1. “AN APPROACH TO A PATIENT IN SHOCK” DR NAILA NAZ HOUSE OFFICER MU 1 Dated:6 th Sept’06

2. REFERENCES: ► James Allen, M.D. Professor of Internal Medicine Pulmonary and Critical Care Medicine Ohio State University ► Principles and practice of medicine by Davidson. ► Current Concepts on the Management of Shock by Max H. WeiL M.D., PH.D.

3. GOALS: ► Definition..? ► Pathophysiology ► Etiology ► Stages ► Shock syndromes ► Management!!

4. SHOCK ► DEFINITION: “a condition in which the cardiovascular system fails to perfuse tissues adequately” “a condition in which the cardiovascular system fails to perfuse tissues adequately” ► An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues

5. ► Inadequate tissue perfusion can result in: -generalized cellular hypoxia (starvation) -generalized cellular hypoxia (starvation) -widespread impairment of cellular metabolism -widespread impairment of cellular metabolism -tissue damage -tissue damage -organ failure -organ failure - death - death

6. PATHOPHYSIOLOGY ► Impaired 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. Cells switch from aerobic to anaerobic metabolism Cells switch from aerobic to anaerobic metabolism lactic acid production lactic acid production Cell function ceases & swells Cell function ceases & swells membrane becomes more permeable membrane becomes more permeable electrolytes & fluids seep in & out of cell electrolytes & fluids seep in & out of cell Na+/K+ pump impaired Na+/K+ pump impaired mitochondria damage mitochondria damage cell death cell death

8. COMPENSATORY MECHANISMS “Sympathetic Nervous System (SNS)- Adrenal Response” “Sympathetic Nervous System (SNS)- Adrenal Response” ► Neurohormonal response ► Hormonal Renin-angiotension system Renin-angiotension system Antidiuretic Hormone Antidiuretic Hormone Adrenal cortex Adrenal cortex

9. NEUROHORMONAL RESPONSE ► Stimulated by baroreceptors ► Increased heart rate ► Increased contractility ► Vasoconstriction (SVR-Afterload) ► Increased Preload

10. RENIN-ANGIOTENSIN SYSTEM ► Decrease renal perfusion ► Releases renin angiotension I ► angiotension II…potent vasoconstriction & ► releases aldosterone adrenal cortex ► sodium & water retention

11. ANTIDIURETIC HORMONE ► Osmoreceptors in hypothalamus stimulated ► ADH released by Posterior pituitary gland  Vasopressor effect to increase BP  Acts on renal tubules to retain water  Acts on renal tubules to retain water

12. ADRENAL CORTEX ► Anterior pituitary releases adrenocorticotropic hormone (ACTH) ► Stimulates adrenal Cx to release glucorticoids ► Blood sugar increases to meet increased metabolic needs

13. FAILURE OF COMPENSATORY RESPONSE ► Decreased blood flow to the tissues causes cellular hypoxia ► Anaerobic metabolism begins ► Cell swelling, mitochondrial disruption, and eventual cell death ► Cell swelling, mitochondrial disruption, and eventual cell death

14. ► If Low Perfusion States persists: ► If Low Perfusion States persists: “IRREVERSIBLE DEATH IMMINENT”!! “IRREVERSIBLE DEATH IMMINENT”!!

15. STAGES OF SHOCK ► Initial stage ► Compensatory stage ► Progressive stage ► Irreversible or refractory stage

16. INITIAL STAGE ► Tissues are under perfused ► Decreased CO ► Increased anaerobic metabolism ► Lactic acid is building

17. COMPENSATORY STAGE ► Reversible. ► SNS activated by low CO..attempting to compensate for the decrease tissue perfusion.

18. PROGRESSIVE STAGE ► Failing compensatory mechanisms.. profound vasoconstriction from the SNS ► Failing compensatory mechanisms.. profound vasoconstriction from the SNS ► Ischemia ► Lactic acid production is high ► Lactic acid production is high ► metabolic acidosis

19. REFRACTORY STAGE ► Irreversible ► Cellular necrosis ► Multiple Organ Dysfunction Syndrome may occur ► Multiple Organ Dysfunction Syndrome may occur

20. ETIOLOGY OF SHOCK 1.Cardiogenic a) acute myocardial infarction (implies > 40% LV muscle loss) -shock accompanies 6-20% of all acute MI's -shock accompanies 6-20% of all acute MI's -more common with patients with anterior MI -more common with patients with anterior MI

21. b) dilated cardiomyopathy c) acute myocarditis d) mechanical -mitral regurgitation -mitral regurgitation -ventricular septal defect -ventricular septal defect -left ventricular aneurysm -left ventricular aneurysm -left ventricular outflow obstruction -left ventricular outflow obstruction e) metabolic and pharmacologic myocardial depression f) arrhythmias

22. 2.Extracardiac Obstructive 2.Extracardiac Obstructive a- massive pulmonary embolism a- massive pulmonary embolism b- severe pulmonary hypertension b- severe pulmonary hypertension c- pericardial tamponade c- pericardial tamponade d- tension pneumothorax d- tension pneumothorax

23. 3.Oligemic a) hemorrhagic a) hemorrhagic b) volume depletion b) volume depletion c) adrenal insufficiency c) adrenal insufficiency

24. 4.Distributive a) septic a) septic b) toxic agents (including adverse reaction to medications and certain drug overdoses) b) toxic agents (including adverse reaction to medications and certain drug overdoses) c) anaphylaxis c) anaphylaxis d) neurogenic d) neurogenic

25. CLINICAL MANIFESTATIONS

26. SHOCK SYNDROMES ► Hypovolemic Shock blood VOLUME problem blood VOLUME problem ► Cardiogenic Shock blood PUMP problem blood PUMP problem ► Distributive Shock blood VESSEL problem blood VESSEL problem

27. HYPOVOLEMIC SHOCK ► Loss of circulating volume “Empty tank” ► ETIOLOGY:  Internal or External fluid loss  Intracellular and extracellular compartments ► Most common causes:  Hemmorhage  Dehydration

28. CLINICAL MANIFESTATIONS ► Tachycardia and tachypnea ► Weak, thready pulses ► Hypotension ► Skin cool & clammy ► Mental status changes ► Decreased urine output: dark & concentrated

29. ASSESMENT OF SEVERITY ► S/S vary depending on severity of fluid loss: 15%(750ml) compensatory mechanism maintains CO compensatory mechanism maintains CO 15-30% (750-1500ml) 15-30% (750-1500ml) Hypoxemia, decreased BP & UOP Hypoxemia, decreased BP & UOP 30-40% (1500-2000ml) 30-40% (1500-2000ml) Impaired compensation & profound shock along with severe acidosis Impaired compensation & profound shock along with severe acidosis 40-50% 40-50% refractory stage: refractory stage: loss of volume loss of volume death death

30. MANAGEMENT OF HYPOVOLEMIC SHOCK ► Goal: Restore circulating volume, tissue perfusion and correct cause. Restore circulating volume, tissue perfusion and correct cause. ► Early Recognition- Do not relay on BP! (30% fluid loss) ► Control hemorrhage ► Restore circulating volume ► Optimize oxygen delivery ► Vasoconstrictor.. if BP still low after volume loading

31. CARDIOGENIC SHOCK “The impaired ability of the heart to pump blood” “The impaired ability of the heart to pump blood” ► Pump failure of the right or left ventricle ► Most common cause is LV MI (Anterior) ► Occurs when > 40% of ventricular mass damage ► Mortality rate of 80 % or >

32. CLINICAL MANIFESTATIONS ► Abnormal heart sounds ► Abnormal heart sounds -Murmurs -Murmurs -Pathologic S3 (ventricular gallop) -Pathologic S3 (ventricular gallop) -Pathologic S4 (atrial gallop) -Pathologic S4 (atrial gallop) ► Pericardial tamponade -muffled heart tones -muffled heart tones -elevated neck veins -elevated neck veins

33. ► Tension pneumothorax - JVP - JVP - tracheal deviation - tracheal deviation - decreased or absent unilateral breath sounds - decreased or absent unilateral breath sounds - chest hyperresonance on affected side - chest hyperresonance on affected side

34. MANAGEMENT OF CARDIOGENIC SHOCK ► Goal of management : ► Treat Reversible Causes ► Protect ischemic myocardium ► Improve tissue perfusion

35. MANAGEMENT ► Increased pumping action & decrease workload of the heart ► Inotropic agents ► Vasoactive drugs ► Intra-aortic balloon pump ► Cautious administration of fluids ► Transplantation ► Consider thrombolytics, angioplasty in specific cases

36. ► Optimizing pumping function of the heart  Pulmonary artery monitoring is a necessity !!  Aggressive airway management: Mechanical Ventilation  Judicious fluid management  Vasoactive agents ► Dobutamine ► Dopamine

37.  Morphine as needed (Decreases preload, anxiety)  Cautious use of diuretics in CHF  Vasodilators as needed for afterload reduction  Short acting beta blocker, esmolol, for refractory tachycardia

38. DISTRIBUTIVE SHOCK ► Inadequate perfusion of tissues through maldistribution of blood flow ► Intravascular volume is maldistributed because of alterations in blood vessels ► Cardiac pump & blood volume are normal but blood is not reaching the tissues

39. ► ETIOLOGY: ► Septic Shock (Most Common) ► Anaphylactic Shock ► Neurogenic Shock

40. SEPTIC SHOCK ► SEPSIS “Systemic Inflammatory Response (SIRS) to INFECTION manifested by two or > of following: “Systemic Inflammatory Response (SIRS) to INFECTION manifested by two or > of following: 1. Temp > 38 or 38 or < 36 centigrade 2. HR > 90 2. HR > 90 3. RR > 20 or PaCO2 20 or PaCO2 < 32 4. WBC > 12,000/cu mm or > 10% Bands (immature wbc) “ 4. WBC > 12,000/cu mm or > 10% Bands (immature wbc) “

41. ► SEPTIC SHOCK: ► Sepsis with: ► Hypotension (SBP 40 reduction from baseline) & ► Tissue perfusion abnormalities invasion of the body by microorganisms & failure of body’s defense mechanism.

42. PATHOPHYSIOLOGY OF SEPTIC SHOCK ► Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses ► Microorganisms enter body ► Mediator Release ► Activation of Complement, kallikrein / kinin/ coagulation & fibrinolytic factors platelets, neutrophils & macrophages…damage to endothelial cells. ► ORGAN DYSFUNCTION ► ORGAN DYSFUNCTION

43. CLINICAL PRESENTATION ► Two phases:  “Warm” shock - early phase ► hyperdynamic response, VASODILATION  “Cold” shock - late phase ► hypodynamic response ► DECOMPENSATED STATE ► DECOMPENSATED STATE

44. MANAGEMENT OF SEPTIC SHOCK ► Prevention !!! ► Find and kill the source of the infection ► Fluid Resuscitation ► Vasoconstrictors ► Inotropic drugs

45. ANAPHYLACTIC SHOCK ► A type of distributive shock that results from widespread systemic allergic reaction to an antigen ► This hypersensitive reaction is LIFE THREATENING.

46. CLINICAL MANIFESTATIONS ► Almost immediate response to inciting antigen ► Cutaneous manifestations  urticaria, erythema, pruritis, angioedema ► Respiratory compromise  stridor, wheezing, bronchorrhea, resp. distress ► Circulatory collapse  tachycardia, vasodilation, hypotension  tachycardia, vasodilation, hypotension

47. MANAGEMENT ► Early Recognition, treat aggressively ► AIRWAY SUPPORT ► IV EPINEPHRINE (open airways) ► Antihistamines, diphenhydramine 50 mg IV ► Corticosteroids ► IMMEDIATE WITHDRAWAL OF ANTIGEN IF POSSIBLE ► PREVENTION ► PREVENTION ► Judicious crystalloid administration ► Vasopressors to maintain organ perfusion ► Positive inotropes ► Patient education ► Patient education

48. NEUROGENIC SHOCK ► A type of distributive shock that results from the loss or suppression of sympathetic tone ► Causes 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! ► Neurogenic is the rarest form of shock!

49. CLINICAL MANIFESTATION ► Hypotension ► Bradycardia ► Hypothermia ► Warm, dry skin ► PAWP ► CO ► Flaccid paralysis below level of the spinal lesion

50. MANAGEMENT ► Hypovolemia- careful fluid replacement for BP<90mmHg, UO<30cc/hr ► Observe closely for fluid overload ► Vasopressors may be needed ► Hypothermia ► Treat Hypoxia ► Maintain ventilatory support ► Maintain ventilatory support

51. ► Observe for Bradycardia-major dysrhythmia…atropine 0.5-1 mg doses to maximum 3 mg ► Observe for DVT- venous pooling in extremities make patients high-risk..P.E. ► Alpha agonist to augment tone if perfusion still inadequate  dopamine  ephedrine

52. CLINICAL ANAYSIS OF SHOCK

53. SUMMARY ► Identify the patient at high risk for shock ► Control or eliminate the cause ► Implement measures to enhance tissue perfusion ► Correct acid base imbalance ► Treat cardiac dysrhythmias

54. THANKS!! THANKS!!