SHOCK

1. SHOCK

2. SHOCK DEFINTION The common denominator in all forms of shock is inadequate capillary perfusion. Shock is Characterized by Inadequate Tissue Perfusion and Cellular Hypofunction/Hypoxia. Total body celular metabolism is malfunctional, usually by inadequate delivery of oxyden to meet celluar needs and occasionally of inability of cells to utilize oxygene( methemoglobinemia, carbon monooxide poisoning).

3. SHOCK shock has been recognised for over 100 years, a clear definition is not estabilished till this moment, the definition of shock varies from time to time and has different meanings according to the etiological and pathogenetic factors, what caused it.

4. Classified by Etiologyby Mark A. Graber, MD:Departments of Family Medicine and Emergency Medicine University of Iowa College of Medicine Peer Review Status: Externally Peer Reviewed by Mosby Hypovolemic shock from volume loss (e.g., dehydration, blood loss, burns) Distributive shock based on loss of vascular tone (e.g., anaphylactic, septic, bacteremic, toxic, neurogenic shock).

5. Classified by Etiologyby Mark A. Graber, MD:Departments of Family Medicine and Emergency Medicine University of Iowa College of Medicine Peer Review Status: Externally Peer Reviewed by Mosby Cardiogenic shock based on pump failure( acute myocardial infarction, ventricular septal defect rupture, papillar muscles rupture, ventricular aneurysm, severe aortic stenosis, arrhythmias, trauma- tensione pneumothorax, pericardial temponade, cardic contusion Dissociative shock based on inability of RBC to deliver oxygen (e.g., methemoglobinemia, carbon monoxide posoning).

6. Most common clinical signs: • Hypotension. Blood pressure drop is a late finding. • An orthostatic systolic decrease of 10 to 20 mm Hg or increase in pulse of 15 beats/min is considered "significant." • Take orthostatic vital signs recumbent and after standing for 1 to 2 minutes. * Orthostatic vital signs may be normal in hypovolemic individuals, or nor-mal individuals may exhibit orthostatic changes; so use clinical judgment and base treatment on symptoms. Alcohol ingestion, a meal, increased age, antihypertensives, etc. may cause orthostatic changes in BP and pulse in the absence of hypovolemia.

7. Most common clinical signs: Tachycardia usually present but may not be, especially in the presence of diaphragmatic irritation, which causes vagal stimulation, in neurogenic shock.

8. Most common clinical signs: Hypoperfusion including decreased urine output, decreased mentation, cool extremities, mottling, etc.* Goal of resuscitation is to maintain urine output between 30 and 60 ml/hr.

9. Hypovolemic shock Definition It is present when marked reduction in oxygen delivery results from diminished cardiac output secondary to inadequate volume of whole blood.

10. Hypovolemic shock The main causes are: • - external bleeding; • - internal bleeding; • - the loss of big amount of plasma due to wide burns; • - the loss of liquids and electrolytes after long lasting and hard diarrhea, vomiting; • - an internal loss of liquids due to pleuritis of peritonitis, acute pancreatitis. * three last sometimes nemed as oligemic shock

11. Hypovolemic shock Pathophysiology: diminishing cardiac output or fluid flow secondary to decreasing venous return

12. Hypovolemic shock Clinicla signs: hypotensia, tachycardia, tachypnoe, oliguria, anxious, skin is pale and cool, often patient have nausea and vomiting, can be restless or comatose

13. Hypovolemic shockacording American Surgeons Committee of Trauma 1988

14. Hypovolemic shock Laboratory determination: • arterial blood gases: pH is considered normal 7.35-7.45, PaCO2 – 35-45mm/ml, in pH <7.35 is associated with a normal or less normal PaCO2 -( metabolic acidosis) • in vomiting by stenosis of pyloric part of ventriculus - alcalosis • serum electrolytes in hemorragic shock near normal, in diarhhoe K↓, vomiting Na↓, pancreatitis Ca↓ ,K↓ and etc. • creatinine is usefule as an indicator of renal function

15. Hypovolemic shock Treatment and menagemant of hypovolemic shock principles: • monitoring of blood pressure, urination, breafing function, HR • replasment of blood volume ( Ringer lactate, solutions similar to plasma in electrolites composition, starch or gelatin solution, in bleading erythrocite mass • supplemental oxygene • after resuscitation surgery manipulations, interventionaly radiology, endoscopy, drugs.

16. Distributive shock septic, bacteremic shock - based on loss of vascular tone, bacteremia and septic shock are closely related conditions.

17. Distributive shock Bacteremic shock develops when hight amount of of bacteremia or fungs and its toxic agents penetrate into the blood and when the host defenses are decreased due to prolonged and hard infectional illness.

18. Distributive shock • Septic shock is sepsis with hypoperfusion and hypotension refractory to fluid therapy. • When bacteremia produces changes in circulation such that tissue perfusion is critically reduced, septic shock ensues.

19. Distributive shock The main causes are: • Septic shock is more often caused by hospital-acquired gram-negative bacilli and usually occurs in immunocompromised patients and those with chronic diseases. • In about 1/3 of patients it is caused by gram-positive cocci and by Candida organisms. • Shock caused by staphylococcal toxins is called toxic shock, a condition more frequently occurring in young women.

20. Distributive shock • Predisposing factors: diabetes mellitus, cirrhosis, leukopenic states, especially those associated with underlying neoplasms or treatment with cytotoxic agents, • antecedent infection in the urinary, biliary or GI tracts, • invasive devices- catheters, drainage tubes, and other foreign materials and prior treatment with antibiotics, corticosteroids, or ventilator devices.

21. Distributive shock Septic shock occurs more often in newborns, patients > 35 yr, pregnant women, and those seriously immunocompromised by underlying diseases or iatrogenic complications of treatment.

22. Distributive shock Pathogenesis The bacterial toxins generated by the infecting organisms trigger complex immunologic reactions: a large number of mediators, including TNF, leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2, have been implicated in addition to endotoxin (the lipid fraction of the lipopolysaccharides released from the cell wall of gram-negative enteric bacilli).

23. Distributive shock Warm shock: initially, vasodilatation of arteries and arterioles occurs, decreasing peripheral arterial resistance with normal or increased cardiac output even though the ejection fraction may be decreased when heart rate increases.

24. Distributive shock Cold shock: later, cardiac output may decrease and peripheral resistance may increase. Despite increased cardiac output, blood flow to the capillary exchange vessels is impaired, and the delivery of vital substrates, especially O2, and the removal of CO2 and waste products are decreased. This decreased organ perfusion particularly affects the kidneys and brain, and subsequently causes failure of one or more of the visceral organs. Ultimately, cardiac output declines and the typical features of shock appear.

25. Distributive shock Clinical signs: • altered mental alertness, chacking chill, rapid rise of body temperature, BP decreased to < 80mm Hg , the skin is warm (paradoxically warm extremities), tachycardia, tachyon, and oliguria; • late cool, pale extremities with peripheral cyanosis and mottling are late signs, with progression, multiorgan failure involves the kidney, lungs, and liver; disseminated intravascular coagulation (DIC) and heart failure may also occur.

26. Distributive shock Laboratory determination: leucocytosis, with marcet shift to left, associated with a sharp decrease in platelet count to <= 50,000/µL, respiratory alcalosis, metabolic acidosis, toxic anemia, positive blood cultures.

27. Distributive shock - Managment should be treated in an ICU, the following should be monitored frequently: systemic pressure, arterial and venous blood pH, arterial blood gas levels, blood lactate level, renal function, electrolyte levels, and possibly tissue PCO2, urine output should be measured, usually with an indwelling catheter, as an indication of splanchnic blood flow and visceral perfusion,

28. Distributive shock - Managment the CVP or pulmonary artery pressure should be measured, and fluid replacement should be given until the CVP reaches 10 to 12 cm H2O or until the pulmonary wedge pressure reaches 12 to 15 mm Hg,

29. Distributive shock - Managment respiration should be supported with nasal O2, tracheal intubation or tracheostomy, and mechanical ventilation as necessary,

30. Distributive shock - Managment • parenteral antibiotics should be given after specimens of blood, body fluids, and wound sites have been taken for Gram stain and culture; • prompt empiric therapy is essential, the choice of an antibiotic requires an educated guess based on the results of previous cultures from the site of the primary infection or on the clinical setting in which the primary infection occurred.

31. Rare cases of shock Shock due to the hormonal insufficiency – gl thyroydea, hipofhysis and etc. (type distributive shock);

32. Rare cases of shock • Neurogenic shock – hypotension secondary to central nervous system dysfunction, it is result of dysruption of the sympathetic nervous system (type is distributive shock). • The main causes are: trauma or lumbal ane-sthesia due to vasomotoric disfunction – paralysis. It results in vaso-dilatation and decresed vascular resistence -> blood insufficiency in a circulatory system.

33. Rare cases of shock Neurogenic shock The main causes are: trauma or lumbal ane-sthesia due to vasomotoric disfunction – paralysis. It results in vaso-dilatation and decresed vascular resistence -> blood insufficiency in a circulatory system.

34. Rare cases of shock Shock due to the hyperergic reactions - allergic reactions develope if the patients is hypersensitive to various antigenes (type distributive shock).