Neurohumoral excess / deficit
 Reduced Oncotic Pressure
Nephrotic syndrome; Liver cirrhosis; Malnutrition; Protein-
losing enteropathies
 Sodium Retention: Excessive salt intake; Reduced renal
function; ↑ Tubular reabsorption, ↓Perfusion,
↑R – A – A secretion;
 Lymphatic Obstruction/Dysfunction:
Inflammatory; Neoplastic; Post-surgical; Post-irradiation ;
 Edema
 Hemodynamic  Inflammatory
 due to imbalance of  due to increased
Starling’s forces vascular permeability
 specific gravity less than  specific gravity more
1.012 than 1.020
 low content of  high content of
proteins/colloids proteins/colloids
 fluid is a  fluid is an EXUDATE
TRANSUDATE
 Edema
 Anasarca – whole body edema; ‘dropsy’
 Hydrothorax – increased pleural fluid
 Hydropericardium – increased pericardial fluid –
may lead to cardiac tamponade
 Ascites / Hydroperitoneum – increased intra-abdominal
fluid
 Lymphedema – edema due to lymphatic obstruction
 Others : Hydrosalphinx; Hydrops of viscera, etc.
Morphology of Edema

 Gross : increased
dimensions (swelling) &
weight; turgor; pitting; wet,
watery cut surface
 Microscopic: colorless to
pale pink, finely granular
material seen in between
cells; widened intercellular
spaces
Morphology of Edema
 Hyperemia
Hyperemia – increased volume of blood in the
affected tissue
 Active hyperemia – due to arterial / arteriolar dilatation &
opening of inactive capillaries--- ↑ blood flow ---↑ redness; may be
neurogenic e.g. blushing; or chemical / humoral e.g. rubor of
inflammation
 Passive hyperemia / Congestion – passive accumulation of
blood due to impaired venous drainage; usually accompanied by
edema; blue-red color (cyanosis);
- may be acute congestion or chronic (CPC)
 Gross Morphology of Hyperemia &
Congestion

 increased redness /
cyanosis of the affected
area;

 tissues are excessively

wet & bloody; oozing of
blood from the cut
surface
Histopathology of
Hyperemia & Congestion
 Active hyperemia –
swollen arteries &
arterioles are full of RBC

 Congestion / CPC –
dilated veins or venules full
of RBC; hemosiderin-laden
macrophages;
 Chronic Passive Congestion
 Pathophysiology:
 dilated venules/veins full of RBC --->
 extravasation into surrounding interstitium --->
 breakdown of hemoglobin into hemosiderin --->
 engulfment of hemosiderin by macrophages --->
“ hemosiderin-laden macrophages ”
 chronic hypoxia ---> necrosis ---> fibrosis
 capillary rupture ---> minute hemorrhages --->
“ hemosiderin-laden scars ”
Chronic Passive Congestion, Lungs

 CPC, Lungs
etiology: left ventricular failure
morphology:
gross: heavy, bloody lobes; cut
surfaces oozing blood;
micoscopic: septal fibrosis-
thickened septa; & hemosiderin-
laden macrophages
‘heart failure cells’
Chronic Passive Congestion, Liver
 CPC, Liver
etiology: right ventricular failure; IVC/hepatic vein obstruction
morphology : gross - “nutmeg” liver
microscopic - centrilobular hemorrhagic necrosis
“cardiac” cirrhosis
Chronic Passive Congestion, Spleen
 CPC, Spleen
etiology : right ventricular
failure
morphology :
gross: congestive
splenomegaly
microscopic: fibrosis &
hemosiderin-laden
macrophages-
“siderofibrotic nodules”
“Gandy-Gamma bodies”
 Hemorrhage

Hemorrhage – escape of blood into the interstitium through

a defect / injury
 Petechia – pinpoint skin hemorrhages
 Purpura – skin hemorrhage up to 1.0 cm. diameter
 Ecchymosis – blotchy confluent skin hemorrhages
 Hemothorax – blood within the pleural cavity
 Hemopericardium – blood w/in the pericardial cavity
 Hemoperitoneum – blood w/in the abdominal cavity
 Subcutaneous Hemorrhages

purpura
petechiae

ecchymosis ecchymosis
hemorrhages
 Hemorrhage

 Epistaxis – bleeding from the nose

 Hemoptysis – coughing out of blood
 Hematemesis – vomiting of blood
 Hematochezia – fresh blood in stools
 Melena – black tarry stoools
 Hemarthrosis – blood within joint spaces
 Hemorrhage

Clinical significance:
 Volume / amount of blood loss
 Rate of blood loss
 Site of hemorrhage
 Chronic blood loss can lead to Iron deficiency
 Hemostasis
hemostasis: the arrest of bleeding from an injured blood
vessel, involving vascular, platelet, & plasma factors
 Vasoconstriction
 Platelet aggregation & formation of a temporary plug
 Plasma coagulation factors activated: extrinsic &
intrinsic pathways
The Coagulation
Cascade
Fluidity of Blood
Factors that keep blood in a fluid state within blood
vessels:
 Smoothness of the endothelium
 Linear flow of blood – central column of blood cells,
peripheral plasma
 Clotting factors in inactive state, dissolved in plasma
 Naturally occuring anti-clotting factors e.g. heparin,
antithrombin,
 Thrombosis & Embolism
 Thrombosis – formation of an intravascular blood
clot in vivo due to one or more of the ff:
 Endothelial injury
 Alterations in blood flow: Turbulence or Stasis
 Hypercoagulability of blood

 Embolism – occurrence of an intravascular space-

occupying lesion – solid, liquid, or gas – in vivo, an
embolus is most commonly a broken-off thrombus
 Thrombosis
Thrombus – intravascular blood clot in vivo
 Mural – attached to the wall of a heart chamber, of the
aorta, iliac a., common carotid a.
 Valvular – on heart valves – infective endocarditis,
thrombotic endocarditis, verrucous endocarditis
 Arterial – most commonly coronary, cerebral, femoral
 Venous - “Phlebothrombosis”- 90% in veins of lower
extremities: deep calf, femoral, popliteal, iliac
Thrombosis
Thrombi
 Arterial vs Venous
 Usually occlusive, due to  almost always occlusive, due
atherosclerotic damage; less to stasis or hypercoagulability
commonly due to acute states
vasculitis, trauma, RHD, MI,
aneurysms  Red, moist, many RBC

 Gray-white, friable
 Less common sites:
periprostatic plexus,
 Tangled strands of fibrin & periuterine & ovarian veins,
platelets; may develop a tail portal vein, dural sinuses
 Lines of Zahn
Arterial & Venous Thrombi

Lines of Zahn
 Thrombosis
Fates of a Thrombus:
 Dissolution by fibrinolytic activity
 Propagation
 Organization &/or recanalization
 Embolization
Clinical significance of Thrombosis
 Obstruction of blood flow
 Source of emboli--- obstruction of blood flow
 Disseminated Intravascular Coagulation

 DIC: “Disseminated Intravascular Coagulation”

 “Consumptive Coagulopathy”
 “Defibrination Syndrome”
 Development of multiple thrombi in the
microcirculation, causing rapid consumption of
platelets, prothrombin, fibrinogen, & coagulation
factors V, VIII, & X; thus leading to bleeding
tendencies
 Post-mortem clot

 not attached to the vessel wall

 a “perfect cast” of the vessel – the clot follows the
exact shape of the blood vessel where it is found
 “currant jelly” or “chicken fat” appearance – due to
stasis and to separation of the serum from the
coagulated RBC
 Embolism
 Embolus – any unattached intravascular space-
occupying mass (solid, liquid, or gas)
 99% are thromboemboli
 the remaining 1% consists of bone marrow,
amniotic fluid, bacterial clusters (septic), fat,
tumor, foreign bodies, air bubbles (most frequently
Nitrogen), atheromatous debris
 may cause sudden death if lodged in coronary or
cerebral arteries; or at the MPA bifurcation as a
saddle embolus
 Pulmonary Embolism
Pulmonary (Venous) Embolism
 most come from deep leg veins;
 up to 80% are clinically silent;
 death occurs when more than
60% of pulmonary vasculature is
occluded;
 chronicity can lead to Pulmonary
hypertension, cor Pulmonale,
pulmonary vascular sclerosis
Venous thrombosis, Pulmonary saddle
embolus,& Lung Infarct
Systemic (Arterial) Embolism
Systemic (Arterial) Embolism-
 60-65% arise from thrombi w/in the LV
post-MI; 5-10% from atrial thrombi; 5%
from cardiomyopathic lesions; 5-10%
from atherosclerotic plaques, aneurysms,
prostheses, IE; 10-15% from unknown
sources;
 almost always causes infarction; 70-
75% lodge in lower extremities; 10% in
the brain, 10% in viscera, & 7-8% in
upper extremities;
 Paradoxical embolus- broken-off
venous thrombus passes through a
defect (VSD, ASD, PFO) into the arterial
circulation
 Fat / Marrow Embolism

Fat / Marrow Embolism

 after traumatic injury to
long bones or to soft
tissues:
 symptoms show 24-72 hrs
after injury – pulmonary &
neurologic deficits, anemia,
thrombocytopenia,
petechiae
 mortality = 10%
 Amniotic fluid Embolism

Amniotic fluid Embolism –

 1 in 50,000 deliveries
 caused by introduction of amniotic fluid into the circulation -
tear in placental membranes, rupture of uterine/cervical veins
in tumultuous labor
 emboli usually lodge in pulmonary vessels;
 Lanugo hair, fetal squames, fat, mucin, bile
 Sx: dyspnea, deep cyanosis, convulsions, coma, DIC,
cardiovascular collapse (shock)
 mortality= 86%
 Air Embolism

Air Embolism
 caused by air entering torn vessels (during delivery,
pneumothorax, abortion, trauma) or by air coming
out of solution due to abrupt decompression
 Significant amount is ≥ 100ml.
 Decompression sickness – acute - “the bends”; “the
chokes”
 Caisson disease – chronic form – multiple minute
ischemic, then necrotic, foci favoring the heads of the
humeri, tibiae, femurs
 Infarction
 def: ischemic necrosis due to occlusion of the arterial
supply or of the venous drainage
 Coagulative pattern is usual, except in the Brain
 nearly 99% caused by thromboembolism, & are arterial
occlusions
 development depends on : circulation of the patient;
type of blood supply; rate of development of the
occlusion; & the susceptibility of the affected tissue to
hypoxia
 Infarct
 Anemic (White) Infarct
 Arterial occlusion in solid
tissues
 Initially hemorrhagic,
becomes pale in 24-48 hrs.
 Heart, Spleen, Kidneys –
single artery (end-arterial)
supply
 May be bland or septic
 Hemorrhagic (Red) Infarct
 Caused by venous occlusion;
or in tissues with a double
circulation; or in previously
congested tissues
 Lung, Liver – dual supply;
ovary – single outlet;
small intestines – rich
collaterals
 Morphology of Infarction
GROSS
 wedge-shaped, the apex being the
focus of the occlusion
 Poorly defined at first, slightly
darker than normal, firmer
consistency; Within 24hrs, more
defined, color intensifies; Within
days, pale infarct becomes yellow-
white & sharply demarcated; red
infarct unchanged, leading to
hyperemia
 Surface of the organ becomes
covered by a fibrinous exudate
Morphology of an Infarct

MICROSCOPIC
 Ischemic coagulative
necrosis (except Brain)
 12-18 hrs: hemorrhagic
suffusion, inflammatory
marginal exudation,
fibroblastic reparative
response
 If sepsis ocurs, the infarct
may become an abscess
Hemorrhagic Infarct
Circulatory failure / Shock
 Circulatory collapse
 Widespread hypoperfusion of tissues due to reduction in
blood volume or cardiac output, or redistribution of
blood, resulting in an inadequate/ineffective circulating
volume
 Insufficient tissue oxygenation--- hypoxia
 Inadequate clearance of metabolites--- accumulation of
lactic acid--- acidosis
 Types of Shock
 CARDIOGENIC – due to intrinsic myocardial damage as in
MI; cardiac tamponade, outflow block, or arrhythmias--- pump
failure
 HYPOVOLEMIC / HEMORRHAGIC – loss of blood (eg
hemorrhage) or plasma (eg severe burns)--- inadequate
circulating blood volume
 SEPTIC / ENDOTOXIC – severe bacterial infections,
usually Gram negative (endotoxins); less common Gram+ or
fungi --- profound peripheral vasodilatation
 NEUROGENIC – spinal cord injury, anesthetic accidents,
severe pain --- massive peripheral vasodilatation
 ANAPHYLACTIC – generalized type I hypersensitivity
reaction--- massive peripheral vasodilatation
 Shock
Cardiogenic Shock
↓cardiac output
↓ venous return ↓ circulating blood
Anaphylactic, Neurogenic Hypovolemic
peripheral vasodilatation ↓ tissue perfusion
Septic shock
tissue hypoxia

metabolic acidosis
 Morphology of Shock
 hypoxic failure of multiple organ systems
 Brain – ischemic encephalopathy – softening; liquefaction
 Liver – fatty change, central hemorrhagic necrosis
 Heart – subendocardial hemorrhages & necrosis; zonal
lesions- hypercontraction of individual myocytes
 Kidneys – acute tubular necrosis
 Lungs - “shock lung” - diffuse alveolar damage (DAD) --- acute
respiratory distress syndrome (ARDS)
 Adrenals – lipid depletion of the zona reticularis & zona
fasciculata --- “stress response”
 GIT – patchy mucosal hemorrhages & necrosis
 Morphology of Shock

Diffuse alveolar Damage, Lung Acute tubular necrosis, Kidney

Thank You !