Pathophysiology of circulatory shock

1. Pathophysiology of circulatoryshock M.Tatár

2. Clinical features of shock -drop of systolicbloodpressure (BP  90 torr) in hypertonicpatients: decrease of 50 torr - low cardiac output and tachycardia - vasoconstriction: skin and splanchnic areas - oliguria (< 20 ml/hour) - cold wet skin - constriction of superficial veins - marked muscle weakness - usualy  body temperature (except septic shock) - disorientation - metabolic acidosis

3. Characteristics of circulatory shock Complexclinicalsyndromeencompassing a group of conditionswithvariablehemodynamicmanifestations Commondenominatorisgeneralisedinadequacy of bloodflowthroughthe body; hypoperfusioncompromisesthedelivery of oxygen and nutrients and theremoval of metabolites; tissuehypoxiashiftsmetabolism to anaerobicpathwayswithproduction of lacticacid if shock is not corrected it leads to: a) cell dysfunction b) irreversible multiorgan insufficiency d) death

4. Cardiovascular dysorders in shock: a) acutecirculatoryinsufficiency b) mismatching between blood volume and volume of vascular bed tissuehypoperfusion

5. Blood pressure Tissue perfusion Cardiac output x Vascularresistance

7. Factors determining tissue perfusion A. cardial:cardiac output B. vascular: changes in vascular resistance regulation of vascular tone: - tonic sympathetic activity - systemic catecholamines • myogenic response- constant tissue blood flow during changed perfusion pressure - metabolic autoregulation - vasodilatory substances - endothelial NO

8. C. humoral: renin, vazopresin, prostaglandins, kinins, atrialnatriureticfactor Factors determining microcirculation: • adhesion of leukocytes and platelets on epithelial lesions - intravascularcoagulation - constriction of precapillary and postcapillary vessels - intense hypoxia  vasodilation of arteriols, venoconstriction continues  intravascular fluid loss -  capillary permeability  tissue edema

9. Hemodynamic classification of shocks 1.Hypovolemic- intravascular fluid volumeloss hemorrhage, fluid depletion or sequestration 2.Cardiogenic- impairment of heartpump myopathiclesions: myocardial infarction, cardiomyopathies dysrhythmias obstructive and regurgitantlesionsof intracardialbloodflowmechanics

10. 3.Obstructive - factorsextrinsic to cardiacvalves and myocardium v. cavaobstruction, pericardial tamponade, pulmonaryembolism, coarctation of aorta 4.Distributive- pathologicredistribution of intravascular fluid volume septicaemia: endotoxic, secondary to specificinfection anaphylactic

11. NORMAL 1. HYPOVOLEMIC 2. CARDIOGENIC 3. DISTRIBUTIVE 4. OBSTRUCTIVE Low Resistance High Resistance

12. Stages of shock 1. Nonprogressivestage (compensated) Compensatorymechanisms(negative feedback) of thecirculationcanreturn CO and BP to normallevels - baroreceptorreflexes sympatheticstimulation  constrictarteriols in most parts of the body and venousreservoirs  protection of coronary and cerebralbloodflow • angiotensin-aldosteron, ADH  vasoconstriction, • water and saltretention by thekidneys - absorption of fluid from ISF and GIT, increasedthirst

14. 2. Progressiveshock • circulatory system themselves begin to deteriorate, without therapy shock becomes steadily worse until death • positive feedback mechanismsare developed and can • causeviciouscircleof progressivelydecreasing CO Cardiacdepression- coronarybloodflow,  contractility Vasomotorfailure- cerebralbloodflow Release of toxins by ischemictissues: histamine, serotonin, tissueenzymes Intestineshypoperfusion  mucosalbarrierdisturbance  endotoxinformation and absorption vasodilation, cardiacdepression - Vasodilation in precapillarybed • Generalisedcellulardeterioration:  K+ ,  ATP, release of • hydrolases – firstsigns of multiorganfailure

15. 3. Irreversibleshock • despitetherapycirculatorysystemcontinues to • deteriorate and deathensues - marked hypoxic tissue damage • endothelial dysfunction adhesive molecules, • neutrophils, macrophagesinflammation - progressive acidosis • microcirculation failure plasma proteins leak to interstitium • advanceddisseminatedintravascular coagulation

16. Cardiogenicshock • infarctionprocess (45% loss of functionalmass of • leftventricle) - ventricle fails as a pump • BP  90 torr for at least 30 min, •  pulmonarycapillarypressure  lungedema - self-perpetuingcyclethenensues(viciouscircle): metabolicacidosis and reducedcoronaryperfusionfurtherimpairingventricularfunction and predisposing to thedevelopment of dysrhythmias Progression of myocardial dysfunction: - hypotension, tachycardia, fluid retention, hypoxemia

17. Septic shock Typicalcauses:peritonitis, gangrenousinfection, pyelonephritis (SIRS) Special features: 1. high fever 2. marked vasodilatation (inflammation) 3.  or normal CO: vazodilation,  metabolic rate 4. disseminated intravascular coagulation clotting factors to be used up hemorrhages occur into many tissue (GIT) IL-1 and TNF: PGE2, leukotrienes and NO - vascularrelaxation -  endothelialpermeability (deficit of intravascularvolume) -  myocardialcontractility

18. Cell dysfunction prolong tissue hypoperfusion  cell membrane lesion, lysosomal enzymes  cell death mechanisms:hypoxia, inflammatory mediators, free radicals

19. Multiorgan failure Kidney -  blood flow (to 10%)   GF oliguria - ischemia acute tubular necrosis - countercurrent mechanism failure izostenuria - marked lesions acute renal failure

20. Lungs • disturbances of pneumocytes and endothelium • accumulation of Tr, Neu in pulmonary • circulation  release of proteases •  leukotriens and free radicals -  permeability -  surfactant, edema and hemorrhagies  respiratory insufficiency(ARDS)

21. 100 % SURVIVAL ( 142 Pts) 75 50 25 0-1 1-2 2-3 3-4 4-6 6-11 11-16 > 16 LACTATE mM/l