shock

classification & description based on guyton & baily & love

1. SHOCK DR .JOJI PETER 1 st YEAR POST GRADUATE ORAL & MAXILLOFACIAL SURGERY AJIDS

2. CONTENTS INTRODUCTION DEFINITION PHYSIOLOGIC CAUSES OF SHOCK THE STAGES OF SHOCK CLASSIFICATION OF SHOCK TREATMENT OF SHOCK CONCLUSION REFERENCE

3. INTRODUCTION Shock is considered as a dreaded medical complication or an emergency condition because of it’s complex nature , its severity & the complexity of its management & most of all its unpredictable nature of outcome. We should be in a position to recognise the type of shock & atleast render initial / emergency treatment until medical help can arrive.

4. DEFINED as . . . . Clinical state of circulatory collapse characterised by a reduction either in cardiac output or in the effective circulating blood volume resulting in hypotension followed by impaired tissue perfusion & cellular hypoxia ( Bailey & love’s Short Practice of Surgery, 24 th Ed.)

5. PHYSIOLOGIC CAUSES OF SHOCK Circulatory Shock Caused by Decreased C.O 1. Cardiac abnormalities that the ability of the heart to pump blood. M.I Severe heart valve dysfunction, heart arrhythmias 2. Factors that venous return & also C.O Diminished blood volume Circulatory Shock That Occurs Without Diminished C.O 1.Excessive metabolism of the body, so that even a normal C.O is inadequate 2.Abnormal tissue perfusion patterns, so that most of the C.O is passing through blood vessels besides those that supply the local tissues with nutrition.

6. What Happens to the Arterial Pressure in Circulatory Shock? The arterial pressure level - principal measure of adequacy of circulatory function . But it can often be seriously misleading . At times, a person may be in severe shock & still have an almost normal arterial pressure because of powerful nervous reflexes that keep the pressure from falling. At other times, the arterial pressure can fall to half of normal , but the person still has normal tissue perfusion & is not in shock. Mostly the Arterial B.P decreases at the same time as the C.O decreases

7. Relationship of Bleeding Volume to C.O & Arterial Pressure 10 % of the total blood volume can be removed with almost no effect on either arterial pressure or C.O , over a period of about 30 minutes. But greater blood loss usually diminishes the C.O 1 ST & later the Arterial pressure Both of which fall to 0 when about 35 -45 %of the total blood volume has been removed.

8. THE STAGES OF SHOCK

9. Demonstration of the effects of different degrees of sudden acute hemorrhage on the subsequent course of arterial pressure Circulatory system can recover as long as the degree of hemorrhage is no greater than a certain critical amount. Thus,hemorrhage beyond a certain critical level causes shock to become progressive. Ie , the shock itself causes still more shock , & the condition becomes a vicious circle deterioration of the circulation & to death

10. NONPROGRESSIVE SHOCK/ COMPENSATED SHOCK If shock is not severe enough to cause its own progression, the person eventually recovers . Therefore, shock of this lesser degree is called Nonprogressive shock It is also called Compensated shock , ie;sympathetic reflexes & other factors compensate enough to prevent further deterioration of the circulation.

11. Negative feedback control mechanisms of the circulation that attempt to return C.O & arterial pressure back to normal levels are: Rapid compensatory mechanism (neural mechanism) 1.Baroreceptor reflexes 2.Chemoreceptor reflexes 3.Central nervous system ischemic response Intermediate compensatory mechanism 4.Reverse stress-relaxation of the circulatory system 5.Formation of angiotensin by the kidneys 6.Formation of vasopressin (ADH) Long term compensatory mechanism 7.Compensatory mechanisms that return the blood volume back toward normal

12. PHYSIOLOGIC SYSTEMS ACTIVATED NERVOUS SYSTEM RENAL SYSTEM ENDOCRINE SYSTEM LOCAL REGULATION

13. NERVOUS SYSTEM Through VMC & Baroceptotor & chemoreceptors

14. 2.ARTERIOLES 1 3.ADRENAL MEDULLA

15. ↓ Blood flow ↓ Arterial pressure ↓O 2 ↑ CO 2 + H + Chemoreceptor stimulation ↓ Baroreceptor firing stimulation Vasoconstrictor area of VMC Vasoconstriction Via sympathetic vasoconstrictor fibres by release of nor- epinephrine Arterial pressure ↑ HR Reduced vagal activity ↓ tissue perfusion

16. RENAL SYSTEM Through Renin - Angiotensin mechanism

17. Blood pressure Angiotensinogen RENIN Angiotensin 1 Angiotensin 2 ACE JG CELLS OF KIDNEY IN LUNGS Aldosterone sectretion Adrenal cortex- Reabsorption of Na & H 2 O from renal tubules Vasoconstriction Blood pressure Blood vol

18. ENDOCRINE SYSTEM

19. Blood loss Arterial pressure Renin Catecholamines Adrenal medulla kidney ADH Baroreceptor stimulation Post. pituitary Angiotensin 2 Aldosterone Adrenal cortex Na & H 2 O Reabsor-ption from Renal tubules

20. LOCAL REGULATION Through local substances-vasoconstrictors

21. Blood vessel injury Stretching of blood vessel Endothelin secretion Phospholipase activation Thromboxane A 2 activation Vasoconstriction Arterial pressure

22. The sympathetic reflexes become activated within 30 seconds to a minute after hemorrhage The angiotensin and vasopressin mechanisms, as well as the reverse stress-relaxation that causes contraction of the blood vessels and venous reservoirs, all require 10 minutes to 1 hour to respond completely, but they aid greatly in increasing the arterial pressure or increasing the circulatory filling pressure and thereby increasing the return of blood to the heart.

23. Finally readjustment of blood volume by absorption of fluid from the interstitial spaces and intestinal tract, as well as oral ingestion and absorption of additional quantities of water and salt, may require from 1 to 48 hours , but recovery eventually takes place, provided the shock does not become severe enough to enter the progressive stage . But when this initial response (peripheral vasoconstriction) is prolonged & treatment is delayed ,it results in the following sequence of events.

24. “Progressive Shock” Is Caused by a Vicious Circle of Cardiovascular Deterioration Cardiac Depression Vasomotor Failure Blockage of Very Small Vessels—“ Sludged Blood.” Increased Capillary Permeability Release of Toxins by Ischemic Tissue Cardiac Depression Caused by Endotoxin Generalized Cellular Deterioration Tissue Necrosis in Severe Shock—Patchy Areas of Necrosis Occur Because of Patchy Blood Flows in Different Organs

25. Prolonged vasoconstriction Tissue anoxia Liver Kidney muscle Intestine Accumulation of metabolic waste Anerobic glycolysis Kidney injury Lactic acid Metabolic acidosis Arterioles sensitive to catecholamine vasodilatation Hydrostatic pressure Interstitial fluid Blood volume # inactivation of VDM Hemorrhagic necrosis Blood loss

26. Blood volume ischemia Capillary injury Vascular permeability Blood volume Cerebral ischemia Myocardial ischemia VM - depression Venous return Depression of cardiac function Cardiac output DECOMPENSATED SHOCK

27. REFRACTORY/IRREVERSIBLE SHOCK After shock has progressed to a certain stage,transfusion or any other type of therapy becomes incapable of saving the person’s life. The person is then said to be in the irreversible stage of shock. Ironically,even in this irreversible stage, therapy can , on rare occasions, return the arterial pressure & even the C.O to normal or near normal for short periods, but the circulatory system nevertheless continues to deteriorate , and death ensues in another few minutes to few hours.

28. Figure shows that transfusion during the irreversible stage can sometimes cause the C.O(as well as the arterial pressure) to return to normal. However, the C.O soon begins to fall again & subsequent transfusions have less & less effect. Multiple deteriorative changes in the muscle cells of the heart that may not necessarily affect the heart’s immediate ability to pump blood but, over a long period,depress heart pumping enough to cause death In severe shock,a stage is eventually reached at which the person will die even though vigorous therapy might still return the C.O to normal for short periods.

29. Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock. In severe degrees of shock -the high-energy phosphate reserves All the creatine phosphate -degraded, and almost all the ATP has downgraded to ADP, AMP and, eventually, adenosine. This adenosine diffuses out of the cells into the circulating blood & is converted into uric acid(cannot reenter the cells) New adenosine - synthesized at 2 % of the normal cellular amount an hour, ie;once stores are depleted, its difficult to replenish. Cellular depletion of high energy compounds causes most devastating end results & leads to irreversibe stage

30. CLASSIFICATION OF SHOCK Hypovolemic shock Cardiogenic shock Distributive shock Septic shock Anaphylactic shock Neurogenic shock Obstructive Shock

31. Most common type of shock in the victim of maxillofacial trauma. DEFINITION Defined as a medical condition in which rapid loss of intravascular blood or plasma volume results in multiple organ failure due to inadequate perfusion . HYPOVOLEMIC/ COLD SHOCK

32. HYPOVOLEMIC SHOCK HEMORRHAGIC SHOCK NONHEMORRHAGIC SHOCK

33. HEMORRHAGIC SHOCK Hemorrhage Filling pressure of the circulation venous return Cardiac output Blood pressure Velocity of blood flow Blood supply to vital organs,esp brain SHOCK

34. HYPOVOLEMIC SHOCK HEMORRHAGIC SHOCK- loss of intravascular blood External source Laceration Trauma Surgical procedure Internal source Gastrointestinal bleeding Femoral fracture Crush injury Ruptered internal organs Post partum hemorrhage “Physiologic response is proportional to volume of blood lost”

35. Clinical signs & staging of acute hemorrhagic shock % Blood loss Clinical signs < 15 Slightly increased heart rate, local swelling, skin- warm,compensate by baro -receptors mediated reflex , vasoconstriction, activation of renin-angiotensin mechanism 15-30 Tachycardia, increased diastolic blood pressure, prolonged capillary refill 30-50 Above findings plus: hypotension, acidosis, decreased urine output , skin-cool , pallor +, cns -lethargic > 50 Refractory hypotension, refractory acidosis, death ,cyanotic skin, thready central pulse, anuria , bradycardia

36. NON HEMORRHAGIC SHOCK Loss of plasma from intravascular compartment than the loss of whole blood Increased hemoconcentration Sluggish blood flow Decreased blood flow to brain Shock

37. Plasma due to shift of massive fluid from intravascular compartment to extravascular compartment Burns Crush injuries Peritonitis Pancreatitis Surgical wounds Pleural effusion Plasma due to dehydration Vomiting/diarrhea Urinary output in renal disease Adrenocortical insufficiency Excessive sweating Excessive diuretic use Diabetes insipidus

38. PATHOPHYSIOLOGY of HYPOVOLEMIC SHOCK Early stage -an attempt is made to maintain adequate cerebral & coronary blood supply by redistribution of blood so that the vital organs ( heart & brain ) are adequately perfused &oxygenated . ie . The heart may receive 25% of the C.O, as opposed to its normal 5% to 8% . Similarly the brain may receive as much as 80% of the C.O, instead of its usual 15% to 20%. Ie . Blood flow to heart & brain & blood flow to extremities, kidneys,skin,muscle & GI tract

39. If shock is adequately treated , recovery by the compensatory mechanism compensated / reversible shock . In hypovolemic shock a great outporing of epinephrine occurs leading to intense vasoconstriction. But this situation results in ischemic anoxia of the involved peripheral tissues in an all out effort to keep the heart & brain function for survival .

40. HISTORY History is vital in determining the possible cause . Symptoms - weakness, lightheadedness, confusion should be assessed In pt with trauma ,determine the mechanism of injury & information of vital organ injuries If conscious-pt may be able to indicate location of pain. In patient with GI bleeding enquire about hematemesis , melena , excessive NSAID use In case of burns , enquire about the type of burn &time of occurrence CLINICAL EVALUATION

41. SIGN & SYMPTOMS MILD HYPOVOLEMIA (<20% of blood loss) Mild tachycardia but relatively few external signs especially in a supine resting young patient Cool extremities Diaphoresis Anxiety MODERATE HYPOVOLEMIA (20-40% of blood loss) Pt becomes increasingly anxious & tachycardic Although normal blood pressure can be maintained in the supine position, there may be significant postural hypotension & tachycardia Mild oliguria SEVERE HYPOVOLEMIA (>40%) Blood pressure declines & unstable even in supine position Marked tachycardia Marked oliguria Mental status deterioration (coma) CLINICAL MANIFESTATION OF HYPOVOLEMIC SHOCK

42. Trauma examination –assess airway , breathing &circulation Later the circulatory system – evaluate signs & symptoms of shock Systolic BP should not be relied upon as main indicator. compensatory mechanism prevents the significant decrease in systolic BP until pt has lost 30% of blood volume. Attention should be paid to pulse, resp. rate & skin perfusion Pts on beta blockers may not have tachycardia regardless degree of shock Plasma loss hemoconcentration & free water loss hypernatremia . These findings should suggest the presence of hypovolemia

43. INVESTIGATION ACID-BASE STATUS Metabolic acidosis/decreased serum bicarbonate OXYGEN SATURATION COMPLETE BLOOD COUNT TC,DC, ESR, Peripheral smear , Hb % ELECTROLYTE LEVELS Na , K, Cl , HCO3 , blood urea, creatinine , Glucose levels ARTERIAL BLOOD GAS This test helps to determine PO 2 of blood , assisting in titration of supplemental oxygen delivery.

44. 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 MORE CAROIOGENIC SHOCK

45. Cardiogenic Shock : Etiologies Mechanical: complications of MI : Papillary Muscle Rupture Ventricular aneurysm Ventricular septal rupture Other causes: Cardiomyopathies Tamponade Tension pneumothorax Arrhythmias Valve disease

46. Cardiogenic Shock: Pathophysiology Impaired pumping ability of LV Decreased stroke volume Decreased CO Decreased BP Compensatory mechanism Decreased tissue perfusion !!!!

47. Cardiogenic Shock: Pathophysiology Impaired pumping ability of LV leads to… Inadequate systolic emptying Left ventricular filling pressures (preload ) Left atrial pressures Pulmonary capillary pressure Pulmonary interstitial & intraalveolar edema !!!!

48. CLINICAL ASSESSMENT Pulmonary & Peripheral Edema JVP Hypotension Tachypnea , Crackles PaO2 Urinary Output Mean arterial pressure below 70 mmhg compromises coronary perfusion (MAP = DBP + PP/3) PP=SPB-DPB

49. SEPTIC SHOCK Formerly known as “blood poisoning” Refers to a bacterial infection widely disseminated to many areas of the body, with the infection being borne through the blood from one tissue to another & causing extensive damage. Septic shock is extremely important to the clinician , because other than cardiogenic shock, septic shock is the most frequent cause of shock-related death in the modern hospital . SEPTIC SHOCK

50. TYPICAL CAUSES OF SEPTIC SHOCK 1. Peritonitis caused by spread of infection from the uterus & fallopian tubes, with instrumental abortion(unsterile conditions) 2. Peritonitis due rupture of the G.I system(intestinal disease & wounds) 3. Generalized bodily infection due spread of a skin infection such as streptococcal or staphylococcal infection. 4. Generalized gangrenous infection resulting specifically from gas gangrene bacilli, spreading first through peripheral tissues and finally by way of the blood to the internal organs, especially the liver. 5. Infection spreading into the blood from the kidney or urinary tract, often caused by colon bacilli.

51. SEPSIS Systemic Inflammatory Response Syndrome(SIRS ) manifested by : two or > of following: Temp > 38 O C or < 36 O C HR > 90/min RR > 20 or PaCO 2 < 32mmHg WBC > 12,000/cu mm Sepsis syndrome : SIRS with confirmed infectious process associated with organ failure or hypotension Septic shock : Sepsis with organ failure & Hypotension (SBP < 90 or > 40 fall from baseline) despite adequate fluid resuscitation

52. Pathophysiology of Septic shock Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses Endotoxins release inflammatory mediators (SIRS) Vasodilation & increase capillary permeability Shock due to alteration in peripheral circulation & massive dilation Cell walls of organisms

53. Clinical Presentation Septic Shock Two phases : “ Warm” shock - early phase ( hyperdynamic response,Vasodilation ) “ Cold” shock - late phase( hypodynamic response,Decompensated state) Early stages –no signs of circulatory collapse but signs of the bacterial infection positive Later the circulatory system usually becomes involved either because of direct extension of the infection or secondarily as a result of toxins from the bacteria,with resultant loss of plasma into the infected tissues through deteriorating blood capillary walls. Finally deterioration of the circulation becomes progressive as in other types of shock.

54. Clinical Manifestations 1. High fever. 2. Often marked vasodilation throughout the body, especially in the infected tissues. 3. High C.O caused by arteriolar dilation in the infected tissues & by high metabolic rate & vasodilation elsewhere in the body, resulting from bacterial toxin stimulation of cellular metabolism & from high body temperature. 4. Sludging of the blood caused by red cell agglutination in response to degenerating tissues. 5. Development of micro–blood clots in widespread areas of the body, a condition called DIC. Also, this causes the blood clotting factors to be used up, so that hemorrhaging occurs in many tissues, especially in the gut wall of the intestinal tract.

55. Mortality Increases in Septic Shock Patients 7-17% Sepsis 400,000 20-53% Severe Sepsis 300,000 Septic Shock 53-63%

56. ANAPHYLACTIC SHOCK Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement IgE mediated Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure Not IgE mediated ANAPHYLATIC SHOCK

57. Anaphylactic Response Vasodilatation Increased vascular permeability Bronchoconstriction Increased mucus production Increased inflammatory mediators recruitment to sites of antigen interaction

58. CLINICALMANIFESTATIONS OF ANAPHYLACTIC SHOCK

59. SIGNS & SYMPTOMS 1. Skin reactions GI disturbances Respiratory disturbances Cardiovascular collapse

60. 1.SKIN REACTIONS Feeling of impending doom sweating flushing conjunctivitis urticaria Pruritis rhinitis

61. 2. GI DISTURBANCES 1.Severe abdominal cramps 2.Nausea & vomiting 3.Diarrhea 4.Fecal & urinary incontinence

62. 3. RESPIRATORY DISTURBANCES 4.Laryngeal edema- stridor 1.Bronchospasm- wheezing 2.dyspnea 3.Cyanosis of nail beds & mucosa

63. 4. CARDIOVASCULAR DISTURBANCES Tachycardia Palpitations 3. Hypotension 4. Cardiac arrhythmias 6. Cardiac arrest 5. Loss of consciousness

64. 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,  C.O. Most common etiology : Spinal cord injury above T6 NEUROGENIC SHOCK IS THE RAREST FORM OF SHOCK! NEUROGENIC SHOCK

65. Pathophysiology of Neurogenic Shock Disruption of sympathetic nervous system Loss of sympathetic tone Venous &arterial vasodilation Decreased venous return Decreased stroke volume Decreased cardiac output Decreased cellular oxygen supply Impaired tissue perfusion Impaired cellular metabolism

66. OBSTRUCTIVE SHOCK A.K.A Extracardiac Obstructive Shock Due to impairment of ventricular filling during diastole due to some external pressure on heart ventricular filling C.O CAUSES Pericardial temponade Tension pneumothorax Constrictive pericarditis Pulmonary embolism OBSTRUCTIVE SHOCK

67. TREATMENT OF SHOCK

68. 1. PREHOSPITAL CARE Prevention of further injury & transportation of patient to hospital as rapidly as possible Prehospital intervention includes Immobilization of the patient Securing adequate airway Ensuring ventilation Maximizing circulation

69. 2. Maximise O 2 delivery Pts airway should be assessed immediately. Depth &rate of respiration assessed. Any pathology that interferes should be addressed immediately High flow supplemental oxygen administered & ventilatory support given

70. Physiology of Treatment in Shock REPLACEMENT THERAPY Blood and Plasma Transfusion. Shock caused by hemorrhage -best possible therapy -transfusion of whole blood. Shock caused by plasma loss-the best therapy is administration of plasma. When dehydration is the cause-provide -appropriate electrolyte solution

71. When Whole blood is unavailable-( battlefield conditions) Plasma can usually substitute adequately for whole blood because it increases the blood volume and restores normal hemodynamics . Plasma cannot restore a normal hematocrit , but the human body can usually stand a decrease in hematocrit to about half of normal before serious consequences result, if C.O is adequate. When plasma is unavailable-plasma substitutes - - dextran solution

72. DEXTRAN SOLUTION AS A PLASMA SUBSTITUTE. Principal requirement of Plasma substitute is that it remain in the circulatory system— Ie , it shouldnot filter through the capillary pores into the tissue spaces for which it must contain substance with large molecular size to exert colloid osmotic pressure. Eg : dextran - a large polysaccharide polymer of glucose Must be nontoxic and Must contain appropriate electrolytes to prevent derangement of the body’s extracellular fluid electrolytes on administration.

73. Treatment of Shock with Sympathomimetic Drugs—Sometimes Useful, Sometimes Not A sympathomimetic drug -mimics sympathetic stimulation. Eg:norepinephrine , epinephrine, 1.In neurogenic shock, in which the sympathetic nervous system is severely depressed.Administering a sympathomimetic drug takes the place of the diminished sympathetic actions and can often restore full circulatory function. 2.In anaphylactic shock, in which excess histamine plays a prominent role. The sympathomimetic drugs have a vasoconstrictor effect that opposes the vasodilating effect of histamine. Therefore, either norepinephrine or another sympathomimetic drug is often lifesaving . 3.In Hemorrhagic shock it is Not valuable because the sympathetic nervous system is almost always maximally activated by the circulatory reflexes ,so much norepinephrine and epinephrine are already circulating in the blood that sympathomimetic drugs have essentially no additional beneficial effect.

74. OTHER THERAPY TREATMENT BY THE HEAD-DOWN POSITION . in hemorrhagic and neurogenic shock when BP is too low,placing the patient in trendenlenburg position promotes venous return, thereby also increasing C.O. First essential step in the treatment of many types of shock. OXYGEN THERAPY. Frequently is far less beneficial,because the problem in most types of shock is not inadequate oxygenation of the blood by the lungs but inadequate transport of the blood after it is oxygenated

75. Treatment with Glucocorticoids (Adrenal Cortex Hormones That Control Glucose Metabolism). (1) glucocorticoids frequently increase the strength of the heart in the late stages of shock; (2) glucocorticoids stabilize lysosomes in tissue cells and thereby prevent release of lysosomal enzymes into the cytoplasm of the cells, thus preventing deterioration from this source; and (3) glucocorticoids might aid in the metabolism of glucose by the severely damaged cells.

76. Conclusion Life threatening: Early goal directed therapy and regular monitoring by trained staff will change outcome. Early detection : DON’T RELY ON BP High index of suspicion Monitor casualties susceptible to shock