Approach to a patient in shock

management of shock

1. SEMINAR APPROACH TO A PATIENT IN SHOCK GUIDE S: DR.A.PAL DR.S.SIDDIQUE BY : DR.ANKUR KAUSHIK

2. Shock is the physiologic state characterized by significant reduction of systemic tissue perfusion, resulting in decreased tissue oxygen delivery. This creates an imbalance between oxygen delivery and oxygen consumption. Prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at the cellular level, which can progress to the systemic level. DEFINITION

3. Hypovolemic Traumatic Cardiogenic Intrinsic Compressive Septic Hyperdynamic (early) Hypodynamic (late) Neurogenic Hypoadrenal CLASSIFICATION OF SHOCK

4. PATHOPHYSIOLOGY OF SHOCK

5. PATHOPHYSIOLOGY MICROCIRCULATION Mean Arterial Pressure (MAP) is dependent on two variables Cardiac Output (CO) Systemic Vascular Resistance (SVR) MAP in shock drops to less than <70 mmHg Α1 receptor mediate vasoconstriction, B2 receptors mediate vasodilation. Norepinepherine acts on A1 receptor, is one of the most fundamental pathway in reduced perfusion pressure.

6. OTHER VASOCONSTRICTOR SUBSTANCES Angiotensin II Vasopressin Endothelin I Thromboxane A2 CIRCULATORY VASODILATORS PGI2 NO PATHOPHYSIOLOGY MICROCIRCULATION

7. Parameters controlling stroke volume Ventricular filling (Preload) Resistance to Ventricular ejection (Afterload) Myocardial contractility CO=SV x HR Myocardial compliance is impaired in shock. Decreased preload Increased filling pressure – lead to secretion of BNP PATHOPHYSIOLOGY CARDIOVASCULAR RESPONSE

8. HEMODYNAMICS OF SHOCK

9. PULMONARY RESPONSE Increased Pulmonary vascular resistance Tachypnea Decreased tidal volume and increased dead space and minute ventilation RENAL RESPONSE ATN PATHOPHYSIOLOGY

10. Elevated Lactate/Pyruvate ratio Significant rise in Triglyceride levels Increased protein catabolism Increased production of glucose PATHOPHYSIOLOGY METABOLIC DERANGEMENTS

11. Activation of compliment cascade (Both classical and alternate pathways) Activation of coagulation pathways Activation of Eicosanoids- Cyclooxygenase derived PGs, Thromboxane A2 and cysteinyl leukotrienes TNF-A - causes hypotension, lactic acidosis and respiratory failure Interleukin 1b PATHOPHYSIOLOGY INFLAMMATORY RESPONSES

12. Compensated shock Decompensated shock Irreversible shock STAGES OF SHOCK

13. Compensatory mechanisms attempts to maintain BP NORMAL BLOOD PRESSURE Unexplained tachycardia Mild tachypnea Delayed capillary refill Orthostatic changes in pressure or pulse irritability COMPENSATED SHOCK

14. Baroreceptors and Chemoreceptors- Disinhibits vasomotor centers which increases adrenergic output Renin- Angiotension system- Angiotensin I and Angiotensin II Antidiuretic Hormone Adrenal Cortex- Aldosterone Posterior Pituitary- Vasopressin ACTH from pituitary- Cortisol COMPENSATORY MECHANISMS

15. It is a state of inadequate end-organ perfusion Compensatory mechanisms fails and HYPOTENSION occurs. Increased tachycardia, increased tachypnea Altered mental state, low urine output, Poor peripheral pulses. Capillary refill markedly delayed Cool extremities DECOMPENSATED SHOCK

16. It occurs as a consequence of decompensated shock not managed properly and at right time. Permanent cellular damage & MODS. Recovery does not occur even with adequate restoration of circulatory volume Death occurs due to refractory acidosis, myocardial and brain ischemia. IRREVERSIBLE SHOCK

17. LOOK FOR SIGNS OF SHOCK Heart Rate: Tachycardia is defined as : Adult : >100 School age: > 120 Preschool : >140 Infant : > 160 (Tachycardia in the elderly may be limited by reduced cardiac reserve, Beta Blockers, pacemakers, so we use narrow pulse pressure to suggest shock) Blood Pressure: Sole reliance on BP may miss early diagnosis of shock because of compensatory mechanisms Respiratory rate: There is tachypnea Altered mental status/Loss of consciousness Pulse pressure: Pulse pressure is narrow (<30 mmHg) Skin: Cold and clumsy or warm urine output: decreased IDENTIFICATION OF TYPE OF SHOCK

18. Decreased consciousness or looks ill HR > 100/min RR > 24/min or PCO2 < 32 mmHg Base Deficit < - 5   mEq /L or lactate > 4 mmol /L Urine output < 0.5 ml/kg/ hr Hypotension (SBP <90 mmHg) > 20 min duration Empiric Criteria for Diagnosis of Shock (Need at least 4)

19. Targeted History Chest pain : MI, Pulmonary Embolism , aortic dissection Trauma : hemorrhage, tamponade , pneumothorax , spinal Immunocompromised /fever : septic Medications : pharmacologic, cardiodepression ; CHRONIC STEROIDS is a clue to adrenal crisis Hemorrhagic :Melena , hematemasis , hemoptysis, hematuria, variceal bleed: GI loss: Vomiting , diarrhea Abdominal pain: pancreatitis, bowel perforation, intestinal ischemia, ectopic rupture,inflammation , sepsis, third spacing, AAA rupture Back pain: AAA rupture Exposures : inhalation, drugs, hypo/hyperthermia, dyshemoglobinopathy APPROACH TO UNDIFFERENTIATED SHOCK

20. General Examination: Level of consciousness, responsiveness, toxic looking, cyanosis. Patient should be fully exposed. Look for evidence of trauma, smell of alcohol etc , raised JVP. Chest : Auscultate for pulmonary edema ( rales ), wheezing with anaphylaxis, Air entry for evidence of pneumothorax or hydrothorax CVS : muffled HS, new murmur. PA: solid organ tenderness, evidence of trauma, peritonitis, AAA CNS: GCS, pupils , movement , reflexes Rectal : ? blood Physical Examination

21. Look for hypoglycemia, electrolyte abnormalities , leukocytosis or leukopenia with sepsis, increased BUN with UGI bleed or dehydration, HB for hemorrhage, blood cultures if febrile . CXR : pulmonary edema, pneumothorax , cardiomegaly, infiltrates, wide aorta ECG : mandatory in adults, look for MI. ABG: Discrepancy between Sa02 on pulse oximeter and Pa02 on think hemoglobinopathy (CO, HS, Methemoglobinemia ) Urinalysis : for focus of infection Toxin screening won’t help unless used as confirmatory test b/c it doesn’t pick up most toxins which cause hypotension Emergency ultrasound Investigations

22. Routine : BP, cardiac, pulsoximeter, input/output. Invasive : arterial pressure (art line), CVP (central line), pulmonary artery pressure (Swan- Ganz ), PCWP Shock index = HR/SBP : > 0.9 as an indicator of incipient shock Arterial - venous blood gas to determine oxygen extraction Lactate : predict poor outcomes, End - tidal CO2 : estimation of cardiac output and response to resuscitation (initially low because poor flow and hyperventilation but increases with resuscitation) Monitoring

23. Consciousness can be maintained until MAP 40 thus LOC a late sign. Shock index : HR/SBP : suggests shock if > 0.9 Lactate clearance index : More resuscitation required if lactate has not decreased by > 50%. Goal lactate < 2 mmol /l Clinical Pearls for DIAGNOSIS of SHOCK

24. Elderly : lack of sympathetic reserve Medications: Beta Blockers, Calcium Channel Blockers, digoxin Intraabdominal pathology (vagal tone) Neurogenic shock also Hypothyroidism Cause of patients in hypovolemic shock with bradycardia or relative bradycardia

25. Unresponsive to fluids or pressors for more than 1hr. MUST think of adrenal crisis Labs of decreased Na, increased K+ only with primary adrenal crisis Dexamethasone 4 mg iv Hydrocortisone 50mg q6h (maximum dose of 200 mg/day) Refractory Shock

26. SEPSIS AND SEPTIC SHOCK

27. Bacteremia = blood culture positive for bacteria SIRS Temp > 38.0 Cor < 36.0 C HR > 90 bpm RR > 24/m Wbc > 12,000/ uL or < 4,000/ uL or > 10% bands Sepsis = SIRS + documented infection Severe Sepsis = Sepsis + MODS: decreased consciousness , ARF, DIC, ARDS, Hepatic dysfunction Septic shock = Sepsis + Hypotension (<90 mmHg or 40 mmHg less than patients normal BP) refractory to volume resuscitation ( requiring pressors ) for more than 1hr.

28. It’s a grading system for sepsis Predisposition: age, chronic obstructive pulmonary disease, liver disease, nursing home residency, and malignancy with and without metastasis. Infection : pneumonia and cellulitis Response : tachypnea , bandemia , and tachycardia Organ dysfunction : renal , respiratory, cardiac, metabolic, and hematologic Predisposition infection response organ dysfunction (PIRO)

29. Inadequate corticosteroid activity for the patient’s severity of illness Should be suspected when hypotension is not relieved by fluid administration Due to adrenal gland failure Critical illness related corticosteroid insufficiency (CIRCI)

30. Mostly due to bacteria and fungal infections. Blood culture + ve in 20-40% patients of severe sepsis, 40-70% cases of septic shock Any bacterium can cause sepsis but most due to gram negative bacteria. (Both of them causes 70% cases of sepsis) Gram positives do not have LPS LPS (lipopolysaccharide) part of gram – ve’s outer membrane (endotoxin) which is a potent activator of mediators of septic shock (lipid A moiety is specific part, hexaacyl moiety) ETIOLOGY

31. LPS binds to CD14 on surfaces of monocytes, macrophages and neutrophils. Which is then transferred to MD-2, that is bound to TLR-4 This transduce signals to interior of cell. This activates various cytokines PATHOPHYSIOLOGY Host sensing microbes

32. THREE MAIN COMPONENTS (i ) hypovolemia (ii) Cardiovascular depression (iii) systemic inflammation Relative hypovolemia due to vasodilation and decreased SVR Absolute hypovolemia due to increased insensible losses and capillary leaking / third spacing Note there is EARLY cardiac depression (was previously thought to be late) ARDS : capillary leaking into lungs PATHOPHYSIOLOGY

33. NO B-Endorphin Bradykinin Platelet activating factor Prostacyclin Hypotensive molecules in Septic shock

34. WARM SHOCK COLD SHOCK TEMP 38 - 40 degrees with chills > 40 degrees or hypothermia SKIN warm cool CNS confused/obtunded stupor/coma CVS tachycardia, hypotension wide pulse pressure bounding pulse good response to fluids/ pressors myocardial depression tachycardia, hypotension narrow pulse pressure thready pulse poor response to fluids/ pressors myocardial depression RESP tachypnea, hypocarbia , mild hypoxemia tachypnea, hypercarbia , hypoxemic respiratory failure BLOOD leukocytosis w/ left shift inc or dec platelets normal coagulation leukocytosis or leukopenia thrombocytopenia DIC RENAL pre-renal failure renal failure METABOLIC hyperglycemia, hypoalbuminemia , mild hepatic enzyme changes, mild respiratory alkalosis hyper or hypoglycemia, lactic acidosis, hepatic failure

35. A cute Renal Failure A dult Respiratory Distress Syndrome (ARDS ) A cute Hepatic Dysfunction D isseminated Intravascular Coagulation L OC A drenal insufficiency D eath : occurs in 20%-80% of the patients Multi-Organ Dysfunction = abnormal function of >2 vital organs in association with SIRS Complications of Sepsis

36. ABC with establishment of 2 large bore ivs , starting oxygen putting on cardiac , BP, and pulsox monitors (may require intubation/ventilation if very sick ) Draw blood for CBC, Ur, Cr, electrolytes , blood cultures, PT, PTT, d-dimer, Type and cross, ABG, order CXR and ECG, put in foley to monitor fluid status, you may want central line and Swan- Ganz , urinalysis and culture , Procalcitonin is very specific marker for sepsis May need LP Brief History and systemic examination Initial treatment: fluids, pressors , empiric antibiotics APPROACH TO MANAGEMENT

37. Fluids To achieve adequate fluid resuscitation, the Surviving Sepsis Guidelines advise at least 30 ml/kg of crystalloids (1.5-3 liters) be infused for most patients ( Grade 1C ) in septic shock. 500 ml NS boluses q10 min until perfusion restored Commonly require 4 - 6 L Consider pressors for requiring > 3 L or signs of fluid overload. Monitor status with foley , central line, Swan- Ganz catheter SPECIFIC MANAGEMENT

38. Norepinephrine   should be provided as the first-line vasopressor ( Grade 1B ). Epinephrine  is considered the next-line agent for septic shock after norepinephrine in the Surviving Sepsis Guidelines. When norepinephrine is insufficient to maintain MAP 65 mm Hg, epinephrine should be added to or substituted for norepinephrine ( Grade 2B ). Vasopressin  at 0.03 units/minute is appropriate to use with norephinephrine , either to improve perfusion (increase MAP) or to reduce the required dose of norepinephrine (ungraded recommendation). Vasopressin is not recommended for use as a single vasopressor for septic shock . Vasopressin doses higher than 0.03 – 0.04 units/min are recommended to be reserved only for dire situations of septic shock refractory to standard doses of multiple vasopressors. GUIDELINES FOR USE OF PRESSORS- GOAL IS TO ACHIEVE MAP OF ≥ 65 mmHg

39. Dopamine  is suggested to  not  be used as an alternative to norepinephrine in septic shock, except in highly selected patients such as those with inappropriately low heart rates (absolute or relative bradycardia ) who are at low risk for tachyarrhythmias ( Grade 2C ). Dopamine is recommended to not be used in low doses in a so-called renal-protective strategy ( Grade 1A ). Phenylephrine  is recommended to not be used for septic shock, except when 1) septic shock persists despite the use of 2 or more inotrope/vasopressor agents along with low-dose vasopressin; 2) cardiac output is known to be high, or 3) norepinephrine is considered to have already caused serious arrhythmias ( Grade 1C ). GUIDELINES FOR USE OF PRESSORS- GOAL IS TO ACHIEVE MAP OF ≥ 65 mmHg

40. Dobutamine  should be tried for patients in septic shock who have low cardiac output with high filling pressures while on vasopressors, or who have persistent evidence of hypoperfusion after attaining an adequate mean arterial pressure and intravascular volume (with or without vasopressors) ( Grade 1C ). A dobutamine infusion up to 20 mcg/kg/min can be added to any vasopressor(s) in use.  Dobutamine is also an appropriate first-line agent in patients with severe sepsis and low cardiac output, with a preserved mean arterial pressure (i.e., who are not in septic shock) ( Grade 1C ). Dobutamine is recommended  not  to be used to deliberately raise cardiac output to higher than normal levels in an attempt to improve perfusion ( Grade 1B ). GUIDELINES FOR USE OF PRESSORS- GOAL IS TO ACHIEVE MAP OF ≥ 65 mmHg

41. Norepinephrine 0.5- 30 ug /min iv Start with or add to dopamine B1 agonist and potent alpha1 agonism with minimal B2 effect thus very effective to increase systemic vascular resistance Dopamine 5- 20 ug /kg/min iv infusion Add norepinephrine if unable to keep SBP > 60 with 20 ug /kg/min of dopamine 1- 2 ug /kg/min (LOW): DOPAMINERGIC; increases renal and mesenteric flow 2 - 10ug/kg/min (MOD): Beta ADRENERGIC; increases contractility by B1 > 20ug/kg/min (HIGH): Alpha ADRENERGIC; increases BP due to alpha1 Doses

42. Mainly B1 agonist, some B2 and some alpha activity B1 is + ve ionotrope and venodilator May lead to hypotension by vasodilation if CO doesn’t increase much Excellent for normotensive, caution with borderline hypotension, don’t use alone in hypotensive Advantage: Less tachycardia for given increase in CO than others (no NE release form nerve endings), greatest ionotropic effect with least chronotropic effect and BP effects Dose is 5 - 25 ug /kg/min: start 2 and increase to 20 ug /kg/min Dobutamine

43. EARLY ANTIBIOTICS have been shown to decrease mortality. Should be started ASAP after cultures drawn Broad-spectrum and maximum doses Broad-spectrum = gram + ve’s , gram – ve’s , anaerobes ANTIBIOTICS

44. Immunocompetent adult: 1. Piperacillin-tazobactam (3.375g q4-6h), 2. Imipenem-cilastine (0.5g q6h). If allergic to B-lactam agents; ciprofloxacin( 400mg q12h) or levofloxacin(500-750 mg q12h) plus clindamycin(600mg q8h). Vancomycin (15mg/kg 12h) should be added to each of the above regimens. EMPERICAL ANTIBIOTICS

45. 1. Imipenem-cilastine (0.5g q6h) or meropenem (1gm/q12h) or cefepime (2g q8h). 2. Piperacillin-tazobactam (3.375g q4-6h ) plus tobramycin(5-7mg/kg q24h) Vancomycin (15mg/kg 12h) should be added to above regimens. Emperical antifungal therapy should be started with caspofungin 70mg loading dose and then 50 mg daily or lipolized Amphotericin-B. EMPERICAL- Neutropenic Patients (<500 neutrophils/ ul )

46. Splenectomy : Cefotaxime (2g q6-8h) or ceftriaxone(2g q12h), if local cephalosporin-resistant pneumococci is high add vancomycin . IV Drug users: Vancomycin (15mg/kg q12h) AIDS: cefepime (2g q8h ), Piperacillin-tazobactam (3.375g q4-6h) plus tobramycin(5-7mg/kg q24h ), If allergic to B-lactam agents; ciprofloxacin( 400mg q12h) or levofloxacin(500-750 mg q12h) plus clindamycin(600mg q8h). Vancomycin (15mg/kg 12h) should be added to each of the above regimens. EMPERICAL- Splenectomy / IV Drug/AIDS

47. Glucocorticoids  —  Evidence from randomized trials suggest that corticosteroid therapy is most likely to be beneficial in patients who have severe septic shock (defined as a systolic blood pressure <90 mmHg) that is unresponsive to adequate fluid resuscitation and vasopressor administration. Data from ongoing clinical trials are needed to confirm that benefit. Nutrition  — There is consensus that nutritional support improves nutritional outcomes in critically ill patients, such as body weight and mid-arm muscle mass. Intensive insulin therapy  — Hyperglycemia and insulin resistance are common in critically ill patients, Most clinicians target blood glucose levels between 140 and 180 mg/ dL  (7.7 to 19  mmol /L). This topic is discussed separately. External cooling  —  External cooling is preferable to no cooling, but they do not provide guidance about whether external cooling is preferable to antipyretic medications . Other therapies in septic shock

48. Recombinant activated protein C ( Apc ): approved by FDA Small molecule endotoxin antagonist: ERITORAN Granulocyte-macrophage colony-stimulating factor Other therapies in septic shock

49. HYPOVOLEMIC SHOCK The most common type of shock

50. It has 4 types: HYPOVOLEMIC SHOCK

51. Physical Exam ABCs are priority Neurologic exam reflects cerebral perfusion Vascular Access At least 2 16 (or larger) gauge needles in upper extremities should not be placed in an injured extremity if peripheral lines cannot be established, femoral or saphenous vein may be used for rapid infusion subclavian and internal jugular veins are useful for CVP monitoring. Initial Management of Hypovolemic shock

52. Rapid infusion of either isotonic saline or ringer lactate should be started. Care must be taken to avoid hyperchloremic acidosis from loss of bicarbonate buffering capacity and replacement with excess chloride. Ringer lactate should be avoided in hyperkalemia and renal dysfunction. Infusion of 2-3 lit fluid over 20-30 mins should restore normal hemodynamic parameters. Initial Fluid Therapy

53. Monitoring Response BP , pulse pressure, HR, skin, level of consciousness Urinary output is the best parameter 0.5cc/Kg/ hr is normal in adults (35cc/ hr in 75kg man ) Acid/Base Balance Early shock : respiratory alkalosis due to hyperventilation Middle : mild metabolic acidosis Late : severe metabolic acidosis due to inadequate tissue perfusion Lactate levels and base deficits have been suggested as best laboratory parameters to monitor hypovolemic shock resuscitation Base deficit = amount of base required to be added to neutralize the pH; normal is > - 2 mmol /l; BD decreases before pH drop or BP drop Monitoring response

54. Packed RBC is preffered over whole blood. Crossmatched blood : preferable but takes 1hr Type-Specific blood : type and screen takes 10min Unmatched blood : type O- is indicated for all pts with exsanguinating hemorrhage, type O + can be given to males and all women above child bearing age Warming Fluids is Essential: heat fluid to 39 degrees; cool blood leads to hypothermia and DIC Coagulopathy : rare in first hour but DIC may develop later; more of a concern with massive transfusion. BLOOD REPLACEMENT

55. Equating BP with CO: an increase in BP does not necessarily mean an increase in CO because increased SVR can increase BP without increase in CO Elderly : reduced catacholamine response, medications, pre-existing hypovolemia , reduced cardiac function, other physiological reserve (lungs, kidneys) is reduced Athletes may not have tachycardia Pregnancy is a hypervolemic state Medications preventing response: BB, CCBs, diuretics . SPECIFIC CONSIDERATIONS

56. Colloids Advantages: less fluid required, more volume remains in vascular space, potential to draw fluids into vascular space Disadvantages : expensive, potential for allergic reactions, coagulopathies, seizures Example: Albumin , hetastarch , pentastarch , dextran Crystalloids Advantages : less volume needed, stays in intravascular space better, draws in interstitial fluid, increases cardiac output and MAP, inotrope, decreases SVR due to vasodilation of precapillary vessels as a result of osmolarity Disadvantages : hypernatremia, hyperosmolarity , seizures, coagulopathy, anaphylactoid reaction with dextran added. Colloids vs Crystalloids

57. CARDIOGENIC SHOCK

58. Decreased cardiac output and evidence of tissue hypoxia in presence of adequate intravascular volume Cardiac Failure = clinical CHF Cardiogenic Shock = clinical CHF + 4/6 empiric criteria for shock (see above) Cardiogenic shock generally occurs when > 40% of myocardium not working Hemodynamic criteria : hypotension (SBP < 90) for > 30 min), cardiac index <2.2L/min/m2 , PCWP > 18 mmHg CARDIOGENIC SHOCK

59. Occurs in 5-10 % of MI patients; Mortality : 50 - 80 % Mean time to onset is 6hrs post admission thus EARLY management important Epidemiology

60. LV failure 74 % acute MR 8%, VSR 4%, isolated RV failure 3%, tamponade or cardiac rupture 2%, other causes 8% Causes

61. elderly DM antior MI previous MI/PVD/CVA previous poor EF large infarctions Female sex Risk Factors

62. Intraarterial BP monitoring essential because of huge differences that can be found between cuff BP and true pressures. Allows agressive use of venodilators and possible avoidance of vasopressors; allow accurate titration of ionotropes , venodilators , vasopressors. Hypotensive : cardiogenic shock versus true volume depletion cannot be determined clinically; needs invasive monitoring of CVP, PAP, PCWP ( low PAP/CVP is hypovolemia ) Vasopressors are good to increase coronary perfusion but bad because increased afterload worsens HF Avoid BZD, morphine, barbituates , ketamine for sedation Choose fentanyl and etomidate for sedation MANAGEMENT OF CARDIOGENIC SHOCK

63. Fluids Small boluses 250 ml NS over 10 min Repeat if respiratory status not deteriorating Should increase BP if hypotension due to hypovolemia . Management of cardiogenic shock

64. Other ETT and ventilation Left Ventriclar Assist Device (LVAD ) PCI/CABG: in cases of acute MI Intra-Aortic Balloon pump (IABP) Indication: cardiogenic shock not stabilized by ionotropes Increases coronary perfusion by 30% Contraindication: aortic insufficiency, severe PVD Management of cardiogenic shock

65. Low doses 2-5 ug /kg/min: dopaminergic; renal/ splanhnic vasodilation Moderate 5-15 ug /kg/min: beta adreneragic ; increased contractility, HR High doses > 15 ug /kg/min: alpha adrenergic; vasoconstrict all vessels, increases BP, HR, contractility (may precipitate ishcemia , may worsen pulmonary edema Indications Hypotension SBP 70 - 100 with signs of hypoperfusion failing fluid challenge:10-20 ug /kg/min oliguria: 2-5 ug /kg/min Dopamine

66. Mainly B1 agonist, some B2 and some alpha activity B1 is + ve ionotrope and venodilator May lead to hypotension by vasodilation if CO doesn’t increase much Excellent for normotensive, caution with borderline hypotension, don’t use alone in hypotensive Advantage : Less tachycardia for given increase in CO than others (no NE release form nerve endings), greatest ionotropic effect with least chronotropic effect and BP effects Dose is 5 - 25 ug /kg/min: start 2 and increase to 20 ug /kg/min Indications Hypotension SBP 70 - 100 with no s/s of hypoperfusion after fluid challenge Dobutamine

67. Mostly alpha agonist (some beta) Drug of choice for volume repleated profound hypotensive (SBP < 70) May add dopaminergic doses (2-5 ug /kg/min) to preserve renal perfusion Goal : temporary management until IABP, PTCA, surgery Dose is 0.5 ug /kg/min Indication hypotension SBP < 70 failing fluid challenge Norepinephrine

68. Isoproteronol : potent beta agonist, profound tachycardia, it should be avoided Digitalis : little role in acute HF, some role in rate control with Afib /flutter Amrinone / Milrinone : phosphodiesterase III inhibitior thus increases cAMP and acts as vasodilator, ionotrope with minimal HR/BP changes Others

69. 5-10% of Mi Mortality 70% Thrombolysis unlikely to be effective b/c of low coronary perfusion pressure thus drug isn’t delivered to site of thrombosis Options for management Thrombolysis PTCA Emergent CABG MI + CARDIOGENIC SHOCK

70. ANAPHYLACTIC SHOCK

71. Assessment : stridor? can patient talk? angioedema of face? Management : chin-lift, jaw thrust, suction excess secretions, nasopharyngeal or oropharyngeal airway Racemic epinephrine : 0.5 ml of 2.25% in 2.5 ml NS as temporizing measure Endotracheal intubation is preferred route of intubation, should be done early before complete obstruction, fiberoptic bronchoscopy may help,nasotracheal intubation is an option in awake, uncooperative patient. Sedation and paralysis is relatively contraindicated because of a distorted airway may preclude intubation after paralysis. Surgical airway may be needed: should be prepared ANAPHYLACTIC SHOCK APPROACH

72. Breathing Assessment : respiratory effort, respiratory rate, wheezing, pulmonary edema Management : ventilate as necessary, oxygen, pulsoximeter Sedation may be necessary for ventilation after intubation ASSESSMENT

73. Drug of choice in anaphylaxis Alpha - agonism : peripheral vasoconstriction reduces vasodilation and vascular permeability to reduce hypotension; can precipitate hypertensive crisis Beta - agonism : bronchodilation , + ve ionotropic , + ve chronotropic ; can precipitate myocardial ischemia, SVT and ventricular tachycardia's, stunned heart syndrome Absolute contraindication: ventricular tachycardias Relative contraindications: elderly, known CAD, hypertension Epinephrine

74. Mild adult : 0.3 - 0.5 ml of 1:1000 subcutaneous Moderate adult : 0.3 - 0.5 ml of 1:1000 intramuscular Severe adult : 10 ml of 1:100,000 intravenous over10 min then infusion of 1 - 4 ug /min if necessary or 1ml of 1:10,000 q 30 sec to effect Route and dose

75. H1 antagonists: Should be used in all cases of anaphylaxis Many options although diphendydramine is the most commonly used Mild: adult:25 - 50 mg po q6h. Moderate:50 - 100 mg im Severe:50 - 100 mg iv over 3 minutes Repeat in 4 - 6 hrs H2 antagonists: H2 antagonism to block myocardial and peripheral vascular tissue responses to histamine Consider with persistent symptoms Adult: cimetidine 300 mg iv followe by 300 mg po q6h X 3/7 Antihistamine

76. Should be added if bronchospasm does not respond to epinephrine Albuterol nebulizer 2.5 - 5.0 mg neb and repeat ( may need continous ) Ipratropium: 250 - 500 ug neb may help Aminophylline : another option, 5.6 mg/kg load over 20 min then 0.1mg/kg/ hr Bronchodilators

77. Limited benefit acutely as onset of action is 4 - 6hrs blunting the late phase Loading : Hydrocortisone 250 mg iv or Methylprednisone 125 mg. A convenient oral corticosteroid is prednisone at dose of 1mg/kg/day. Have role in biphasic anaphylaxis Corticosteroids

78. Fluids: 1 st thing to do in anaphylactic shock is giving fluids in form of crystalloids. Consider vasopressors for refractory hypotension Dopamine:5 ug /kg/min Intravenous epinephrine (1:10,000 v/v preparation) can be administered as a continuous infusion Management of hypotension

79. Positive ionotropic and chronotropic cardiac effects (independent of alpha and beta adrenergic receptors) Enhances CAMP synthesis Consider in patients refractory to treatment and epinephrine – resistant patients who are on beta blockers Adults : 1 mg sc , im , iv then infusion 1 - 5 mg/ hr Watch for hypokalemia and hyperglycemia Glucagon

80. Anti- IgE ( omalizumab ) complexes circulating (but not receptor-bound) IgE and keeps it from binding to its receptors. It does not remove IgE bound to receptors and can take several weeks to months to have a substantial effect. It should not be used in an acute setting and would not be expected to influence IgE -independent or nonimmunologic events. OMALIZUMAB

81. NEUROGENIC SHOCK

82. I nitial loss of somatic motor, sensory, and sympathetic, autonomic function due to spinal cord injury. Sympathetic component : this is neurogenic shock (one manifestation of spinal shock which is systemic hypotension due to loss of sympathetic function but preservation of parasympathetic function) Motor component : flaccid paralysis, areflexia Sensory component : anesthesia to all modalities SPINAL/NEUROGENIC SHOCK

83. Hypotension + Paradoxical Bradycardia + warm/dry skin and adequate urine output May not have actual bradycardia ; may simply have failure to respond to become tachycardia with hypotension BRADYCARDIA : loss of sympathetic innervation to the heart ( unopposed vagal stimulation); occurs with injuries at or above T4 HYPOTENSION : due to vasodilation due to loss of sympathetic tone; usually occurs with injuries at or above T6 because if it is below T6 there is enough sympathetic tone left to the torso and upper body that the BP doesn’t drop. Signs of Neurogenic shock

84. Fluid is always the initial treatment of shock, especially since concomitant hemorrhagic shock must be excluded following trauma. Most institutions will additionally utilize  pressor  agents to achieve hemodynamic stability. Dopamine is often used either alone or in combination with other inotropic agents. Vasopressin (antidiuretic hormone [ADH ]) Certain vasopressors (ephedrine, norepinephrine). Phenylephrine may be used as a first line treatment, or secondarily in patients who do not respond adequately to dopamine. Atropine (administer if bradycardia is severe.) MANAGEMENT OF NEUROGENIC SHOCK

85. THANK YOU……