physiology shock

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  • 1. The Physiology of Shock2R.E.B,, 2003

2. Shock occurs whenthe rate of arterial blood flow is inadequate to meet metabolic tissue needs and is the consequence of cardio-vascular collapse Essentials of diagnosis are Hypotension (100 beats/min (sympathetic response) oliguria blood pressure may be maintained in supine patient Severe (loss of > 40% blood volume) Classic signs of shock appear with hemodynamic instability (Cave: if mental confusion occurs is an ominous clinical sign) Only very short time frame may separate mild and severe shock symptoms that lead, when left untreated, to progressive and irreversible cell injury and death 6. Signs and Symptoms Low Blood Pressure Systolic BP is usually below 90 mmHg Pulse is rapid and weak Respiration is rapid and shallow Skin is pale, cool, and clammy Drowsiness 7. Hypovolemic Shock Results from trauma in which there is bloodloss Decreased blood volume causes a decrease inblood pressure Insufficient amounts of O2 is being transportedto body tissues and organs 8. Compensated Shock Early stages of shock where the bodyscompensatory mechanisms are able tomaintain normal perfusion 9. Decompensated Shock Advanced stage of shock that occurs when thebodys compensatory mechanisms fail tomaintain normal perfusion 10. Irreversible Shock Stage of shock that has progressed to the pointthat the body nor medical interventions correctthe problem 11. Compensated and Decompensatedshock Usually the body is able to compensate butwhen these mechanisms fail shock developsand may progress 12. Compensation Mechanisms Catecholamines may be secreted ( I.E.Epinephrine and norepinephrine) The Renin-Angitensin system aids inmaintaining blood pressure Endocrine Response by pituitary gland resultsin secretion of anti-diuretic hormone (ADH) 13. Catecholamine Release Epinephrine and Norepinephrine releaseaffects the cardiovascular system, causingincrease in HR, increase in Cardiac contractilitystrength, arteriolar constriction whichelevates blood pressure 14. Renin-Angiotensin system Renin is released from the kidneys and acts onspecialized plasma protein called Angiotensinthe produces AngiotensinI. AngiotensinI is converted to AngiotensinII byenzymes in the lungs called AngiotensinConverting Enzyme (ACE) 15. Anti-Diuretic Hormone Causes the kidneys to reabsorb water creatingan additive to the aldostrone 16. Stages of Shock Initial non-progressive stage Baro-receptor reflexes Release of catecholamine Activation of renin-angiotensin-aldosteron system ADH releaseresults in tachycardia, peripheral vasoconstriction (cool skin) and renal fluidconservation Progressive stage Widespread tissue hypoxia results in anaerobic glycolysis and Lactate acidosis (pH < 7.35) Vasodilation with blood pooling in microcirculation Declined cardiac output Oligouria Widespread tissue hypoxia Irreversible stage Widespread cell injury leading to Further decreased myocardial contractility Anuria with tubular necrosis Ischemic bowl may lead to leakage of bacterial flora Fluid lung (ARDS) 17. S/S of Hypovolemic Shock Altered LOC Pale, cool, clammy skin Blood pressure may be normal then fall Pulse may be normal then become rapid, finallyslowing and disappearing Urination decreases Cardiac dysrhythmias may occur 18. Tx for Hypovolemic Shock Airway control Administer high flow oxygen Control severe bleeding Keep patient warm Elevate lower extremities Establish IV and administer bolus of crystalloidsolution for fluid replacement 19. Cardiogenic shock Pump failure Secondary to myocardial infarction (most common) Cardio-myophathy Acute valvular dysfunction (regurgitations) Rupture of the ventricular septum Arrhythmia Tachyarrhythmia Bradyarrhythmia Obstructions Tension pneumothorax Pericardial diseases (tamponade or constrictive pericarditis) Pulmonary hypertension (emboli or other vascular diseases) 20. Characteristics of Cardiogenic Shock Low cardiac output Peripheral vasoconstriction Left sided heart failure leads to pulmonary venouscongestion and pulmonary edema Right sided heart failure leads to systemic venouscongestion and peripheral edema 21. It is essential to distinguish a cardiogenic from a hypovolemicshock!Both forms are associated with reduced cardiac out put, and increasedperipheral vascular resistance, however:Cardiogenic shock:jugular venous distention (high CVP)Hypovolemic shock: collapsedcapacitance veins (low CVP) 22. Cardiogenic Shock The heart loses the ability to supply all bodyparts with blood Usually the result of left ventricular failuresecondary to acute MI or CHF Many patients will have normal bloodpressures 23. S/S of Cardiogenic Shock Major difference between other types of shockis presence of Pulmonary Edema Difficulty breathing Wheezes, Crackles, Rales are heard as fluidlevels increase Productive cough with white or pink-tingedfoamy sputum Cyanosis Altered mentation Oliguria ( decreased urination) 24. TX for Cardiogenic Shock Assure open airway Adminster oxygen Assist ventilations as needed Keep patient warm Place patient in position of comfort Establish Iv with minimal fluid administration Monitor Vitals May need to administer Dopamine orDobutamine 25. Distributive Shock Sepsis Due to gram negative or gram positive bacteria Anaphylaxis Due to previous sensitization to an allergen Neurogenic Due to traumatic spinal cord injury Effects of epidural or spinal anesthetics Reflex parasymapthetic stimulation 26. Types of ShockNeurogenic Shock Results due to the overall dilation of the bloodvessels within the cardiovascular system Decreased blood pressure Insufficient amounts of O2 is being transportedto body tissues and organs 27. Neurogenic Shock Results from injury to brain or spinal cordcausing interruption of nerve impulses toarteries Arteries lose tone and dilate causinghypovolemia Sympathetic nerve impulses to the adrenalglands are lost, which prevents the release ofcatecholamines and their compensatory effects 28. Neurogenic Shock (cont) High cervical injuries cause interruption ofimpulse to peripheral nervous system causing Neurogenic shock is most commonly due tosevere injury to spinal cord or total transectionof cord (spinal shock) 29. S/S of Neurogenic Shock Warm, Dry, Red Skin Low Blood Pressure Slow Pulse 30. TX for Neurogenic Shock Airway control Maintain body temperature Immobilization if indicated Consider other causes of shock IV and medications that increase peripheralvascular resistance (I.E. Norepinephrine,Dopamine) 31. Anaphylatic Shock Severe immune response to foreign substance S/S most often occur within minutes but cantake up to hours to occur The faster the reaction develops the moresevere it is likely to be Death will occur if not treated promptly 32. S/S of Anaphylactic Shock Skin- Flushing- Itching- Hives-Swelling-Cyanosis 33. S/S of Anaphylactic Shock Respiratory System- Breathing difficulty- Sneezing, Coughing- Wheezing, Stridor- Laryngeal edema- Laryngospasm 34. S/S of Anaphylactic Shock Cardiovascular System- Vasodilation- Increased heart rate- Decreased blood pressure 35. S/S of Anaphylactic Shock Gastrointestinal System- Nausea, vomiting- Abdominal cramping- Diarrhea 36. TX for Anaphylactic Shock Airway protection which may includeEndotracheal Intubation Establish IV with crystalloid solution Pharmacological interventions: Epinephrine,Antihistamines(Benadryl),Corticosteroids(dexamethasone),Vasopressors(dopamine, Epinephrine), andinhaled beta agonist(albuterol) 37. Pathogenesis of Septic Shock (vasodilatory shock) Sepsis is defined as a systemic inflammatory responseto a bacterial infection with bacteriemia (thoughblood cultures can be negative) Severe sepsis is defined by additional end-organdysfunction (mortality rate: 25-30%) Septic shock is defined as sepsis with hypotensiondespite fluid resuscitation and evidence of inadequatetissue perfusion (40-70%) 38. NEJM 2004, Vol. 351;2 pp 159-169 39. Clinical Spectrum of InfectionInfectionBacteremiaSepsisSevere SepsisSeptic Shock 40. The syndrome of septic shock is characterized by Systemic vasodilation (hypotension) Diminished myocardial contractility Widespread endothelial injury and activation leadingto fluid leakage (capillary leak) resulting in acuterespiratory distress syndrome (ARDS) Activation of the coagulation cascade (DIC) 41. Disseminated intravascular coagulation (DIC) is characterized by widespread activation of coagulationresulting in the intravascular formation of fibrin and ultimatelythrombotic occlusion of small and midsize vessels leads to compromise of blood supply to organs and maytherefore contribute to multiple organ failure subsequent depletion of platelets and coagulation factors canresult in severe bleeding and may be the presenting symptom 42. Virtually all patients with sepsis have coagulation abnormalities. The extreme form of it is called:Acute disseminated intravascular coagulation (DIC)Severe cutaneous bleeding as a result of fulminant Meningococcal septicemia due to activation and consumption of all coagulationfactors (consumption coagulopathy) 43. Septic Shock An infection enters bloodstream and is carriedthroughout body Toxins released overcome compensatorymechanisms Can cause dysfunction of one organ system orcause multiple organ dysfunction 44. S/S of Septic Shock Increased to low blood pressure High fever, no fever, hypothermic Skin flushed, Pale, Cyanotic Difficulty breathing and altered lung sounds Altered LOC 45. TX of Septic Shock Airway control Administer oxygen IV of crystalloid solution Dopamine for blood pressure support Monitor other vitals