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IVMS-CV -Pathophysiology, Pharmacology and Treatment of Shock

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Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com

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IVMS-CV -Pathophysiology, Pharmacology and Treatment of Shock

  1. 1. CV Pharmacology- Pathophysiology and Treatment of Shock Recommended Reading: Autonomic pharmacology Formatives: Practice Question Set #1 Clinical: E-Medicine Articles Shock, Cardiogenic Shock, Hypovolemic Shock, Septic Prepared and presented by: Marc Imhotep Cray, M.D. BMS / CK-CS Teacher http://www.imhotepvirtualmedsch.com/
  2. 2. 2 Shock (circulatory) See: Shock (circulatory) Effects of inadequate perfusion on cell function From: http://en.wikipedia.org/wiki/Shock_%28circulatory%29
  3. 3. 3 Shock, Circulatory Defined  Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition where insufficient blood flow reaches body tissues  As blood carries oxygen and nutrients around body, reduced flow hinders delivery of these components to tissues, and can stop tissues from functioning properly  The process of blood entering tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state See: Shock: An Overview PDF by Michael L. Cheatham, MD, Ernest F.J. Block, MD, Howard G. Smith, MD, John T. Promes, MD, Surgical Critical Care Service, Department of Surgical Education, Orlando Regional Medical Center Orlando, Florida
  4. 4. 4 The problem in shock  Altered circulatory parameters  Compromised microcirculation  Persistent severe hypoxia  Multiple organ failure From: http://www.cvpharmacology.com/clinical topics/hypotension.htm
  5. 5. 5 Main types of Shock  Vasoconstrictive  Trauma, bleeding, burning, ileus (volumen loss)  Pulmonary embolism (impaired cardiac filling)  Myocardial infarction (impaired cardiac contraction)  Vasodilatative  Anaphylaxis, sepsis (maldistribution of blood flow)  Spinal medullary injury (venous pooling)  Hypothermia
  6. 6. 6 Classification  In 1972 Hinshaw and Cox suggested the following classification which is still used today  It uses four types of shock: 1. hypovolemic, 2. cardiogenic, 3. distributive and 4. obstructive shock
  7. 7. 7 Classification (based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox)  Hypovolaemic  Hemorrhagic, Fluid depletion, Increased vascular capacitance  Cardiogenic  Myopathic, Mechanical, Arrhythmic  Distributive  Septic, etc.  Obstructive  PE, pericarditis, pnumothorax etc.
  8. 8. 8 Hypovolemic shock Hypovolemic shock –  This is the most common type of shock and based on insufficient circulating volume.  Its primary cause is loss of fluid from the circulation from either an internal or external source.  An internal source may be haemorrhage.  External causes may include extensive bleeding, high output fistulae or severe burns.
  9. 9. 9 Cardiogenic shock Cardiogenic shock –  This type of shock is caused by the failure of the heart to pump effectively.  This can be due to damage to the heart muscle, most often from a large myocardial infarction.  Other causes of cardiogenic shock include arrhythmias, cardiomyopathy, congestive heart failure (CHF), and cardiac valve problems.
  10. 10. 10 Distributive shock Distributive shock –  As in hypovolaemic shock there is an insufficient intravascular volume of blood.  This form of "relative" hypovolaemia is the result of dilation of blood vessels which diminishes systemic vascular resistance. Examples of this form of shock are: 1. Septic shock 2. Anaphylactic shock 3. Neurogenic shock
  11. 11. 11 Obstructive shock Obstructive shock –  In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest.  Several conditions result in this form of shock. 1. Cardiac tamponade 2. Tension pneumothorax 3. pulmonary embolism 4. Aortic stenosis
  12. 12. 12 Endocrine shock based on endocrine disturbances. Recently a fifth form of shock has been introduced:  Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency  Thyrotoxicosis may induce a reversible cardiomyopathy  Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage  However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition  Relative adrenal insufficiency in critically ill patients where present hormone levels are insufficient to meet the higher demands
  13. 13. 13 Comparison of types of shock (Early stage) Vasoconstrictive Vasodilatative Hypovolamic Cardiogenic Circulatory Septic Cardiac index Cardiac index Peripheral resistance Peripheral resistance Blood Volume Blood Volume Malperfusion and organ dysfunction are the ultimate end point of any shock stage
  14. 14. 14 Decreased cardiac output Decreased blood pressure Decreased tissue perfusion Decreased coronary perfusion Decreased myocardial function Microcirculatory obstruction Cellular aggregation Microcirculatory demage Cell hypoxia Metabolic acidosis Decreased myocardial contraction Inracellular fluid loss Decreased venous return BP = CO x SVR Pathophysiology Concept Map
  15. 15. 15 Hypovolemic Shock loss in circulatory volume  Decreased venous return  Decreased filling of the cardiac chambers  Decreased cardiac output  increase in the systemic vascular resistance (SVR). low central venous pressure (CVP), a low pulmonary capillary wedge pressure (PCWP), low cardiac output (CO) and cardiac index (CI), and high SVR. The arterial blood pressure may be normal or low.
  16. 16. 16 HYPOVOLEMIC (oligemic) SHOCK  Hemorrhagic  - Trauma  - Gastrointestinal  - Retroperitoneal  • Fluid depletion (nonhemorrhagic)  External fluid loss  Dehydration  Vomiting  Diarrhea  Polyuria  Interstitial fluid redistribution  Thermal injury  Trauma  Anaphylaxis  • Increased vascular capacitance (venodilatation)  - Sepsis  - Anaphylaxis  - Toxins/Drugs
  17. 17. 17 Cardiogenic Shock  dependent on poor pump function  acute catastrophic failure of left ventricular pump function high PCWP, low CO and CI, and generally a high SVR
  18. 18. 18 CARDIOGENIC  Myopathic  -Myocardial infarction (Left ventricle, Right ventricle)  -Myocardial contusion (trauma)  -Myocarditis  -Cardiomyopathy  -Post ischemic myocardial stunning  -Septic myocardial depression  -Pharmacologic Anthracycline cardiotoxicity Calcium channel blockers
  19. 19. 19  Mechanical  -Valvular failure Regurgitant Obstructive  -Hypertropic cardiomyopathy  -Ventricular septal defect  Arrhythmic  -Bradycardia Sinus (e.g.,vagal syncope)Atrioventricular blocks  -Tachycardia SupraventricularVentricular CARDIOGENIC (2)
  20. 20. 20 DISTRIBUTIVE  Septic (bacterial, fungal, viral, rickettsial)  Toxic shock syndrome  Anaphylactic, anaphylactoid  Neurogenic (spinal shock)  Endocrinologic  Adrenal crisis  Toxic (e.g., nitroprusside, bretyllium)
  21. 21. 21 Extracardiac obstructive shock Impaired diastolic filling (decreased ventricular preload)  a physical impairment to adequate forward circulatory flow involving mechanisms (different than primary myocardial or valvular dysfunction)  Frank decrease in filling pressures (as in mediastinal compressions of great veins) or  trends towards equalization of pressures in the case of cardiac tamponade or  markedly increased right ventricular filling pressures High CVP, low PCWP Cardiac output is usually decreased with increased SVR.
  22. 22. 22 Symptoms  Narrowing of pulse pressure  Tachycardia, hypotension  Restlessnes  Disphoria  Decreased urine output  Anxiety  Cool, clammy skin  Obtundation  Dyspnea  Unconsciousness
  23. 23. 23 Treatment of shock Generalities:  Positioning, avoiding hypothermia  Maintaining adequate oxygenization  Fluid resuscitation  Pain relief ?  (inotropic treatment?)
  24. 24. 24 Enhance compensatory phase of the shock  Maintenance of mean circulatory pressure  Maximizing cardiac function  Redistributing perfusion to vital organs  Optimizing unloading of oxygen at tissues
  25. 25. 25 Maintain Volume  -Fluid redistribution to vascular space  From interstitium (Starling effect)  From intracellular space (Osmotic effect)  -Decreased renal fluid losses  Decreased glomerular filtration rate (GFR) Increased aldosterone  Increased vasopressin
  26. 26. 26 Mintain Pressure  Decreased venous capacitance  Increased sympathetic activity  Increased circulating (adrenal) epinephrine  Increased angiotensin  Increased vasopressin
  27. 27. 27 Maximize Cardiac Performance  Increased contractility  Sympathetic stimulation  Adrenal stimulation
  28. 28. 28 Early mechanical ventilation  allows blood flow to be redistributed  tends to reverse lactic acidosis  supports the patient until other therapeutic measures can be effective Tidal volumes in the order of 7-10 mlkg-1 of lean body mass, an O2 concentration that results in arterial saturation not less than 92%, adequate ventilator rate and sedation to minimize the work of breathing.
  29. 29. 29 Fluid resuscitation  IV line  Large bore cannula  More iv line  Choice of infusion  Lactated Ringer's solution (initial bolus: 10-25 ml/kg / 10 min.)  Colloids  Dextrane  Hydroethylstrach  Gelatine  Small volume resuscitation  Rate, amount  General conditions  parameters ( BP, Pulse, CVP, SatO2 etc)
  30. 30. 30 Dextrane  Molecular weight: 40K - 60/70K Dalton  Concentration: 10% (40K)*; 6% (60/70K)**  Water binding: 25 ml/g -- 4 - 6 h  Plasma expanding effect: * 180-200; ** 150%  Elimination:  metabolic  kidney
  31. 31. 31 Hydroxyethylstrach  Molecular weight: 450K - 200K - 40K Dalton  Substitution: 0,5 - 0,62 - 0,7  Water binding: 15 - 20 ml/g -- 3 - 6 h  6% HES (200K/0,5) -- plasma substitution (100%)  10%HES (200K/0,5) -- plasma expanding (140%)  Elimination:  kidney  12 - 24 h (65 - 70 %) --- 168 h
  32. 32. 32 Inotropic drugs Inotropie Heart rate SVR Kidney Blood flow Cornarry Blood flow Cardiac Output Dose Epinephrin ++ + + - + + 10-30 mcg/min Norepinephrin ++ 0 ++ -- + + 2-8 mcg/min Dopamin ++ + - ++ + ++ 2-5 mcg/min/kg Dobutamin +++ (+) -- + + ++ 5-15 mcg/min/kg Isoproterenol ++ ++ - + + ++ 5 mcg/mi Amrinon +++ 0 -- + + ++ Bolus 0.5 - 1.5 mg/kg Cont.: 2 to 10 mcg/kg/min
  33. 33. 33 Reference Resource Joynt, Gavin (April 2003). "Introduction to management of shock for junior ICU trainees and medical students". The Chinese University of Hong Kong. Retrieved on 9 October, 2006.

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