Shock is a condition where the cardiovascular system fails to adequately perfuse tissues. It can be caused by an impaired pump (cardiogenic shock), reduced circulating volume (hypovolemic shock), or maldistribution of blood flow (distributive shock). The main effects are cellular hypoxia, impaired metabolism, and organ damage or failure if not treated. Compensatory mechanisms aim to increase perfusion but eventually fail, leading to irreversible cellular damage and death if shock persists.

1. SHOCKPATHOPHYSIOLOGY

2. shockShockis a condition in which the cardiovascular system fails to perfuse tissues adequatelyAn impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues

3. ShockInadequate tissue perfusion can result in: generalized cellular hypoxia (starvation)

4. widespread impairment of cellular metabolism

5. Tissue damage organ failure

6. deathPathophysiology of shockImpaired tissue perfusion occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand. All Types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome.

7. PATHOPHYSIOLOGYCells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & swells membrane becomes more permeable electrolytes & fluids seep in & out of cellNa+/K+ pump impairedmitochondria damagecell death

8. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response SNS - Neurohormonal response Stimulated by baroreceptorsIncreased heart rate Increased contractility Vasoconstriction (Afterload) Increased Preload

9. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response SNS - Hormonal: Renin-angiotension systemDecrease renal perfusion Releases renin angiotension I angiotension II potent vasoconstriction & releases aldosterone adrenal cortex sodium & water retention ( intravascular volume )

10. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response SNS - Hormonal: Antidiuretic HormoneOsmoreceptors in hypothalamus stimulated ADH released by Posterior pituitary gland Vasopressor effect to increase BP Acts on renal tubules to retain water

11. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response SNS - Hormonal: Adrenal Cortex Anterior pituitary releases adrenocorticotropic hormone (ACTH) Stimulates adrenal Cx to release glucorticoids Blood sugar increases to meet increased metabolic needs

12. Failure of Compensatory ResponseDecreased blood flow to the tissues causes cellular hypoxia

13. Anaerobic metabolism begins

14. Cell swelling, mitochondrial disruption, and eventual cell death

15. If Low Perfusion States persists:IRREVERSIBLE DEATH IMMINENT!!

16. Stages of Shock❇Initial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building❇Compensatory stage - Reversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion. ❇Progressive stage - Failingcompensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high metabolic acidosis❇Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndromemay occur DEATH IS IMMINENT!!!!

17. Pathophysiology Systemic Level Net results of cellular shock:decreased myocardial contractility

18. systemic lactic acidosis

19. decreased vascular tone

20. decrease blood pressure, preload, and cardiac outputClinical Presentation: Generalized ShockVital signs

21. Hypotensive: (may be WNL or due to compensatory mechanism)

22. MAP

23. Tachycardia: Weak and Thready pulse

24. Tachypneic : blow off CO2 Respiratory alkalosisClinical Presentation: Generalized ShockMental status: (LOC)restless, irritable, apprehensive unresponsiveDecreased Urine output

25. Shock Syndromes Hypovolemic Shockblood VOLUMEproblem Cardiogenic Shockblood PUMP problem Distributive Shock [septic;anaphylactic;neurogenic]blood VESSEL problem

26. HYPOVOLEMIC SHOCK Loss of circulating volume “Empty tank ” decrease tissue perfusion general shock response ETIOLOGY: Internal or External fluid lossIntracellular and extracellular compartments Most common causes:HemmorhageDehydration

27. External loss of fluid Fluid loss: DehydrationNausea & vomiting, diarrhea, massive diuresis, extensive burns Blood loss: trauma: blunt and penetratingBLOOD YOU SEEBLOOD YOU DON’T SEE

28. Internal fluid lossLoss of Intravascular integrityIncreased capillary membrane permeabilityDecreased Colloidal Osmotic Pressure (third spacing)

29. Pathophysiology of Hypovolemic ShockDecreased intravascular volume leads to…. Decreased venous return (Preload, RAP) leads to... Decreased ventricular filling (Preload, PAWP) leads to…. Decreased stroke volume (HR, Preload, & Afterload) leads to ….. Decreased CO leads to...(Compensatory mechanisms)Inadequate tissue perfusion!!!!Assessment & ManagementS/S vary depending on severity of fluid loss:15%[750ml]- compensatory mechanism maintains CO15-30% [750-1500ml- Hypoxemia, decreased BP & UOP30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis40-50% - refactory stage: loss of volume= death

30. Clinical PresentationHypovolemic ShockTachycardia and tachypneaWeak, thready pulsesHypotension Skin cool & clammyMental status changesDecreased urine output: dark & concentrated

31. Initial Management Hypovolemic ShockManagement goal:Restore circulating volume, tissue perfusion, & correct cause:Early Recognition- Do not relay on BP! (30% fld loss)Control hemorrhageRestore circulating volumeOptimize oxygen deliveryVasoconstrictor if BP still low after volume loading

32. The impaired ability of the heart to pump bloodPump failure of the right or left ventricleMost common cause is LV MI (Anterior)Occurs when > 40% of ventricular mass damageMortality rate of 80 % or MORECAROIOGENIC SHOCK

33. Cardiogenic Shock : EtiologiesOther causes:Cardiomyopathiestamponadetension pneumothoraxarrhythmiasvalve diseaseMechanical: complications of MI:Papillary Muscle RuptureVentricular aneurysmVentricular septal rupture

34. Cardiogenic Shock: PathophysiologyImpaired pumping ability of LV leads to…Decreased stroke volume leads to…..

35. Decreased CO leads to …..

36. Decreased BP leads to…..

37. Compensatory mechanism which may lead to

38. Decreased tissue perfusion !!!!Cardiogenic Shock: PathophysiologyImpaired pumping ability of LV leads to…Inadequate systolic emptying leads to ...

39. Left ventricular filling pressures (preload) leads to...

40. Left atrial pressures leads to ….

41. Pulmonary capillary pressure leads to …

42. Pulmonary interstitial & intraalveolar edema !!!!Clinical PresentationCardiogenic ShockSimilar catecholamine compensation changes in generalized shock & hypovolemic shockMay not show typical tachycardic response :if pt on Beta blockers, in heart block, or if bradycardic in response to nodal tissue ischemiaMean arterial pressure below 70 mmHg compromises coronary perfusion(MAP = SBP + (2) DBP/3)

43. Clinical PresentationCardiogenic ShockPericardial tamponademuffled heart tones, elevated neck veinsTension pneumothoraxJVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side

44. CLINICAL ASSESSMENTPulmonary & Peripheral Edema JVD CO HypotensionTachypnea, Crackles PaO2 UOP LOC

45. MANAGEMENT Goal of management :Treat Reversible CausesProtect ischemic myocardiumImprove tissue perfusionEarly assessment & treatment!!!Optimizing pump by:Increasing myocardial O2 deliveryMaximizing CODecreasing LV workload (Afterload)

46. MANAGEMENTLimiting/reducing myocardial damage during Myocardial Infarction:Increased pumping action & decrease workload of the heartInotropic agentsVasoactive drugsIntra-aortic balloon pumpCautious administration of fluidsTransplantationConsider thrombolytics, angioplasty in specific cases

47. Management Cardiogenic ShockOPTIMIZING PUMP FUNCTION:Pulmonary artery monitoring is a necessity !!Aggressive airway management: Mechanical VentilationJudicious fluid managementVasoactive agentsDobutamineDopamine

48. Management Cardiogenic ShockOPTIMIZING PUMP FUNCTION (CONT.):Morphine as needed (Decreases preload, anxiety)Cautious use of diuretics in CHFVasodilators as needed for afterload reductionShort acting beta blocker, for refractory tachycardia

49. Inadequate perfusion of tissues through maldistribution of blood flowIntravascular volume is maldistributed because of alterations in blood vesselsCardiac pump & blood volume are normal but blood is not reaching the tissuesDISTRIBUTIVE SHOCK

50. Vasogenic/Distributive ShockEtiologiesSeptic Shock (Most Common)Anaphylactic Shock Neurogenic Shock

51. Anaphylactic ShockA type of distributive shock that results from widespread systemic allergic reaction to an antigenThis hypersensitive reaction isLIFE THREATENING

52. Pathophysiology Anaphylactic ShockAntigen exposurebody stimulated to produce IgE antibodies specific to antigendrugs, bites, contrast, blood, foods, vaccinesReexposure to antigenIgE binds to mast cells and basophilsAnaphylactic response

53. Anaphylactic ResponseVasodilatationIncreased vascular permeabilityBronchoconstrictionIncreased mucus productionIncreased inflammatory mediators recruitment to sites of antigen interaction

54. Clinical Presentation Anaphylactic ShockAlmost immediate response to inciting antigenCutaneous manifestationsurticaria, erythema, pruritis, angioedemaRespiratory compromisestridor, wheezing, bronchorrhea, resp. distressCirculatory collapsetachycardia, vasodilation, hypotension

55. Management Anaphylactic ShockEarly Recognition, treat aggressively AIRWAY SUPPORTIV EPINEPHRINE (open airways)AntihistaminesCorticosteroids IMMEDIATE WITHDRAWAL OF ANTIGEN IF POSSIBLEPREVENTION

56. Management Anaphylactic ShockJudicious crystalloid administration Vasopressors to maintain organ perfusionPositive inotropesPatient education

57. NEUROGENIC SHOCKA type of distributive shock that results from the loss or suppression of sympathetic toneCauses massive vasodilatation in the venous vasculature,  venous return to heart,  cardiac output.Most common etiology: Spinal cord injury above T6 Neurogenic is the rarest form of shock!

58. Pathophysiology of Neurogenic ShockDisruption of sympathetic nervous systemLoss of sympathetic toneVenous and arterial vasodilationDecreased venous returnDecreased stroke volumeDecreased cardiac outputDecreased cellular oxygen supplyImpaired tissue perfusionImpaired cellular metabolism

59. Assessment, Diagnosis and Management of Neurogenic ShockPATIENT ASSESSMENTHypotensionBradycardiaHypothermiaWarm, dry skinCO Flaccid paralysis below level of the spinal lesionMEDICAL MANAGEMENTGoals of Therapy are to treat or remove the cause & prevent cardiovascular instability, & promote optimal tissue perfusion

60. MANAGEMENT OF NEUROGENIC SHOCKHypovolemia- RX with careful fluid replacement for BP Changes in LOCObserve closely for fluid overload

61. Vasopressors may be needed

62. Hypothermia- warming avoid large swings in pts body temperatureTreat Hypoxia

63. Maintain ventilatory supportMANAGEMENT OF NEUROGENIC SHOCKObserve for Bradycardia-major dysrhythmiaObserve for DVT- venous pooling in extremities make patients high-risk>>P.E.Use prevention modalities [TEDS,anticoagulation]