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“AN APPROACH TO A PATIENT IN SHOCK”

“AN APPROACH TO A PATIENT IN SHOCK”. DR NAILA NAZ HOUSE OFFICER MU 1 Dated:6 th Sept’06. REFERENCES:. James Allen, M.D. Professor of Internal Medicine Pulmonary and Critical Care Medicine Ohio State University Principles and practice of medicine by Davidson.

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“AN APPROACH TO A PATIENT IN SHOCK”

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  1. “AN APPROACH TO A PATIENT IN SHOCK” DR NAILA NAZ HOUSE OFFICER MU 1 Dated:6th Sept’06

  2. REFERENCES: • James Allen, M.D.Professor of Internal MedicinePulmonary and Critical Care MedicineOhio State University • Principles and practice of medicine by Davidson. • Current Concepts on the Management of Shock by Max H. WeiL M.D., PH.D.

  3. GOALS: • Definition..? • Pathophysiology • Etiology • Stages • Shock syndromes • Management!!

  4. SHOCK • DEFINITION: “a condition in which the cardiovascular system fails to perfuse tissues adequately” • An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues

  5. Inadequate tissue perfusion can result in: -generalized cellular hypoxia (starvation) -widespread impairment of cellular metabolism -tissue damage    -organ failure - death

  6. PATHOPHYSIOLOGY • Impaired tissue perfusion occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand. • All Types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome.

  7. Cells switch from aerobic to anaerobic metabolism lactic acid production   Cell function ceases & swells   membrane becomes more permeable    electrolytes & fluids seep in & out of cell  Na+/K+ pump impaired   mitochondria damage  cell death   

  8. COMPENSATORY MECHANISMS “Sympathetic Nervous System (SNS)-Adrenal Response” • Neurohormonal response • Hormonal Renin-angiotension system Antidiuretic Hormone Adrenal cortex

  9. NEUROHORMONAL RESPONSE • Stimulated by baroreceptors • Increased heart rate • Increased contractility • Vasoconstriction (SVR-Afterload) • Increased Preload

  10. RENIN-ANGIOTENSIN SYSTEM • Decrease renal perfusion • Releases renin   angiotension I • angiotension II…potent vasoconstriction & • releases aldosterone adrenal cortex • sodium & water retention

  11. ANTIDIURETIC HORMONE • Osmoreceptors in hypothalamus stimulated • ADH released by Posterior pituitary gland • Vasopressor effect to increase BP • Acts on renal tubules to retain water  

  12. ADRENAL CORTEX • Anterior pituitary releases adrenocorticotropic hormone (ACTH) • Stimulates adrenal Cx to release glucorticoids • Blood sugar increases to meet increased metabolic needs

  13. FAILURE OF COMPENSATORY RESPONSE • Decreased blood flow to the tissues causes  cellular hypoxia • Anaerobic metabolism begins • Cell swelling, mitochondrial disruption, and eventual cell death

  14. If Low Perfusion States persists:  “IRREVERSIBLE DEATH IMMINENT”!!

  15. STAGES OF SHOCK • Initial stage • Compensatory stage • Progressive stage • Irreversible or refractory stage

  16. INITIAL STAGE • Tissues are under perfused • Decreased CO • Increased anaerobic metabolism • Lactic acid is building

  17. COMPENSATORY STAGE • Reversible. • SNS activated by low CO..attempting to compensate for the decrease tissue perfusion.

  18. PROGRESSIVE STAGE • Failing compensatory mechanisms.. profound vasoconstriction from the SNS     • Ischemia • Lactic acid production is high    • metabolic acidosis

  19. REFRACTORY STAGE • Irreversible • Cellular necrosis • Multiple Organ Dysfunction Syndrome may occur 

  20. ETIOLOGY OF SHOCK 1.Cardiogenic • acute myocardial infarction (implies > 40% LV muscle loss) -shock accompanies 6-20% of all acute MI's -more common with patients with anterior MI

  21. b) dilated cardiomyopathy c) acute myocarditis d) mechanical -mitral regurgitation -ventricular septal defect -left ventricular aneurysm -left ventricular outflow obstruction e) metabolic and pharmacologic myocardial depression f) arrhythmias

  22. 2.Extracardiac Obstructive a- massive pulmonary embolism b- severe pulmonary hypertension c- pericardial tamponade d- tension pneumothorax

  23. 3.Oligemic a) hemorrhagic b) volume depletion c) adrenal insufficiency

  24. 4.Distributive a) septic b) toxic agents (including adverse reaction to medications and certain drug overdoses) c) anaphylaxis d) neurogenic

  25. CLINICAL MANIFESTATIONS

  26. SHOCK SYNDROMES • Hypovolemic Shock blood VOLUME problem • Cardiogenic Shock blood PUMP problem • Distributive Shock blood VESSEL problem

  27. HYPOVOLEMIC SHOCK • Loss of circulating volume “Empty tank” • ETIOLOGY: • Internal or External fluid loss • Intracellular and extracellular compartments • Most common causes: • Hemmorhage • Dehydration

  28. CLINICAL MANIFESTATIONS • Tachycardia and tachypnea • Weak, thready pulses • Hypotension • Skin cool & clammy • Mental status changes • Decreased urine output: dark & concentrated

  29. ASSESMENT OF SEVERITY • S/S vary depending on severity of fluid loss: 15%(750ml) compensatory mechanism maintains CO 15-30% (750-1500ml) Hypoxemia,  decreased BP & UOP 30-40% (1500-2000ml) Impaired compensation & profound shock along with severe acidosis 40-50% refractory stage: loss of volume death 

  30. MANAGEMENT OF HYPOVOLEMIC SHOCK • Goal: Restore circulating volume, tissue perfusion and correct cause. • Early Recognition- Do not relay on BP! (30% fluid loss) • Control hemorrhage • Restore circulating volume • Optimize oxygen delivery • Vasoconstrictor.. if BP still low after volume loading

  31. CARDIOGENIC SHOCK “The impaired ability of the heart to pump blood” • Pump failure of the right or left ventricle • Most common cause is LV MI (Anterior) • Occurs when > 40% of ventricular mass damage • Mortality rate of 80 % or >

  32. CLINICAL MANIFESTATIONS • Abnormal heart sounds  -Murmurs -Pathologic S3 (ventricular gallop) -Pathologic S4 (atrial gallop) • Pericardial tamponade -muffled heart tones -elevated neck veins

  33. Tension pneumothorax - JVP - tracheal deviation - decreased or absent unilateral breath sounds - chest hyperresonance on affected side

  34. MANAGEMENT OF CARDIOGENIC SHOCK • Goal of management : • Treat Reversible Causes • Protect  ischemic myocardium • Improve tissue perfusion

  35. MANAGEMENT • Increased pumping action  & decrease workload of the heart • Inotropic agents • Vasoactive drugs • Intra-aortic balloon pump • Cautious administration of fluids • Transplantation • Consider thrombolytics, angioplasty in specific cases

  36. Optimizing pumping function of the heart • Pulmonary artery monitoring is a necessity !! • Aggressive airway management: Mechanical Ventilation • Judicious fluid management • Vasoactive agents • Dobutamine • Dopamine

  37. Morphine as needed (Decreases preload, anxiety) • Cautious use of diuretics in CHF • Vasodilators as needed for afterload reduction • Short acting beta blocker, esmolol, for refractory tachycardia

  38. DISTRIBUTIVE SHOCK • Inadequate perfusion of tissues through maldistribution of blood flow • Intravascular volume is maldistributed because of alterations in blood vessels • Cardiac pump & blood volume are normal but blood is not reaching the tissues

  39. ETIOLOGY: • Septic Shock (Most Common) • Anaphylactic Shock • Neurogenic Shock

  40. SEPTIC SHOCK • SEPSIS “Systemic Inflammatory Response (SIRS) to INFECTION manifested by two or > of following: 1. Temp > 38 or < 36 centigrade 2. HR > 90 3. RR > 20 or PaCO2 < 32 4. WBC > 12,000/cu mm or > 10% Bands (immature wbc) “

  41. SEPTIC SHOCK: • Sepsis with: • Hypotension (SBP < 90 or > 40 reduction from baseline) & • Tissue perfusion abnormalities invasion of the body by microorganisms & failure of body’s defense mechanism.

  42. PATHOPHYSIOLOGY OF SEPTIC SHOCK • Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses • Microorganisms enter body • Mediator Release • Activation of Complement, kallikrein / kinin/ coagulation & fibrinolytic factors platelets, neutrophils & macrophages…damage to endothelial cells. • ORGAN DYSFUNCTION 

  43. CLINICAL PRESENTATION • Two phases: • “Warm” shock - early phase • hyperdynamic response, VASODILATION • “Cold” shock - late phase • hypodynamic response • DECOMPENSATED STATE

  44. MANAGEMENT OF SEPTIC SHOCK • Prevention !!! • Find and kill the source of the infection • Fluid Resuscitation • Vasoconstrictors • Inotropic drugs

  45. ANAPHYLACTIC SHOCK • A type of distributive shock that results from widespread systemic allergic reaction to an antigen • This hypersensitive reaction is LIFE THREATENING.

  46. CLINICAL MANIFESTATIONS • Almost immediate response to inciting antigen • Cutaneous manifestations • urticaria, erythema, pruritis, angioedema • Respiratory compromise • stridor, wheezing, bronchorrhea, resp. distress • Circulatory collapse • tachycardia, vasodilation, hypotension  

  47. MANAGEMENT • Early Recognition, treat aggressively • AIRWAY SUPPORT • IV EPINEPHRINE (open airways) • Antihistamines, diphenhydramine 50 mg IV • Corticosteroids • IMMEDIATE WITHDRAWAL OF ANTIGEN IF POSSIBLE • PREVENTION  • Judicious crystalloid administration • Vasopressors to maintain organ perfusion • Positive inotropes • Patient education  

  48. NEUROGENIC SHOCK • A type of distributive shock that results from the loss or suppression of sympathetic tone • Causes massive vasodilatation in the venous vasculature, venous return to heart, cardiac output. • Most common etiology: Spinal cord injury above T6 • Neurogenic is the rarest form of shock!

  49. CLINICAL MANIFESTATION • Hypotension • Bradycardia • Hypothermia • Warm, dry skin • PAWP • CO • Flaccid paralysis below level of the spinal lesion

  50. MANAGEMENT • Hypovolemia- careful fluid replacement for BP<90mmHg, UO<30cc/hr • Observe closely for fluid overload • Vasopressors may be needed • Hypothermia • Treat Hypoxia • Maintain ventilatory support

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