hypovolemic ang cardiogenic shock FINAL.pptx

SHOCK, HYPOVOLEMIC SHOCK

1. shock Presenter: dr.Annamalai Moderatot : dr.T.MUNEER

2. HYPOVOLEMIC SHOCK Hypovolemic shock encompasses disease process that reduces CO and oxygen delivery via reduction in preload.

3. DETERMINANTS OF OXYGEN DELIVERY (DO2) The two major components of DO2 are cardiac output(CO) and arterial oxygen content(cao2): DO2=CO X Cao2 The two major components of CO are heart rate (HR) and stroke volume ( sv ) DO2 = (HR X SV) x Cao2 The major determinants of SV are preload, afterload(SVR) and cardiac contractility SV = (preload x contractility) xSVR The Cao2 is composed of oxygen carried by convection with hemoglobin and oxygen dissolved in blood Ca02 = (Hb x 1.39 x Sa02) + (pao2 x 0.03)

4. Heart pumps well, but not enough blood volume to pump MAP = CO x SVR HR x Stroke volume Hypovolemic shock is a consequence of decreased preload due to intravascular volume loss. -The decreased preload diminishes stroke volume, resulting in decreased cardiac output (CO).

5. etiology Haemorrhagic causes: 1 . internal Hematoma Hemothorax Hemoperitoneum 2.external Trauma bleeding

6. Non haemorrhagic causes 1.internal Third space loss Pancreatitis Ascitis 2.external Vomitting Diarhea burns

7. Clinical features Cold clammy pale skin Thready pulse Tacchycardia & tacchypnea Hypotension Oliguria Confusion Decreased CVP Decreased CO Decreased PCWP Elevated SVR Decreased CVP

8. AMERICAN COLLEGE OF SURGEON CLASSIFICATION OF ACUTE HAEMORRHAGE PARAMETERS GRADE I GRADE II GRADE III GRADE IV %Blood loss <15% 15-30% 30-40% >40% ml blood loss <750 750-1500 1500-2000 >2000 PR/min <100 >100 >120 >140 SBP N N 90-70 <60 Pulse pressure 36 30 20-3. 10-20 RR 14-20 20-30 30-40 >40 Urine output ml/ hr 30-35 25-30 5-15 <5 Mental status oriented anxious confusion lethargic

9. management Resuscitation of these patients should be considered in two phases: Early, while active bleeding is still ongoing Late, once all hemorrhage has been controlled

10. GOALS OF THE TREATMENT ABCDE A irway control work of B reathing optimize C irculation assure adequate oxygen D elivery achieve E nd points of resuscitation

11. Fluid administration is the cornerstone of resuscitation rapid infusion of up to 2 L of warmed isotonic crystalloid solution in any hypotensive patient with the goal of restoring normal blood pressure

12. Goals of early resuscitation Maintain systolic blood pressure at 80 to 100 mm Hg Maintain hematocrit at 25% to 30% Maintain the prothrombin time and partial thromboplastin time in normal ranges Maintain the platelet count at greater than 50,000 per high-power field Maintain normal serum ionized calcium

13. crystalloids Isotonic crystalloids (normal saline, lactated Ringer's solution [LR], Plasma- Lyte A) are the initial resuscitative fluids administered to any trauma patient . advantage of being inexpensive, readily available, nonallergenic, noninfectious , and efficacious in restoring total-body fluid. easy to store and administer, mix well with infused medications, and can be rapidly warmed to body temperature. Disadvantages of crystalloids include lack of oxygen-carrying capacity, lack of coagulation capability, and limited intravascular half-life.

14. H ypertonic saline solution will draw fluid into the vascular space from the interstitium and thereby reverse some of the non hemorrhagic fluid loss caused by shock and ischemia .

15. colloids Colloids, including starch solutions and albumin, have been advocated for rapid plasma volume expansion. Like crystalloids, colloids are readily available, easily stored and administered colloids will increase intravascular volume by drawing free water back into the vascular space.

16. colloid resuscitation will restore intravascular volume more rapidly than crystalloid infusion will and at a lower volume of administered fluid. Disadvantage : expensive, allergic reaction If there is any endothelial injury colloids leaks out . It will increase the oncotic pressure in extravascular space which worsen the condition. It takes 12-24hrs for endothelial cells to repair

17. Red blood cells are the mainstay of treatment of hemorrhagic shock. With an average hematocrit of 50% to 60%, a unit of RBCs will predictably restore oxygen-carrying capacity and expand intravascular volume as well as any colloid solution.

18. When the patient is in shock, however, and blood loss is likely to be substantial, platelets should be empirically administered in proportion to RBCs and plasma (1 : 1 : 1)

19. ASSESMENT OF INTRAVASCULAR VOLUME STATUS PASSIVE LEG RAISE TEST: Predict the responsiveness to additional intravenous fluid by providing the patient withendogenous volume bolus While the patient is resting in a semirecumbent position at 45 degree angle, the bed is placed in Trendelenburg such that the patients head becomes horizontal and the legs are extended at 45 degree angle There is an immediate assesement of changes in CO or pulse pressure variation occur.

20. The most commonly used parameters to assess the adequacy of volume resuscitation are IVC diameter and IVC collapse using echocardiography.

21. OXYGENATION AND VENTILATION In addition to cellular hypoxia caused by circulatory failure patient with shock may present with hypoxemia In shock there can be development of ARDS and subsequent V/Q mismatch and shunt. Supplement oxygen should be initiated and titrated to maintain spo2 of 92-95% If patient requires intubation this should be provided promptly so as to minimize the duration of tissue hypoxia

22. Patient with shock may have need high minute ventilatory needs to compensate for metabolic acidosis. It is important to provide ventilation with lung protective stratergies focussed on low tidal volume ventilation and optimization of positive end expiratory pressure to minimize ventilator induced lung injury.

23. Cardiogenic shock Cardiogenic shock results from cardiac failure with the inability of the heart to maintain adequate tissue perfusion. The clinical definition of cardiogenic shock is evidence of tissue hypoxia due to decreased cardiac output (cardiac index < 2.2 L/min/m2)and sustained systolic arterial hypotension (<90 mmHg) in the presence of adequate intravascular volume.

24. This is most often caused by cardiac dysfunction due to myocardial infarction .. The initiating event in cardiogenic shock is a primary pump failure.

25. etiology 1.compressive type Associated with external compression to the heart Cardiac tamponade Tension pneumothorax Positive pressure ventilation

26. 2.obstructive type: Associated with obstruction to outflow or inflow to the heart AS MS TS PS

27. 3.Functional type Overall most common type IHD arryhthmias

28. Hemodynamics The pulse is typically weak and rapid, Often in the range of 90–110 beats/min, elevated PCWP Elevated CVP Decreased CO

29. Criteria for cardiogenic shock Sys BP <= 90 mmHg and HR > 90/min BP mean <= 65 mmHg Signs of organ insuff : oliguria, cold extremities CI < 2.2 L/min/m2 PCWP > 15 mmHg

30. treatment Correction of hypovolemia The first priority in treating cardiogenic shock is to expand the circulating blood volume with IV fluids , Treatment of arrhythmias Treatment of hypotension Treatment of metabolic acidosis Treatment of electrolyte disturbances

31. Therapy should minimize myocardial oxygen demand and raise oxygen delivery to the ischemic area; This goal is complicated by the fact that many resuscitative approaches to correct hypotension (preload augmentation, inotropes, and vasopressors; increase myocardial oxygen consumption. In patients without hypotension, pharmacologic vasodilatation using nitrates or sodium nitroprusside may reduce myocardial oxygen consumption and improve ventricular ejection by reducing left ventricular afterload and possibly produce a shift of blood from the lungs to the periphery by reducing venous tone .

32. Medications:- 1. Vasoactive therapy — Vasopressors and inotropic agents are administered only after adequate fluid resuscitation. Choice of vasoactive therapy depends on the presumed etiology of shock as well as cardiac output. If there is evidence of low cardiac output with high filling pressures, inotropic support is needed to improve contractility.

33. If there is continued hypotension with evidence of high cardiac output after adequate volume resuscitation, then vasopressor support is needed to improve vasomotor tone.

34. Dobutamine, predominantly ß-adrenergic agonist , 1 st line of drug for cardiogenic shock, Increasing contractility and decreasing afterload . Initial dose is 0.5–1 mcg/kg/min as a continuous iv infusion,

35. Which can be titrated every few minutes as needed to hemodynamic effect; The usual dosage range is 2–20 mcg/ kg/min intravenously. Tachyphylaxis can occur after 48 hours secondary to the down-regulation of b-adrenergic receptors

36. Epinephrine: Increases the myocardial contractility Powerful cardiac stimulant Increases the heart rate

37. End points of resucitation 1.clinical: most important: urine output Adults:>0.5ml/kg/hr Children:1-1.5ml/kg/hr Infants:>2ml/kg/hr

38. 2.check for arterial blood lactate level 3.mixed venous oxygen saturation: It is a measure of oxygen saturation at right atrium It indicates the utilisation of oxygen by the organs Normal value is 70% In hypovolemic shock : blood volume is l,ow , so the oxygen is overutilized by the organs so M.V.O.S - < 50% In cardiogenic shock: blood volume is normal but heart cannot pump enough blood so oxygen is over utilized so M.V.O.S <50%

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