Pharmacotherapy of shock

Pharmacotherapy of shock

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  DR. D. K.BRAHMA ASSOCIATE PROFESSOR DEPARTMENT OF PHARMACOLOGY NEIGRIHMS, SHILLONG Pharmacotherapy of Shock
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  Introduction • Definition: Complexacute circulatory failure associated with hypoperfusion of tissues, which is incompatible with life if untreated and persisting for more than a short time • Initiated by – trauma, acute blood loss, depletion of body fluids, severe infection or acute myocardial dysfunction • Mechanism of Shock: Hypovolemic, Cardiogenic, Obstructive, Distributive and Septic
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  Classification of Shock I.Hypovolemic or Oligemic: i. Acute blood loss – burns and haemorrhage ii. Dehydration and Sodium depletion – vomiting, diarrhoea, diabetic ketoacidosis and Addison`s disease II. Bacteremic endotoxic or septic: Severe infections in gm –ve bacteria like E. coli, gm +ve resistant streptococci TSS. Deficiency of adrenal gland function and vasopressin production III. Cardiogenic shock: MI, Acute myocarditis and severe paroxysmal tachycardia IV. Anaphylactic shock V. Neurogenic shock: Spinal anaesthesia, spinl chord injury, abdominal and testicular trauma and perofration of hollow viscus VI. Haemo-obstructive shock – massive pulmonary embolism
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  Hypovolemia Mechanism Hypovolemia – Reductionin circulating blood volume Reduced blood flow to skin, kidneys and intestines Slowing of blood flow, local haemoconcentration in capillaries – thrombi formation Tissue hypoxia – acidosis – liberation of histamine, PG and cardio depressant peptides to circulation Baroreceptor - Generalized Compensatory Sympatho adrenal discharge Excessive sympatho- adrenal discharge Peripheral vasoconstriction – clinical manifestations. Pooling of blood to periphery, sluggish micro circulation Damage to intracellular structures & fall in diastolic BP – less coronary flow (cardiogenic element of shock) – also less cerebral blood flow
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  Septic Shock Mechanism Toxinsreleased by Microorganisms – Exotoxins (TSS) and Endotoxins (gm –ve) PHAGOCYTES and ENDOTHELIAL CELLS Release of Cytokines - TNFα, IL (IL-1β) and PAF Release of LTs, PGs and TXA2Injury to BV, inflammation, vasodilatation increased permeability, coagulation and complement cascades and fluid loss – hypovolemia Depression of myocardium and Diffuse Cell Injury, – multiple organ failure
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  Clinical Picture  Generally– pallor, sweating, cold extremities, rapid and thready pulse and air hunger  Cyanosis of the extremities  Oliguria – urine output < 25 ml per hour for 4 hours or <500 ml/24 hours  Mental changes (somnolence, confusion, restlessness) and acidosis  Difference of temperature between rectum and skin  Central venous pressure (CVP) - guide to hypovolemia estimation  Fluid replacement – 10-20 ml per minute for 10-15 minutes  No rise in of CVP – hypovolemia  CVP exceeds 15 cm of water or rise > 5 cm of water – Pump Failure  Pulmonary artery occlusive pressure (PAOP)  Remember - Diagnose before BP falls significantly – 25% deficit
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  Management – Hypovolemicshock  Early recognition of shock state - Restoration of effective blood volume suitable fluids – CVP measurement  Whole blood and plasma  Colloidal plasma substitutes – Dextran, hydroxyethyl starch, polyvinylpyrrolidone etc.  Crystalloid plasma substitutes – NaCl and 5% Dextrose  Lactic acidosis correction - Sodium bicarbonate  Abnormalities of electrolyte balance correction  Correction of causative factor – haemostasis, surgical removal of necrotic tissue, antibiotics, defibrillation etc.  Injection Morphine for pain relieving – except head injury and acute abdomen  Vasopressor agents – DA (0.2 – 1 mg/min) or NA to correct hypotension – after fluid replacement only (NA – 4 mg in 50 ml)  Oxygen administration to correct tissue hypoxemia
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  IV Fluid Severe hypovolemia,low/unrecordable BP, feeble/unpalpable pulse etc. IV fluid wide open rate (10 – 20 ml/min) for 1 hour (approx.) for fluid replacement  If improvement – reduce to IF fluid and continue till 24 hours  If no improvement – Increase/Prolong the IF fluid administration  If no improvement – haemtocrit rise - IV Colloid 10 mg/kg/hour  If no improvement – Blood/Plasma transfusion
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  Management - BacteremicShock Endotoxic Shock: Severe infection and tissue hypoperfusion – organ dysfunction Antibiotics – empirical to start with Surgical Removal if required Blood volume expansion, correction of acidosis, Casopressor agents, correction of hypoglycaemia Lung protective ventilation – low tidal volumes (6 ml/kg of ideal body weight)
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  Acute Myocardial Infarction Beforehospitalization  Sublingual Nitroglycerine 0.4 mg every 5 minutes till pain subsides (max 3 doses)  Relief of Pain: Morphine Injection 10 mg IV for 10 minutes together with IV Metoclpramide  Repeat after 30 minutes if necessary – alternatively Pethidine or Bupreonorphine (SC)  Absolute confinement to bed - Oxygen 100% by face mask  Antiplatelet therapy – 80 to 160 mg Aspirin to be chewed
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  AMI – afterhospitalization  Bed Rest  Maintenance of blood volume and tissue perfusion – elevated lower limbs and IV fluid 5% Dextrose – CVP or PAOP  Treatment of hypotension (to decrease preload and increase CO) – IV inotropic drugs – Dopamine or Dobutamine or IV furosemide  Correction of acidosis – sod. Bicarbonate infusion  Prevention of arrhythmia – IV Beta blockers – Propranolol (0.1 mg/kg in 3 divided doses at 5-10 minutes interval followed by orally every 6 hourly) … . Tachyarrhythmia (IV Lignocaine – 1 – 2 mg/minute IV or Procainamide)  Continue IV Vasodilators (GTN) or Nitroprusside  Thrombolytic Therapy – continue with Aspirin and start Streptokinase or Urokinase or Alteplase (rt-PA) or tenecteplase … 2.5 lac IU IV over 10 minutes followed by 5 Lac IU over next 60 minutes …. 100 mg for 1 hr 15 mg – 50 mg – 15 mg … PCI (stent implantation)  Prevention of remodeling and future attacks – ACEIs or ARBs Platelet inhibitors
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  Anaphylactic shock Management Lay the patient flat and raise legs  Torniquet if possible to obstruct draining blood flow from the site of antigen deposition  Airway maintenance  Adrenaline Injection (1:1000) IM – 0.5 ml slowly - if severely ill give IV adrenaline (1:10,000) 3-5 ml slowly … can be repeated after 15-20 minutes (Beta blocker ?)  IF fluid – large fluid amount – colloids – with Dopamine or NA  Corticosteroids – IV Hydrocortisone 100 mg follwed by prednisolone  Antihistaminics: Chlorpheniramine 10 – 20 mg slow IV over 1 minute – can be repeated  Bronchodilators – aminophylline IV or nebulized salbutamol  Supportive measure – Oxygen and assisted ventilation
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  Other types ofShocks Neurogenic shock: Treated like hypovolemic shock with use of vasopressor agents Haemo-obstructive shock – Like cardiogenic shock
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  Case Study -Example  First Aid Staff initiated transport of a 25-year-old female who cut both of her wrists in an apparent suicide attempt. On arrival of the First Aid Staff at the scene, the patient was awake, but drowsy, with active bleeding from both wrists. The field team estimates a 900-ml blood loss on scene. The bleeding is now controlled with direct pressure, and a large-bore IV catheters have been established. The patient’s present systolic blood pressure is 60 mm Hg. Normal saline IV lines are running wide open. How do you manage the case in Hospital ???  This patient is suffering from hypovolemic shock and requires fluid resuscitation. In this case, the hemorrhage is controlled, and fluids should be administered at a wide open rate with pressure applied to the IV fluid bag to increase the flow. Unlike the uncontrolled hemorrhage model in which aggressive fluid administration may lead to increased bleeding, the bleeding here is controlled. Therefore, fluid volume should be rapidly replaced to normalize blood pressure
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  Thank you –Khublei shibun