Shock...............................pptx

Shock

1. SHOCK

2. DEFINITION Profound hemodyamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate perfusion of vital organs

3. Types of Shock Cardiogenic (intracardiac vs extracardiac) Hypovolemic Distributive sepsis**** neurogenic (spinal shock) adrenal insufficiency anaphylaxis

4. Cardiogenic Shock, intracardiac Myocardial Injury or Obstruction to Flow Arrythymias valvular lesions AMI Severe CHF VSD Hypertrophic Cardiomyopathy

5. Presentation of Cardiogenic Shock Pulmonary Edema JVD hypotensive weak pulses oliguria

6. Cardiogenic Shock, extracardiac (Obstructive) Pulmonary Embolism Cardiac Tamponade Tension Pneumothorax Presentation will be according to underlying disease process.

7. Hypovolemic Shock Reduced circulating blood volume with secondary decreased cardiac output Acute hemorrhage Vomiting/Diarrhea Dehydration Burns Peritonitis/Pancreatitis

8. Presentation of Hypovolemic Shock Hypotensive flat neck veins clear lungs cool, cyanotic extremities evidence of bleeding? Anticoagulant use trauma, bruising oliguria

9. Distributive Shock Peripheral Vasodilation secondary to disruption of cellular metabolism by the effects of inflammatory mediators. Gram negative or other overwhelming infection. Results in decreased Peripheral Vascular Resistance.

10. Distributive Shock: Presentation Febrile Tachycardic clear lungs, evidence of pneumonia warm extremities flat neck veins oliguria

11. Diagnosing Shock Response to fluids Echo/EKG CXR Evidence of infection Swan-Ganz Catheter?

12. Swan-Ganz Catheter Utilized to differentiate types of shock and assist in treatment response. Probably overused by physicians. Studies documenting increased mortality in patients with catheters versus no catheters, although somewhat swayed by selection bias.

13. Swan-Ganz Catheter

14. Swan-Ganz Interpretation

15. Management Correct underlying disorder if possible and then direct efforts at increasing the blood pressure to increase oxygen delivery to the tissues. Maintain a mean arterial pressure of 60 (1/3 systolic + 2/3 diastolic) Keep O 2 sats >92%, intubate if neccesary

16. Correction of hypotension Normal Saline should be administered anytime a patient is hypotensive. If hypotension exists give more NS. *** If possible give blood as it replaces colloid. Vasopressors Inotropic agents for cardiogenic shock Intra-aortic Balloon Pump for cardiogenic

17. Management of Cardiogenic Shock Attempt to correct problem and increase cardiac output by diuresing and providing inotropic support. IABP is utilized if medical therapy is ineffective. Catheterization if ongoing ischemia Cardiogenic shock is the exception to the rule that NS is always given for hypotension NS will exacerbate cardiac shock.

18. Intra-Aortic Balloon Pump

19. Management of Septic Shock Early goal directed therapy Identification of source of infection Broad Spectrum Antibiotics IV fluids Vasopressors Steroids ?? Recombinant human activated protein C ( Xygris) Bicarbonate if pH < 7.1

20. Management of Hypovolemic Shock Correct bleeding abnormality If PT or PTT elevated then FFP Aggressive Fluid replacement with 2 large bore IV’s or central line. Pressors are last line, but commonly required.

21. Addison’s Disease Deficiency of cortisol and aldosterone production in the adrenal glands This is suspected when patient is non-responsive to fluids and antibiotics. Electrolytes may reveal hyponatremia and hyperkalemia Hydrocortisone 100 mg IV immediately then taper appropriately

22. Figure 1. Simplified schematic of postulated intracellular actions of β-adrenergic agonists. β-Receptor stimulation, through a stimulatory Gs-GTP unit, activates the adenyl cyclase system, which results in increased concentrations of cAMP . Overgaard C B , and Džavík V Circulation. 2008;118:1047-1056 Copyright © American Heart Association, Inc. All rights reserved.

23. Figure 2. Schematic representation of postulated mechanisms of intracellular action of α1-adrenergic agonists. α1-Receptor stimulation activates a different regulatory G protein ( Gq ), which acts through the phospholipase C system and the production of 1,2-diacylglycerol (DAG) and, via phosphatidyl-inositol-4,5-biphosphate (PiP2), of inositol 1,4,5-triphosphate (IP3). Overgaard C B , and Džavík V Circulation. 2008;118:1047

24. Figure 3. A, Endogenous catecholamine synthesis pathway. Overgaard C B , and Džavík V Circulation. 2008;118:1047-1056

25. Figure 4. Basic mechanism of action of PDIs. PDIs lead to increased intracellular concentration of cAMP , which increases contractility in the myocardium and leads to vasodilation in vascular smooth muscle. Overgaard C B , and Džavík V Circulation. 2008;118:1047-1056

26. Background Vasopressors are class of drugs that elevate Mean Arterial Pressure (MAP) by inducing vasoconstriction. Inotropes increase cardiac contractility. Many drugs have both vasopressor and inotropic effects. Vasopressors are indicated for a decrease of >30 mmHg from baseline systolic blood pressure or MAP <60 mmHg, when either condition results in end-organ dysfunction secondary to hypoperfusion .

27. Receptor Physiology Main categories of adrenergic receptors relevant to vasopressor activity: Alpha-1adrenergic receptor Beta-1, Beta-2 adrenergic receptors Dopamine receptors

28. Receptor Physiology Receptor   Location Effect Alpha-1 Adrenergic   Vascular wall Vasoconstriction     Heart Increase duration of contraction without       increased chronotropy Beta Adrenergic Beta-1 Heart ↑ Inotropy and chronotropy   Beta-2 Blood vessels Vasodilation Dopamine   Renal Vasodilation     Splanchnic (mesenteric)       Coronary       Cerebral     Higher doses   Vasoconstriction

29. Drug Alpha-1 Beta-1 Beta-2 Dopaminergic Predominant Clinical Effects ( Phenylephrine *** SVR ↑ ↑, CO ↔/↑ Noradrenaline *** ** SVR ↑ ↑, CO ↔/↑ Adrenaline (Epinephrine) *** *** ** CO ↑ ↑, SVR ↓ (low dose) SVR/↑ (higher dose)     Dopamine (mcg/kg/min)           0.5 to 2 * ** CO 5 to 10 * ** ** CO ↑, SVR ↑ 10 to 20 ** ** ** SVR ↑ ↑   Dobutamine 0/* *** ** CO ↑, SVR ↓ Isoproterenol *** *** CO ↑, SVR ↓ *** Very Strong Effect, ** Moderate effect, * Weak effect, 0 No effect. Vasoactive Medication Receptor Activity and Clinical Effects

30. Clinical Application     1st Line Agent 2nd Line Agent Septic Shock Norepinephrine ( Levophed ) Vasopressin     Phenylephrine ( Neosynephrine ) Epinephrine (Adrenalin) Heart Failure   Dopamine   Milrinone     Dobutamine   Cardiogenic Shock   Epinephrine ((Adrenaline)     Dobutamine   Anaphylactic Shock   Epinephrine (Adrenalin) Vasopressin Neurogenic Shock   Phenylephrine ( Neosynephrine )   Hypotension Anesthesia-induced Phenylephrine ( Neosynephrine )     Following CABG Epinephrine (Adrenalin)  

31. Based on Rivers et al article re: Early Goal Directed Therapy, what is the ultimate goal in the first 6 hours? CVP of 8-12 unventilated/12-15 ventilated MAP >65 Cardiac Output > 8 LPM Hemoglobin > 10 gm / dL ScvO2 > 70%

32. Initial Resuscitation: Goals of Early Goal Directed Therapy CVP 8-12 cmH 2 O 12-15 cmH 2 O on ventilator MAP > 65 mmHg May need to be higher in patients with HTN UOP > 0.5 mL/Kg /hour ScvO 2 > 70% SvO 2 > 65 % Goal: Normalize lactate Goal in the first 6 hours after diagnosis 16-17% decrease in mortality Rivers E. N Engl J Med 2001; 345:1368-77

33. Clinical Scenario I 72 year-old woman with DM type II, hypertension and CKD is transferred for altered mental status. Her vitals upon arrival are as follows: Temp 101F, BP 70/45, Hr 140, RR 20, O2 Sat 95% RA. Pertinent lab findings: WBC 21, Cr 3.5, Lactic Acid 3.4. After adequate IVF resuscitation, pt continues to remain hypotensive BP 60-70s/30-40s and tachycardic Hr 130. What is the most appropriate 1 st line vasopressor / inotropic agent? A. Epinephrine B. Dobutamine C. Norepinephrine D. Dopamine

34. Clinical Scenario II 64 year-old man with CAD and PCI ( drug-eluting stents), ischemic cardiomyopathy (EF 20-25%) with AICD, who presents with 1 week history of progressively worsening shortness of breath, orthopnea and bilateral lower extremity edema, after running out of all medications about 10 days ago. Vitals: Temp 99F, BP 75/48, Hr 75, RR 25, O2 Sat 91% on RA. CXR reveals vascular congestion and bilateral pleural effusion. Bedside ultrasound reveals significantly diminished EF. What is the most appropriate 1 st line vasopressor / inotropic agent? A. Adrenaline B. Dobutamine C. Noradrenaline D. Dopamine

35. Clinical Scenario III 56 year-old obese man with COPD and OSA, who was initially admitted for acute COPD exacerbation secondary to community-acquired pneumonia, was found to be in acute respiratory failure. Emergency intubation done. Vitals after intubation are as follows: Temp 99.8F, BP 74/48, Hr 74. What is the most appropriate 1 st line vasopressor / inotropic agent? A. Phenylephrine B. Dobutamine C. Noradrenaline D. Dopamine