5_Circulatory Disorders & Shock

8/13/2019 5_Circulatory Disorders & Shock

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Circulatory disorders & Shock

Jan Laco, M.D., Ph.D.


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Summary

1. Edema

2. Hyperemia and Congestion

3. Hemorrhage

4. Thrombosis

5. Embolism 6. Infarction


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1. Edema

= fluid in interstitium

cavitieshydrothorax, hydropericardium, ascites

anasarca = severe generalized edema

3 major factors:

hydrostatic pressure

plasma colloid osmotic pressure lymphatic obstruction

inflammation


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1. Edema

1. hydrostatic pressure

impaired venous return

congestive heart failure

constrictive pericarditis

liver cirrhosisascites

venous obstruction or compression thrombosis

external pressure


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1. Edema

2. plasma colloid osmotic pressure

loss or reduced albumin synthesis

nephrotic syndrome

protein-losing gastroenteropathy

liver cirrhosis

malnutrition


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1. Edema

3. lymphatic obstruction

lymphedema

inflammatoryfilariasis elephantiasis

neoplasticbreast carcinoma

postsurgical (LN resection) + postirradiation


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1. Edema

subcutaneous tissue (pitting edema) + cavities

generalized x local prominent

right heart failurelower limbs

left heart failure - pulmonary edema

nephrotic syndromeperiorbital edema (eyelids) brain edemalocalized x generalized

gyri flattening + sulci narrowing herniation


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= blood volume in particular tissue

2a. hyperemiaactive (arteriolar dilation)

red striated muscle exercise

2b. congestionpassive (impaired venous return)

systemic x localblue-red color (cyanosis)

accumulation of deoxygenated Hb

chronic chronic hypoxia regressive changes +

small hemorrhages siderophages


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pulmonary congestion

acute

blood fulfilled septal capillaries

septal + alveolar edema + small hemorrhages

chronic

septa thickening fibrosis

alveoli - siderophages (heart failure cells)


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liver congestion

acute

blood fulfilled central vein + sinusoids chronicnutmeg red-brown + fatty collor

centrolobular necrosis + hemorrhage

periportal fatty change

cardiac fibrosis

bowel congestion

hemorrhagic necrosis


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3. Hemorrhage

= extravasation of blood from blood vessels

external (+ hollow organ)

within tissuehematoma

hemorrhagic diathesesinsignificant injury

vasculopathies trombocytopenia + -patia

coagulopathy


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3. Hemorrhage

arterial + venous + capillary

H. per rhexininjury - brain

H. per diabrosinerosionpeptic ulcer

H. per diapedesintransmigration of RBC(no damage of capillaries)toxic injury +

stasis


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3. Hemorrhage - sequelae

1. loss volume

> 20% hemorrhagic shock

2. loss rate acute hemorrhagic shock

chronic (peptic ulcer, menstrual bleeding)

iron deficiency anemia

3. site

subcutaneous x brain


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Disseminated Intravascular

Coagulation (DIC)basis: widespread activation of thrombin

Mi: fibrin thrombi in microcirculation

1. stage multiple fibrin thrombi in microcirculation

consumption of PLT + coagulation proteins

2. stage fibrinolytic system activation serious

bleeding


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DIC - causes

1. obstetric complications

abruption placentae retroplacental hematoma

amniotic fluid embolism

septic abortion

2. infections

sepsis (Gram +, Gram- bacteria)

meningococcemia 3. neoplasms

carcinoma of pancreas, prostate, lung, leukemia

4. tissue injury

burns


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4. Thrombosis

= intravital intravascular blood clotting

Virchow triad

1. endothelial injuryphysicalhypertension, turbulence

chemicalhypercholesterolemia, smoking, vasculitis

2. alteration of blood flow

stasisimmobilization, cardiac chamber dilation

3. hypercoagulability

primary (genetic) x secondary

factor V mutation (Leiden) x neoplasms, drugs,


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4. Thrombosis

Grossly: mural x occlusive

Mi: RBC + WBC + PLT + fibrin

lines of Zahn - lamination

Sites

arteries + veins + capillaries

cardiac chambers + valve cusps


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4. Thrombosis

1. Arterial thrombi

occlusive

coronary + cerebral + femoral aa.

upon AS plaque + bifurcation

G: gray-white, friable

Mi: PLT + fibrin, RBC + WBC


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4. Thrombosis

2. venous thrombi (phlebothrombosis)

occlusive

deep veins of LL + pelvic plexus

G: firm, red, attached to wall

Mi: RBC + fibrin

!!! asymptomatic (50%) !!!

X postmortal clots (not attached to wall,gelatinous red centre + fat supernatant)


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4. Thrombosis

3. cardiac chambers

upon infarction + dilated cardiomyopathy

mural

4. valve cusps

infective endocarditis (vegetations) non-bacterial thrombotic endocarditis (sterile)

Libman-Sacks endocarditissystemic LE


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4. Thrombosis

fate of thrombus

1. propagation

2. embolization

3. dissolution fibrinolysis (recent thr.)

4. organization

endothelial cells, smooth muscle cells, fibroblasts,

capillaries 5. recanalization

new small lumina


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5. Embolism

= detached i.v. solid, liguid or gaseous masscarried by blood to distant site from point of origin

1. thrombembolism (99%)pulmonary x systemic infarction

2. cellular - amniotic fluid, tumor cells

3. subcellular - AS debries, BM bits

4. fat 5. air

6. foreign bodies - catheter


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Pulmonary thrombembolism

source - deep veins of LL + pelvic plexus

v. cava inf. right heart a. pulmonalis

paradoxical embolism - IA or IV defect systemic emboli

+ left heart failure pulmonary infarction

large - sudden death (acute right heart failure)

bifurcationsaddle embolus 60% pulmonary circulation obtructed

small (60-80%) - pulmonary hypertension

branching arterioles fibrinolysis bridging web


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Systemic thrombembolism

source: intracardial thrombi (80%) + AS

infarctions

LL (75%) + brain (10%)

bowel + kidney + spleen


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Fat embolism

source: fractures of bones with fatty BM + softtissue trauma + burns

1. stage (after 1-3 days)

veins lungs pulmonary insufficiency

2. Stage

lungs systemic circulation neurologic

symtoms + thrombocytopenia 10% fatal

Mi: fat droplets in lung, brain, kidney capillaries


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Air embolism

1. systemic veins lungs

obstetric procedures, goiter operation, chest wall injury

2. pulmonary veins

systemic circulation cardiosurgery

100mL of air symptoms (chokes)

air bubblesphysical vessel obstruction

Decompression sickness

deep sea divers (nitrogen)

chronic formcaisson diseasebone necrosis


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Amniotic fluid embolism

source: abruptio placentae retroplacentalhematoma

a.f. infusion into maternal circulation uterineveins lungs

dyspnea, cyanosis, hypotensive shock, seizures,coma + lung edema + DIC

Mi: pulmonary capillaries (mother) - squamouscells + lanugo hair + fat

+ DAD


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7. Infarction

= ischemic necrosis due to occlusion ofarterial supply or venous drainage

causes: thrombotic or embolic events (99%)

vasospasm, hemorrhage in AS plaque

external compression (tumor)

twisting (testicular + ovarian torsion, bowelvolvulus)


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7. Infarction

- determinants 1. nature of blood supply

duallung + liver

end-arterialkidney + spleen

2. rate of occlusion

acuteinfarction

chroniccollateral circulation, interart. anastomoses

3. vulnerability to hypoxia neurons3-4 min

cardiomyocytes - 20-30 min

fibroblasts - hours

4. oxygen blood contentheart failure, anemia


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7. Infarction

- morphology 1. red infarcts

venous occlusion

loose tissue (lung)blood collection dual circulationlung + bowel

previously congested organs

reperfusion (angioplasty, drug-induced thrombolysis)

2. white infarcts

arterial occlusion

solid organsheart (yellow), spleen, kidney


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7. Infarction

- morphology healing

granulation tissue (5-7 day) fibrous scar (6-8

weeks) !!! brainliquefactive necrosis pseudocyst !


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7. Infarction

septic infarctions

source

infective endocarditis (vegetations)

suppurative thrombophlebitis

infarction abscess granulation tissue

scar


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Shock

= systemic hypoperfusion due to reduction of

cardiac output / effective blood volume circulation

hypotension cellular hypoxia featureshypotension, tachycardia, tachypnea,

cool cyanotic skin (x septic s.warm)

initial threat + shock manifestations in organs

prognosis

origin + duration


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Shock

1. cardiogenicfailure of myocardial pump

myocardial infarction, arrhythmias

pulmonary embolism

2. hypovolemic - inadequate blood/plasma volume

hemorrhage

fluid loss (vomiting, diarrhoea, burns, trauma)

3. septicvasodilation + endothelial injury Gram+, Gram- bacteria

4. neurogenic - loss of vascular tone

spinal cord injury

5. anaphylacticIgEmediated hypersensitivity


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Shock - stages

progressive disorder multiorgan failure death

1. nonprogressive

compensatory mechanism (neurohumoral) activation

centralization of blood circulation

2. progressive

tissue hypoperfussionmetabolic dysbalancies 3. irreversible

incurred cellular damage + tissue injury


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Shock - morphology

brain - ischemic encephalopathy

tiny ischemic infarctions (border zones)

heart

subendocardial hemorrhage + necroses, contr. bands

kidney - acute tubular necrosis (shock kidney)

pale, edematous

tubular epithelium necroses casts lungdiffuse alveolar damage (shock lung)

heavy, wet

congestion + edema + hyaline membranes


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Shock - morphology

adrenal gland

lipid depletion

GIThemorrhagic enteropathy

mucosal hemorrhages + necroses

liver

fatty change, central necrosis

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5_Circulatory Disorders & Shock