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![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](https://image.slidesharecdn.com/classdrugtherapyofshock-160310043509/75/Class-drug-therapy-of-shock-29-2048.jpg)
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Class drug therapy of shock
1. Shock is defined as inadequate tissue perfusion resulting in cellular dysfunction. It can occur with normal or low blood pressure and results from various causes like sepsis, hemorrhage, cardiac failure, etc. 2. Early goal-directed therapy for septic shock involves rapid fluid resuscitation, antibiotics, and vasopressors to maintain adequate perfusion. Dopamine, norepinephrine, and epinephrine are commonly used vasopressors. 3. Cardiogenic shock results from inadequate cardiac output, usually from acute myocardial infarction or myocarditis. It requires fluids, inotropes like dobutamine, and revascularization when possible.
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Discusses the definition and physiology of shock, inadequate oxygen delivery, symptoms, and progression leading to end organ failure.
Focuses on the history, physical examination, lab investigations, imaging studies, and diagnostic evaluations necessary for shock.
Outlines various types of shock: hypovolemic, septic, cardiogenic, and others, distinguishing causes and effects on the body.
Details fluid resuscitation methods, including crystalloid and colloid solutions for shock treatment.
Discusses vasoactive drugs and their roles in managing shock, emphasizing dosages and effects on cardiac output.
Details various inotropic agents used in shock, their dosing, and effects on different types of shock.
Defines systemic inflammatory response syndrome (SIRS) and discusses the management of septic shock with vasopressors.
Details clinical signs of shock, acute myocardial infarction, treatment strategies, and monitoring parameters.
Describes management protocols for anaphylaxis, focusing on emergency treatment and medication administration.
Explains neurogenic shock, its cause, symptoms, fluid resuscitation needs, and treatment protocols.
Outlines urgent complications associated with shock such as tension pneumothorax, cardiac tamponade, and pulmonary embolism.
Provides information on where to download related materials and resources from the author.
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Class drug therapy of shock
- 1. Dr. RAGHU PRASADAM S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
- 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. • Inadequate systemicoxygen 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
- 5. Progression of physiologiceffects as shock ensues Cardiac depression Respiratory distress Renal failure DIC Result is end organ failure
- 6. • History • Recentillness • 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
- 7. • Infectious source Cardiorespiratorymonitor Pulse oximetry Supplemental oxygen IV access ABG, lab investigations-CBC, Chemistries, Lactate Coagulation studies, Cultures Foley catheter
- 8. CT of head/sinuses Lumbarpuncture Wound cultures Acute abdominal series Abdominal/pelvic CT or US Cortisol level Fibrinogen, FDPs, D-dimer
- 9.
- 10. 10 Type Preload COPVR SVR Hemmorrhagic Anaphylactic Cardiogenic Septic (Hyperdynamic) Septic (Hypodynamic) /
- 11. Non-hemorrhagic Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Environmental (dehydration) Hemorrhagic GI bleed Trauma Massivehemoptysis Abdominal Aortic Aneurysm rupture(AAA) Ectopic pregnancy, post-partum bleeding
- 12. Airway Breathing Circulation Establish2 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
- 13. 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.
- 14. “Crystalloids” Normal saline (justNaCl). 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.)
- 15. Crystalloids enter entireECF: 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
- 16. Blood trasfusion Packed redcells- 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
- 17. DEXTRAN-isolated from beetroot 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
- 18. 18 Vasoactive drugs arean 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
- 19. 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
- 20. 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)
- 21. 21 An endogenous precursorof 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)
- 22. DRUG Common Uses PhenylephrineSeptic 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
- 23. Epinephrine—catecholamine. Lowdoses 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.
- 24. Isoxsuprine(isoproterenol)—synthetic catecholamine. Works exclusivelyon 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.
- 25. Milrinone—used in combinationwith 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.
- 26. Norepinephrine—catecholamine. Primarily alpha 1stimulation 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.
- 27. Neosynephrine (phenyleprine)—adrenergicthat stimulates alpha receptors. Longer duration of action than epinephrine. Reduction of renal and mesenteric blood flow limits prolonged use.
- 28. Two or moreof 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!
- 29. Sepsis plus refractoryhypotension 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
- 30. High fever Diffuse rashwith 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
- 32. • 2 largebore 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
- 33. Zosyn(piperacillin+ tazobactum) 3.375grams 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
- 34. Vasoactive Drugs inSepsis 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 + +/- -
- 35. • 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
- 36. AMI Sepsis Myocarditis Myocardial contusion Aortic ormitral stenosis, HCM Acute aortic insufficiency
- 37. 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
- 38. Goals- Airway stabilityand improving myocardial pump function Cardiac monitor, pulse oximetry Supplemental oxygen, IV access Intubation will decrease preload and result in hypotension -fluid bolus
- 39. 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)
- 40. Correct hypotension: Fluid resuscitationto 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
- 41. 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
- 42. • 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
- 43. Pruritus, flushing, urticariaappear Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse
- 44. ABC’s Angioedema and respiratorycompromise require immediate intubation IV, cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line Corticosteriods H1 and H2 blockers
- 45. Epinephrine 0.3 mg IMof 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
- 46. Corticosteroids Methylprednisolone 125 mgIV 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
- 47. • Occurs afteracute 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)
- 48. Loss of sympathetictone 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
- 49. A,B,Cs Remember c-spine precautions Fluidresuscitation 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
- 50. Methylprednisolone Used only forblunt spinal cord injury High dose therapy for 23 hours Must be started within 8 hours Controversial- Risk for infection, GI bleed
- 51. Tension pneumothorax Air trappedin 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
- 52. Cardiac tamponade Blood inpericardial 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
- 53. 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
- 54. Aortic stenosis Resistance tosystolic ejection causes decreased cardiac function Chest pain with syncope Systolic ejection murmur Diagnosed with echo Vasodilators (NTG) will drop pressure! Rx: Valve surgery
- 55.