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Class drug therapy of shock

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Class drug therapy of shock

  1. 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
  2. 2. Term “choc” – French for “push” or impact was first published in 1743 by the physician LeDran Belief – symptoms arose from fear or some other form of altered cerebral function Inadequate oxygen delivery to meet metabolic demands Results in global tissue hypoperfusion and metabolic acidosis Shock can occur with a normal blood pressure and hypotension can occur without shock
  3. 3. • Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery • Sympathetic nervous system • NE, epinephrine, dopamine, and cortisol release •Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) • Renin-angiotensin axis • Water and sodium conservation and vasoconstriction • Increase in blood volume and blood pressure
  4. 4. Progression of physiologic effects as shock ensues Cardiac depression Respiratory distress Renal failure DIC Result is end organ failure
  5. 5. • History • Recent illness • Fever • Chest pain, • Abdominal pain • Comorbidities • Medications • Toxins/Ingestions • Recent hospitalization or surgery • Baseline mental status • Physical examination • Vital Signs • CNS – mental status • Skin – color, temp, rashes, sores • CV – heart sounds • Resp – lung sounds, RR, oxygen sat, ABG • GI – abd pain, rigidity, guarding, rebound • Renal – urine output
  6. 6. • Infectious source Cardiorespiratory monitor Pulse oximetry Supplemental oxygen IV access ABG, lab investigations-CBC, Chemistries, Lactate Coagulation studies, Cultures Foley catheter
  7. 7. CT of head/sinuses Lumbar puncture Wound cultures Acute abdominal series Abdominal/pelvic CT or US Cortisol level Fibrinogen, FDPs, D-dimer
  8. 8. Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive
  9. 9. 10 Type Preload CO PVR SVR Hemmorrhagic Anaphylactic Cardiogenic Septic (Hyperdynamic) Septic (Hypodynamic) /
  10. 10. Non-hemorrhagic Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Environmental (dehydration) Hemorrhagic GI bleed Trauma Massive hemoptysis Abdominal Aortic Aneurysm rupture(AAA) Ectopic pregnancy, post-partum bleeding
  11. 11. Airway Breathing Circulation Establish 2 large bore IVs or a central line Crystalloids Normal Saline or Lactate Ringers-Up to 3 liters Packed Red Blood Cells O negative or cross matched Control any bleeding Arrange definitive treatment
  12. 12. TBW (42 L) = 2/3 of body weight (70 kg). ICF (28 L) = 2/3 of TBW. ECF (14 L) = 1/3 of TBW. Interstitial fluid (ISF, 10.5 L) = ¾ of ECF Intravascular fluid (IVF, 3.5 L) = ¼ of ECF.
  13. 13. “Crystalloids” Normal saline (just NaCl). Lactated ringers Plasmalyte-balanced crystalloid solution with multiple electrolye solution Normosol-solution of balanced electrolytes in water for injection. Last 3 have K+ and other stuff (acetate, Mg++, etc.)
  14. 14. Crystalloids enter entire ECF: ISF (3/4 of ECF) and IVF (1/4 of ECF). 3 or 4:1 for replacement of blood loss with crystalloid Colloids only enter IVF (in short term– 16 hour half- time for entrance into ISF) 1:1 replacement of blood loss with colloid
  15. 15. Blood trasfusion Packed red cells- increase O2 carrying capacity Plasma-fresh frozen plasma contains all stable proteins-albumin, globulin and clotting factors Normal human serum albumin-reduce edema, hypovolemic shock
  16. 16. DEXTRAN-isolated from beet root Inhibit rouleaux formation HYDROXYETHYL STARCH-resistant to hydrolysis by amylase, maintains blood volume longer POLYVINYL PYROLIDINE (PVP)-synthetic water soluble hydrophilic polymer Gelatin polymers-HAEMACCEL-polypeptide dissolved in electrolyte DEXTROSE-5% in water
  17. 17. 18 Vasoactive drugs are an important pharmacologic defense in the treatment of shock. May be required to support BP in the early stages of shock. These agents may be needed to: Enhance CO through the use of inotropic agents Increase SVR through the use of vasopressors
  18. 18. 19 Epinephrine , β1, (β2) 2-10 µg/min Norepinephrine , β1 0 - 2-20 µg/min Dopamine β1, DR, (α ) 1 - 30 Dobutamine β1, β2 2 - 20 Phenylphrine  20-200µg/min Vasopressin Angiotensin III 5 - 20 Amrinone PDI 2 -15 Drug Receptor CO SVR Dose Range 0 - (µg/kg/min) 1 0
  19. 19. 20 Nifedipine 0 - 0.5 - 10 Nitroglycerin 0 - 3 - 5 Nitroprusside 0 - 0.5 - 5 Prostacyclin 10 - 40 2 Drug CO SVR Dose Range (µg/kg/min)
  20. 20. 21 An endogenous precursor of norepinephrine with multiple dose-related effects stimulates alpha, beta and dopaminergic receptors. Low Dose (0.5 - 3 µg/kg/min) Predominantly dopaminergic (DR) effects Enhanced blood flow to renal and splanchnic beds Moderate Dose (5 -10 µg/kg/min) Positive inotropic effects (1) High Dose (>10 µg/kg/min) a-actions (vasoconstriction)
  21. 21. DRUG Common Uses Phenylephrine Septic Shock, neurogenic shock Norepinephrine Septic shock Epinephrine Anaphylaxis, ACLS, septic shock Dopamine Renal Insufficeny, septic shock, cardiogenic shock Dobutamine Cardiogenic shock (CS) Isoproterenol bradycardia due to heart block, effects HR Milrinone Cardiogenic shock- in those who don’t respond to dobutamine
  22. 22.  Epinephrine—catecholamine. Low doses stimulates beta receptors (so increases CO), causes bronchodilation as well. Larger doses act on alpha receptors.  Drug of choice in anaphylaxis. Prevents release of histamine, so reverses vasodilation and bronchoconstriction.  Can be given IV, subcut or even via ETT.
  23. 23. Isoxsuprine(isoproterenol)—synthetic catecholamine. Works exclusively on beta receptors. Increases heart rate, myocardial contractility and variable BP effects. Limited usefulness as vasopressor. Increases myocardial oxygen consumption and decreases coronary flow. Causes cardiac dysrhythmias.
  24. 24. Milrinone—used in combination with other agents in cardiogenic shock. Increases cardiac output and decreases SVR without increasing heart rate or myocardial oxygen consumption. Improved CO then increases renal perfusion, thus urinary output with decrease in circulating volume and decreased cardiac workload.
  25. 25. Norepinephrine—catecholamine. Primarily alpha 1 stimulation but also beta1 receptors. Useful in cardiogenic and septic shock. Does cause reduced renal blood flow so limits its long term use. Phenylephrine—adrenergic that stimulates alpha receptors. Longer duration of action than epinephrine. Reduction of renal and mesenteric blood flow limits prolonged use.
  26. 26.  Neosynephrine (phenyleprine)—adrenergic that stimulates alpha receptors. Longer duration of action than epinephrine. Reduction of renal and mesenteric blood flow limits prolonged use.
  27. 27. Two or more of Criteria-Systemic Inflammatory Response Syndrome (SIRS) Temp > 38 or < 36 C HR > 90 RR > 20 WBC > 12,000 or < 4,000 Plus the presumed existence of infection Blood pressure can be normal!
  28. 28. Sepsis plus refractory hypotension After bolus of 20-40 mL/Kg patient still has one of the following: SBP < 90 mm Hg MAP < 65 mm Hg MAP = [(2 x diastolic)+systolic] / 3
  29. 29. High fever Diffuse rash with desquamation on the palms and soles over subsequent 1-2 weeks Hypotension (may be orthostatic) and evidence of involvement of 3 other organ systems Streptococcal TSS more frequently presents with focal soft tissue inflammation and less commonly is associated with diffuse rash. Streptococcus pyogenes (group A Streptococcus) S aureus
  30. 30. • 2 large bore IVs • NS IVF bolus- 1-2 L wide open (if no contraindications) • Supplemental oxygen • Empiric antibiotics, based on suspected source, as soon as possible Antibiotics- Survival correlates with how quickly the correct drug was given Cover gram positive and gram negative bacteria
  31. 31. Zosyn(piperacillin+ tazobactum) 3.375 grams IV and ceftriaxone 1 gram IV or Imipenem 1 gram IV Add additional coverage as indicated Pseudomonas- Gentamicin or Cefepime MRSA- Vancomycin Intra-abdominal or head/neck anaerobic infections- Clindamycin or Metronidazole Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae Neutropenic – Cefepime or Imipenem
  32. 32. Vasoactive Drugs in Sepsis and Usual Hemodynamic Responses Drug Dose Cardiac Output Blood Pressure Systemic Vascular Resistance Dopamine* 2.5-20 mcg/kg/min + + + Norepinephrine† 0.05-2 mcg/kg/min + ++ ++ Epinephrine 0.05-2 mcg/kg/min ++ ++ + Phenylephrine 2-10 mcg/kg/min - ++ ++ Dobutamine‡ 2.5-10 mcg/kg/min + +/- -
  33. 33. • Signs: • Cool, mottled skin • Tachypnea • Hypotension • Altered mental status • Narrowed pulse pressure • Rales, murmur • Defined as: • SBP < 90 mmHg • CI < 2.2 L/m/m2 • PCWP > 18 mmHg • Pulmonary Arterial Wedge pressure
  34. 34. AMI Sepsis Myocarditis Myocardial contusion Aortic or mitral stenosis, HCM Acute aortic insufficiency
  35. 35. Often after ischemia, loss of LV function Lose 40% of LV clinical shock ensues CO reduction lactic acidosis, hypoxia Stroke volume is reduced Tachycardia develops as compensation Ischemia and infarction worsens
  36. 36. Goals- Airway stability and improving myocardial pump function Cardiac monitor, pulse oximetry Supplemental oxygen, IV access Intubation will decrease preload and result in hypotension -fluid bolus
  37. 37. AMI Aspirin, beta blocker, morphine, heparin If no pulmonary edema, IV fluid challenge If pulmonary edema Dopamine – will ↑ HR and thus cardiac work Dobutamine – May drop blood pressure Combination therapy may be more effective PCI(Percutaneous Coronary Intervention) or thrombolytics RV infarct Fluids and Dobutamine (no NTG) Acute mitral regurgitation or VSD Pressors (Dobutamine and Nitroprusside)
  38. 38. Correct hypotension: Fluid resuscitation to correct hypovolemia Inotropic or Vasopressor support: Dobutamine Milrinone Norepinephrine Dopamine Epinephrine Oxygenation If MI – ASA, Heparin, and Revascularization If arrhythmia – correct arrhythmia If extracardiac abnormality – reverse or treat cause
  39. 39. Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm Edema Most likely major underlying disturbance? Acute Pulmonary Edema Hypovolemia Low-output cardiogenic shock Arrhythmia Administer Furosemide Morphine Oxygen intubation Nitroglycerin Dopamine Dobutamine Administer Fluids Blood transfusions Cause-specific interventions Check Blood Pressure Brady cardia Tachyc ardia Check Blood Pressure Systolic BP (>100 mm Hg) Systolic BP (NO signs/sympto ms of shock) Systolic BP (signs/symptoms of shock) Systolic BP (<70 mm Hg + signs/symptoms of shock) See Sec. 7.7 in ACC/AHA Guidelines for patients with STEMI ACE Inhibitors Nitroglycerin Dobutamine Dopamine Norepinephrine Systolic BP (>100 mm Hg) Further Diagnostic/Therapeutic Considerations (for non-hypovolemic shock) Diagnostic / Therapeutic Pulmonary artery catheter, Intra-aortic balloon pump, echo, angiography, etc Reperfusion revascularization 41
  40. 40. • 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
  41. 41. Pruritus, flushing, urticaria appear Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse
  42. 42. ABC’s Angioedema and respiratory compromise require immediate intubation IV, cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line Corticosteriods H1 and H2 blockers
  43. 43. Epinephrine 0.3 mg IM of 1:1000 Repeat every 5-10 min as needed Caution with patients taking beta blockers- can cause severe hypertension due to unopposed alpha stimulation For CV collapse, 1 mg IV of 1:10,000 If refractory, start IV drip
  44. 44. Corticosteroids Methylprednisolone 125 mg IV Prednisone 60 mg PO Antihistamines H1 blocker- Diphenhydramine 25-50 mg IV H2 blocker- Ranitidine 50 mg IV Bronchodilators Albuterol nebulizer Atrovent nebulizer Magnesium sulfate 2 g IV over 20 minutes Glucagon For patients taking beta blockers and with refractory hypotension 1 mg IV q5 minutes until hypotension resolves
  45. 45. • Occurs after acute spinal cord injury • Sympathetic outflow is disrupted leaving unopposed vagal tone • Results in hypotension and bradycardia • Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)
  46. 46. Loss of sympathetic tone results in warm and dry skin Shock usually lasts from 1 to 3 weeks Any injury above T1 can disrupt the entire sympathetic system Higher injuries = worse paralysis
  47. 47. A,B,Cs Remember c-spine precautions Fluid resuscitation Keep MAP at 85-90 mm Hg for first 7 days Thought to minimize secondary cord injury If crystalloid is insufficient use vasopressors Search for other causes of hypotension For bradycardia Atropine Pacemaker
  48. 48. Methylprednisolone Used only for blunt spinal cord injury High dose therapy for 23 hours Must be started within 8 hours Controversial- Risk for infection, GI bleed
  49. 49. Tension pneumothorax Air trapped in pleural space with 1 way valve, air/pressure builds up Mediastinum shifted impeding venous return Chest pain, SOB, decreased breath sounds Confirmation -CXR Rx: Needle decompression, chest tube
  50. 50. Cardiac tamponade Blood in pericardial sac prevents venous return to and contraction of heart Related to trauma, pericarditis, MI Beck’s triad: hypotension, muffled heart sounds, JVD Diagnosis: large heart CXR, echo Rx: Pericardiocentisis
  51. 51. Pulmonary embolism Virchow’s triad: Hypercoagulability. Hemodynamic changes (stasis, turbulence) Endothelial injury/dysfunction. Signs: Tachypnea, tachycardia, hypoxia Low risk: D-dimer Higher risk: CT chest Rx: Heparin, consider thrombolytics
  52. 52. Aortic stenosis Resistance to systolic ejection causes decreased cardiac function Chest pain with syncope Systolic ejection murmur Diagnosed with echo Vasodilators (NTG) will drop pressure! Rx: Valve surgery
  53. 53. Download slides from Authorstream-raghuprasada Slideshare-raghuprasada Youtube-raghuprasada

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