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Acute medicine Lecture Series 2010
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  1. Acute medicine Lecture Series 2010 Shock How to water a garden? Ahmad F. Mady MD

  2. Before we go anywhere, let’s startat the beginning • What do you need to maintain a nice garden? WATER

  3. What do you need to get the water to the garden ?

  4. 4 things • Water pump • Release valve • Hose • Water amount

  5. What is Shock? • Theoretical: Inability to meet cellular requirements for oxygen • Practical: When the nurse calls you for a low blood pressure

  6. what are the types of shock? Think about the garden: The garden will die without enough water • Pump failure • Release valve failure • Hose failure • Water failure

  7. What the hell are you talking about?

  8. Aetiological Shock Categories • Pump failure = Cardiogenic shock • Release valve failure = Obstructive shock • Hose failure = Distributive shock • Water failure = Hypovolemic shock

  9. Hypovolemic Shock Not enough stuff • Blood • plasma

  10. Hemorrhagic Shock

  11. Cardiogenic Shock • The heart cannot pump enough blood to meet the metabolic demands of the body • Causes Muscle Valve Heart rate Too fast Too slow Poor coordination Mortality ( 60-90%)

  12. Obstructive Shock • Tension pneumothorax • Cardiac tamponade • Pulmonary embolism • Aortic stenosis

  13. Distirutive shock Caused by systemic vasodilatation from • Infection -Septic shock (35-40% ,1 month mortality) • Spinal / Neurogenic Shock • Anaphylaxis

  14. Septic shock

  15. Pathophysiology • DO2 = Q X CaO2 • DO2 = Q X (1.34 X Hb X SpO2) Normal DO2 is 520 to 570 mL/min/m2 • VO2 = Q X (CaO2 - CvO2) • VO2 = Q X 13.4 X Hb X (SpO2-SvO2) Normal VO2 is 110-160 ml/min/ m2 • O2ER = VO2 / DO2 X 100 Normal O2ER = 0.2-0.3 (20 to 30%)

  16. Pathophysiology • MRO2 : • The metabolic demand for oxygen at the tissue level. • The rate at which oxygen is utilized in the conversion of glucose to energy and water through glycolysis and Kreb’s cycle. VO2 ≥ MRO2 = Normal Metabolism VO2 < MRO2 = SHOCK

  17. Pathophysiology • When demand is insufficient the first compensatory mechanism is increase in CO. • autonomic responses. • Arteriolar vasoconstriction. • Increase in HR and contractility . • Constriction of venous capacitance, which augments VR. • Release of vasoactive hormones epi, norepi, dopamine, and cortisol to increase arteriolar and venous tone. • Release of ADH and activation of the renin-angiotensin axis

  18. Pathophysiology • The cellular response to a decrease in systemic O2 delivery is ATP depletion leading to ion-pump dysfunction (influx Na+ and efflux K+) leading to membrane instability and cellular dysfunction. • When compensatory mechanisms failure the body starts anaerobic metabolism forming lactic acid.

  19. Clinical manifestation • Characterized by three stages • Preshock (warm shock, compensated shock) • Shock • End organ dysfunction • Compensated shock • Low preload shock – tachycardia, vasoconstriction, mildly decreased BP • Low afterload (distributive) shock – peripheral vasodilation, hyperdynamic state

  20. Shock Initial signs of end organ dysfunction • Tachycardia • Tachypnea • Metabolic acidosis • Oliguria • Cool and clammy skin

  21. End Organ Dysfunction Progressive irreversible dysfunction • Oliguria or anuria • Progressive acidosis and decreased CO • Agitation, obtundation, and coma • Patient death

  22. Invasive hemodynamic monitoring

  23. Also diagnosis of hyperdynamic septic shock optimizing fluids/intorops/vasopressors Invasive hemodynamic monitoring • Arterial line • CVP • Is CVP or PAOP reliable in shock ??? • Is there a role for Swan-Ganz in shock ?!

  24. Treatment • General objective Rapid recognition and restoration of perfusion Fluids vasopressors inotrops

  25. Fluids Two broad categories related to a shock discussion • Crystalloids • Colloids Crystalloids • Hypoosmolar D5, 1/4, ½ NS not helpful for our patient in shock • Iso-osmolar NS, RL RL has lower chloride concentration vs. NS so tendency of non-AG metabolic acidosis • Hyper: mannitol, 3%NS no great advantage..cell dehydration

  26. Fluids Colloids • Natural vs Synthetic • Natural • Blood • FFP • Platelets • Human albumin • Drawbacks: • Limited supply • High cost • Possible allergic reactions • Risk of infection

  27. Fluids • Synthetic • Dextran • HES high MW , medium MW , low MW • Drawbacks: • Alterd hemostasis if large dose • relative High cost • Hyperamylesmia....? misinterpretation • Dextrane (bleeding,x-matched RBCs,anaphylaix,renal)

  28. Which is best ? Crystalloid vs Colloid • Evidence has been conflicting Tailoring the type of resuscitation fluid to the specific clinical condition seems a more logical approach than using the same type of fluid without exception for all ICU patients

  29. Vasopressors / Inotropes Essential few principles to remember • Alpha Peripheral squeeze on vessels • Beta Inotropic and/or chronotropic effect . with most beta effect, comes a degree of vasodilation >decreased afterload • Other pathways exist c AMP Phosphodiesterase inhibitors

  30. Vasopressors / Inotropes • epinepherin • Alpha and beta effect • Great increase on cardiac O2 demand • Splanchnic vasoconstriction • Should be 2nd or 3rd line trope • Dopamine • Alpha and beta depending on dose BUT Overall alpha effect is weaker than levo • Beta effect increases cardiac O2 requirements • Beta also increases amount of dysrhythmias • works indirectly at nerve endings to release norepi and epi.

  31. Vasopressors / Inotropes • Norepinepherine(levophed) • Mostly alpha, some beta • Potent vasoconstrictor, less effect on increase in HR • Reflex bradycardia in response to increase in MAP, HR remains unchanged or even slight decrease Vasopressin • Vasoconstriction of peripheral blood vessels via V1 receptor • Weak pressor in normal patients • Patel 1999, Sharshar 2003- 1/3 of septic patients have relative vasopressin deficiency • Although used commonly, needs future studies.

  32. Vasopressors / Inotropes • Dobutamine • Mostly beta effect • Increase in inotropy • Increase in chronotropy • Peripheral vasodilation • Overall will increase cardiac output and decrease afterload Others

  33. So… • Now we discuss shock types • We discuss fluid principles • We discuss pressors/tropes Let’s put it all together to treat “shock”

  34. Case 1 52 yr old male with crushing retrosternal chest pain, diaphoresis. • ECG: depression in V56, II, III, aVF • BP 110/70, HR 110, in CCU BP drops to 80/60 Cardiogenic shock • Treatment Judicious fluid Inotropes Little need for pressors

  35. Case 2 60 yr female with chest pain and shortness of breath • Sa02 82% BP 75/50 • Elevated JVP, S1Q3T3 • CT chest: massive saddle pulmonary embolism Obstructive Shock Treatment: • Fluids + pressors or tropes ? • RELIEVE THE OBSTRUCTION Pulmonary embolism Thrombolysis Tension pneumo Needle decompression and ICT TamponadePericardiocentesis

  36. Case 3 78 yr female with productive cough, fever,confusion • BP 85/35, HR 125 • CXR: RLL infiltrate, 25% bands, urea 19 Distributive Shock Treatment: • fluids, pressors, inotropes? • ANTIBIOTICS (in under one hour)

  37. Septic Shock Rivers et al. Early Goal Directed Therapy in the Treatment of Severe Sepsis and Septic Shock. NEJM 2001; 345:1368-77 • randomized partially blinded • 263 patients; 130 Tx, 133 control • Standard therapy vs. six hours of EGDT CVP 8-12 MAP >65 SvO2 >70 UOP >0.5cc/kg/hr

  38. So... • You have to Fill the tank...early A dry patient not in heart failure will die much sooner than a resuscitated patient in heart failure What about pressors/inotropes ? • If your MAP <65, likely will need vasopressor • If your MAP>65, and Scv02<70, may benefit from inotrope

  39. Treatment Algorithm

  40. Case 4 53 yr old male on GI ward, Hx of Portal HTN, esophageal varices, recent sever hematemesis • HR 135, BP 80/60, 8L 02. • Anxious, confused, diaphoretic Hypovolemic shock Treatment Your staff will bring the scope in about 30 minutes The MET team will respond in 15 minutes Your patient will be dead in 10 minutes • Stop the bleeding • fluids, pressors, inotropes?

  41. Resuscitation endpoints....?? • Blood pressure • Heamatocrite/Hb • Filling pressures • All of the above • Non of the above

  42. Resuscitation endpoints • Lactic acid production Elevated serum lactate is an indirect measure of the oxygen debt, and an approximation of the magnitude and duration of the severity of shock. The rate of clearance of lactate is a better marker of adequate resuscitation rather than absolute value. • Base deficit BD is the amount of base in millimoles that is required to titrate 1 L of whole blood to a pH of 7.40 with the sample fully saturated with O2 at 37°C and a PaCO2 of 40. Elevated BD correlate with the severity of shock. Correction of BD is a guide for resuscitation.

  43. Resuscitation endpoints • Intramucosal pH monitoring Mesenteric organs have earlier and greater hypoperfusion than other organs. Gastric tonometry measure intragastric intramucosal pH and is an early indicator of hypoperfusion in shock and correlate with the mortality.(technically difficult to use)

  44. So…what was our objective ? Have a nice garden

  45. So…our objectives were • Definition of shock • Pathophysiology • Shock Categories • Management of shock • Case scenarios

  46. ? any question..

  47. Thank you A H M A D F. M A D y