Circulatory disorders Shock Assoc Prof Jan Laco MD

Circulatory disorders & Shock Assoc. Prof. Jan Laco, MD, Ph. D

Summary l 1. Edema l 2. Hyperemia and Congestion l 3. Hemorrhage l 4. Thrombosis l 5. Embolism l 6. Ischemia / Infarction

1. Edema = fluid in interstitium l cavities – hydrothorax, hydropericardium, ascites l anasarca = severe generalized edema l 3 major factors: – hydrostatic pressure – plasma colloid osmotic pressure – lymphatic drainage l inflammation

1. Edema l 1. hydrostatic pressure – impaired venous return congestive heart failure l constrictive pericarditis l liver cirrhosis – ascites l – venous obstruction or compression thrombosis l external pressure l

1. Edema plasma colloid osmotic pressure l loss or reduced albumin synthesis l 2. – nephrotic syndrome – protein-losing gastroenteropathy – liver cirrhosis – malnutrition

1. Edema l 3. lymphatic obstruction l lymphedema – inflammatory elephantiasis Filariasis - Wuchereria bancrofti l Erysipelas – Streptococcus pyogenes l – neoplastic – breast carcinoma (orange peel skin) – post-surgical (LN resection) + postirradiation

1. Edema subcutaneous tissue (pitting edema) + cavities l generalized x locally prominent l right-sided heart failure – lower limbs l left-sided heart failure - pulmonary edema l nephrotic syndrome – periorbital edema (eyelids) l brain edema – localized x generalized l – gyri flattening + sulci narrowing herniation

2. Hyperemia and Congestion = blood volume in particular tissue l 2 a. hyperemia – active (arteriolar dilation) – red color – striated muscle exercise l 2 b. congestion – passive (impaired venous return) – – – systemic x local blue-red color (cyanosis), edema event. hypoxemic necrosis, e. g. bowel accumulation of deoxygenated Hb chronic hypoxia regressive changes + small hemorrhages siderophages

2. Hyperemia and Congestion l pulmonary congestion l acute – by blood fulfilled septal capillaries – septal + alveolar edema + small hemorrhages l chronic – septa thickening fibrosis (induration) – alveoli - siderophages (heart failure cells)

2. Hyperemia and Congestion liver congestion l acute l – by blood fulfilled central veins + sinusoids l chronic – “nutmeg liver“ – red-brown + fatty color – centrilobular necrosis + hemorrhage – periportal fatty change – in time - cardiac fibrosis l bowel congestion – hemorrhagic necrosis

3. Hemorrhage = extravasation of blood from blood vessels l external (+ in hollow organs) l internal: within tissue – hematoma l hemorrhagic diatheses – insignificant – vasculopathies – trombocytopenia + -patia – coagulopathy injury

3. Hemorrhage l 1. Petechiae (1 -2 mm) - skin + mucosa – intravascular pressure, platelets l 2. Purpuras (3 -5 mm) – trauma, vasculitis, vascular fragility l 3. Ecchymosis (1 -2 cm) = hematoma (bruise) – RBC phagocytosis by macrophages – Hb (red-blue) bilirubin (blue-green) hemosiderin (golden-brown) l 4. Cavities – hemothorax, hemopericardium, hemoperitoneum – hemarthros

3. Hemorrhage l arterial l H. + venous + capillary per rhexin – injury - brain l H. per diabrosin – erosion – peptic ulcer l H. per diapedesin – transmigration of RBC (no damage of capillaries) – toxic injury + stasis

3. Hemorrhage - sequelae l 1. loss volume – > 20% hemorrhagic shock l 2. loss rate – acute hemorrhagic shock – chronic (peptic ulcer, metrorhagia, colonic adeno. Ca) l l 3. iron deficiency anemia site – subcutaneous x brain

Disseminated Intravascular Coagulation (DIC) l basis: widespread activation of thrombin l Mi: fibrin thrombi in microcirculation l 1. stage – multiple fibrin thrombi in microcirculation consumption of PLT + coagulation proteins l 2. stage – fibrinolytic system activation serious bleeding

DIC - causes l 1. obstetric complications – abruptio placentae retroplacental hematoma – amniotic fluid embolism – septic abortion l 2. infections – sepsis (Gram +, Gram- bacteria) – meningococcemia l 3. neoplasms – carcinomas of pancreas, prostate, lung, leukemias l 4. tissue injury – burns

4. Thrombosis = intravital intravascular blood clotting l Virchow triad l 1. endothelial injury – physical – hypertension, turbulence – chemical – hypercholesterolemia, smoking, vasculitis l 2. alteration of blood flow – stasis – immobilization, cardiac chamber dilation l 3. hypercoagulability – primary (genetic) x secondary – factor V mutation (Leiden) x neoplasms, drugs

4. Thrombosis l Grossly: mural x occlusive l Mi: RBC + WBC + PLT + fibrin lines of Zahn - lamination l Sites – arteries + veins + capillaries – cardiac chambers + valve cusps

4. Thrombosis l 1. Arterial thrombi l occlusive l coronary + cerebral + femoral aa. l upon AS plaque + bifurcation l G: gray-white, friable l Mi: PLT + fibrin, RBC + WBC

4. Thrombosis l l l l 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)

4. Thrombosis 3. cardiac chambers, atrial auricles l upon infarction + dilated cardiomyopathy l mural l 4. valve cusps l infective endocarditis (vegetations) l non-bacterial thrombotic endocarditis (sterile) l Libman-Sacks endocarditis – systemic LE l

4. Thrombosis – fate of thrombus 1. propagation l 2. embolization l 3. dissolution l – fibrinolysis (recent thrombi) l 4. organization – endothelial cells, smooth muscle cells, fibroblasts, capillaries l 5. recanalization – new small lumina

5. Embolism = detached i. v. solid, liguid or gaseous mass carried by blood to distant site from point of origin l 1. thrombembolism (99%) – pulmonary x systemic infarction 2. cellular - amniotic fluid, tumor cells l 3. subcellular - AS debries, BM bits l 4. fat l 5. air l 6. foreign bodies – catheter -------------------paradoxical retrograde l

Pulmonary thrombembolism l l l 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) – bifurcation – saddle embolus – 60% pulmonary circulation obstructed l small (60 -80%) - pulmonary hypertension – branching arterioles fibrinolysis bridging web

Systemic thrombembolism l source: intracardial thrombi (80%) aortic AS plaques l infarctions – LL (75%) + brain (10%) – bowel + kidney + spleen

Fat embolism source: fractures of bones with fatty BM + soft tissue trauma + burns l 1. stage (after 1 -3 days) l – veins lungs respiratory insufficiency l 2. stage – lungs systemic circulation neurologic symtoms + thrombocytopenia 10% fatal l Mi: fat droplets in lung, brain, kidney capillaries l

Air embolism l 1. systemic veins lungs – obstetric procedures, goiter operation, chest wall injury l 2. pulmonary veins systemic circulation – cardiosurgery 100 m. L of air symptoms (dyspnea) l air bubbles – physical vessel obstruction l l Decompression sickness – deep sea divers (nitrogen) – chronic form – caisson disease – bone necrosis

Amniotic fluid embolism l l l source: abruptio placentae retroplacental hematoma a. f. infusion into maternal circulation uterine veins lungs dyspnea, cyanosis, hypotensive shock, seizures, coma + lung edema + DIC Mi: pulmonary capillaries (mother) - squamous cells + lanugo hair + fat + DAD

Metastasis similar to embolism x secondary focus is formed l hematogenous – sarcomas l lymphogenous – carcinomas l – regional LNs – sentinel LN l porogenous – gastric and ovarian carcinomas – through hollow organs, along serosas

7. Ischemia / Infarction = ischemic necrosis due to occlusion of arterial supply (or venous drainage? ) l causes: – – thrombotic or embolic events (99%) vasospasm, hemorrhage in AS plaque external compression (tumor) twisting (testicular + ovarian torsion, bowel volvulus)

7. Infarction - determinants l 1. nature of blood supply – dual – lung + liver – end-arterial – kidney + spleen l 2. rate of occlusion – acute – infarction – chronic – collateral circulation, interart. anastomoses l 3. vulnerability to hypoxia – neurons – 3 -4 min – cardiomyocytes - 20 -30 min – fibroblasts - hours l 4. oxygen blood content – heart failure, anemia

7. Infarction - morphology l 1. red infarcts – venous occlusion – loose tissue (lung) – blood collection – dual circulation – lung + bowel – previously congested organs – reperfusion (angioplasty, drug-induced thrombolysis) l 2. white infarcts – arterial occlusion – solid organs – heart (yellow), spleen, kidney

7. Infarction - morphology l wedge shape – apex to occluded artery – base to organ periphery + fibrinous exudate (pleuritis, pericarditis epistenocardiaca) l onset – poorly defined, hemorrhagic l later – sharper margins + hyperemic rim

7. Infarction - morphology ischemic coagulative necrosis – 3 zones l 1. total necrosis - centre l – loss of nuclei, eosinophilia of cytoplasm, architecture is preserved l 2. partial necrosis – some cells survive – inflammation (neutrophils) – 1 -2 day degradation of dead tissue l 3. hyperemic rim

7. Infarction - morphology l healing – granulation tissue (5 -7 day) fibrous scar (6 -8 weeks) – !!! brain – liquefactive necrosis pseudocyst !

7. Infarction l septic infarctions l source – infective endocarditis (vegetations) – suppurative thrombophlebitis l infarction scar abscess granulation tissue

Shock l l = systemic hypoperfusion due to reduction of cardiac output / effective blood volume circulation hypotension cellular hypoxia features – hypotension, tachycardia, tachypnea, cool cyanotic skin (x septic s. – warm) initial threat + shock manifestations in organs prognosis – origin + duration

Shock l 1. cardiogenic – failure of myocardial pump – myocardial infarction, arrhythmias – pulmonary embolism l 2. hypovolemic - inadequate blood/plasma volume – hemorrhage – fluid loss (vomiting, diarrhoea, burns, trauma) l 3. septic – vasodilation + endothelial injury – Gram+, Gram- bacteria l 4. neurogenic - loss of vascular tone – spinal cord injury l 5. anaphylactic – Ig. E–mediated hypersensitivity

Shock - stages progressive disorder multiorgan failure death l 1. non-progressive l – compensatory mechanism (neurohumoral) activation – centralization of blood circulation l 2. progressive – tissue hypoperfussion – metabolic dysbalancies l 3. irreversible – incurred cellular damage + tissue injury – death

Shock - morphology l brain - ischemic encephalopathy – tiny ischemic infarctions (border zones) l heart – subendocardial hemorrhage + necroses, contr. bands l kidney - acute tubular necrosis (shock kidney) – pale, edematous – tubular epithelium necroses granular casts l lung – diffuse alveolar damage (shock lung), ARDS – heavy, wet – congestion + edema + hyaline membranes

Shock - morphology l adrenal gland – lipid depletion l GIT – hemorrhagic enteropathy – mucosal hemorrhages + necroses l liver – fatty change, central necrosis