Shock #2 PDF

Week 13 Care of Patients in Shock Shock Impaired delivery of oxygen to the tissues aerobic metabolism with oxygen anaerobic metabolism without oxygen ○ development of lactic acidosis develops when lactate is produced as a result of carbohydr...

Week 13 Care of Patients in Shock Shock Impaired delivery of oxygen to the tissues aerobic metabolism with oxygen anaerobic metabolism without oxygen ○ development of lactic acidosis develops when lactate is produced as a result of carbohydrate metabolism with tissue hypoxia you have a lack of oxygenation getting to the tissues ○ cells are forced to become anaerobic metabolism ○ then more lactate is being produced ○ when it accumulates within the body faster than it is being metabolized then we have the development of lactic acidosis ○ it can happen at any time when the demand for oxygen is greater than its availability ***Cause of the shock Blood loss hx of stroke and patient is on anticoagulant hx of heart attack is patient on antiplatelet MAP (mean arterial pressure) 70-110 mm HG to have adequate perfusion Sometimes when patients come in you might not be able to get diastolic so you would use a tool called Doppler You would say the systolic number over doppler this means RELISTEN!!! Stages of Shock (hemorrhagic shock) Initial stage ○ loss of 750 cc of blood  ○ body will try to compensate for blood loss Minimal tachycardia (HR 110) Normal or increase of pulse pressure tells us how well heart is contracting to get pulse pressure we take the difference from systolic - diastolic 40-60 mm Hg normal levels pulse pressure increases with age the higher the stiffer and more damage the vessels are thought to be if high this means stiff arteries or fatty deposits ○ atherosclerosis it shows how well your heart is contracting treating high blood pressure reduces pulse pressure ○ high blood pressure the vessels are stiff ○ it requires more to contract effectively and pump blood throughout the body nonprogressive stage/ compensatory stage ○ MAP decreases by 10 to 15 mm Hg ○ compensatory stage ○ more than 750-1500 cc of blood loss ○ anxiety ○ restlessness loss of oxygen ○ adrenal medulla stimulated epinephrine and norepinephrine it increases HR and blood pressure ○ kidney tries to save themselves less than 30 cc of urine antidiuretic hormone is secreted  it is sensing that the blood is more concentrated allowing more water to be reabsorbed this will decrease blood concentration ○ tissue hypoxia in non vital organs we shunt blood from these organs to give to important organs brain heart Liver these organs need adequate perfusion this will not cause damage to other parts of the body during this phase ○ Anaerobic effect will produce acidosis ○ in this stage everything is reversible if we intervene and provide interventions ○ if not recognized patient will go into next stage progressive stage ○ Sustained decrease in MAP of more than 20 mm Hg ○ 1500-2000 cc of blood loss ○ HR >120 beats per minute compromises diastolic filling time when heart is resting it doesn’t have adequate time to fill before the next contraction to pump blood throughout the circulation ○ RR 30-40 per minute called tachypnea ○ narrow pulse pressure low pulse pressure decrease perfusion to all major organs ○ vital organs develop hypoxia ○ hyperventilating pulse pressure is low decrease perfusion  ○ life threatening emergency ○ immediate interventions are needed ○ conditions causing shock need to be corrected within an hour of the onset of the progressive stage refractory stage ○ too much cell death and tissue damage result from too little oxygen reaching the tissues ○ more than 2 liters of blood loss ○ lethargic, sleepy ○ skin is cool to touch blood is shunted to all organs that is the reason why this feels this way ○ severe hypotension ○ narrow pulse pressure ○ body can no longer respond effectively to interventions, and shock continues ○ there is irreversible cell and tissue death ○ anaerobic metabolism is occurring during this stage Multiple Organ Dysfunction Syndrome (MODS) Metabolites are released from dead cells micro thrombi are also released throughout the body MODS occurs first in ○ liver ○ heart ○ brain ○ kidney Classification of Shock by Functional Impairment Hypovolemic Shock intravascular volume decrease MAP decreases ○ stimulates baroreceptor  ○ located aortic arch and carotid sinus ○ stimulation of SNS ○ tachycardia ○ increase in contractility increase in cardiac output temporarily coronary arteries dilate then decrease of blood pressure decrease in tissue perfusion Causes ○ hemorrhage ○ dehydration ○ fluid shifts trauma ruptured spleen ○ massive bleeding stores platelets ○ removes old red blood cells burns treatment ○ control the source of the blood loss ○ replace the volume loss ○ increase the perfusion to all organs ○ we always stop the bleeding first because if we increase the blood pressure patient will bleed out more ○ Colloids increase serum osmotic pressure not first class unless they have interstitial edema example albumin dextran hetastarch ○ crystalloids  first line of use Isotonic solutions which increase BP example normal saline lactated ringers ○ blood products replace the blood loss you never want to contaminate blood products and ALWAYS REMOVE anything that has glucose this will cause blood clots example packed RBCs whole blood Cardiogenic Shock we have problems with left, right, or both ventricles actual heart muscle is unhealthy, and pumping is directly impaired high left ventricular pressure this leads to fluids moving from pulmonary beds to interstitial area RELISTEN!!! myocardial infarction is the most common cause of direct pump failure normal pressures are 6-12 on left side of heart right side of heart 2-5 When the vessels are dilated the heart uses less oxygen Clinical manifestations ○ Tachycardia ○ decrease in cardiac output ○ decrease blood pressure ○ narrowing pulse pressure ○ vasoconstriction ○ crackles treatment of Cardiogenic Shock ○ beta adrenergic agonists  norepinephrine dobutamine Dopamine different effects depending on dosage the dosage given will depend on the condition of the patient each dosage has the different effect ○ low dose: 2mcg/kg/min dilates real and mesenteric arteries and increase renal perfusion ○ moderate dose: 5mcg/kg/min increase HR, contractility and cardiac output ○ high dose: 10mcg/kg/min increase vasoconstriction ○ Vasodilators decreases the workload of the heart by decrease preload decrease afterload: force where heart has to pump against to eject blood into the circulatory system medications nitroprusside nitroglycerin ○ mechanical assist devices the intra-aortic balloon pump (IABP) allows the heart to rest increase cardiac output increase blood flow to heart decrease the afterload decrease the amount of oxygen that the heart has to use mobility restricted this is in the femoral artery  pedal pulses if pedal pulses are not palpable we need to auscultate with Doppler we always need to be able to hear this pulse when this device is in a person this would mean that the device has migrated and this will occlude the heart Obstructive Shock Caused by problems that impair the ability of the normal heart muscle to pump effectively Causes ○ pulmonary embolism blood clot in pulmonary vasculature If it occludes ○ difficulty breathing ○ deterioration of the lung ○ cardiac tamponade medical emergency compressing the heart accumulation of fluid in the pericardial sac Pressures are identical on both sides of the heart Treatment for Obstructive Shock ○ pulmonary embolism heparin ○ fibrinolytic therapy breakup clots that have already formed streptokinase alteplase ○ cardiac tamponade pericardiocentesis- needle that removes the fluid pericardial window  drain Distributive Shock Blood volume has not been lost but distributed in interstitial space ○ loss of sympathetic tone vessels being dilated pooling of blood capillary leaks discoloration of extremities ○ septic, anaphylactic, and neurogenic shock vasodilation major characteristic sepsis when WBC count is low the body enters into a sepsis shock and this doesn’t allow the body to fight an infection organ failure (severe sepsis) all tissues have some degree of hypoxia microthrombi formation is extensive amplified systemic inflammatory response (inflammation in the entire body) anaerobic metabolism continues septic shock local infection ○ in one part of the body if not addressed then it becomes systemic systemic infection (bacteremia) ○ all over the body ○ caused by gram negative e coli klebsiella pneumoniae ○ caused by gram positive staphylococcus  streptococcus pneumoniae frequent portal of entry into the body genitourinary tract but there can be other portals of entry ○ GI tract ○ respiratory ○ skin wherever you have a break in the skin tissue level you have ○ White blood cells that are producing a pro inflammatory cytokines ○ cytokines produce systemic inflammation systemic inflammatory response syndrome mortality rate is 60% and as high as 80% most common in non cardiac ICUs in the US elderly are at greater risk most cases are nosocomial increased incidence due to advanced invasive technology we are concerned with very young and older population and immunocompromised treatment blood cultures antibiotic therapy oxygen therapy vancomycin aminoglycosides ○ tobramycin ○ gentamicin penicillins ○ Cephalosporins are family with this medication if allergic these two can not be given  ○ systemic penicillin ○ amoxicillin ○ piperacillin cephalosporins ○ ancef steroid therapy ○ hydrocortisone ○ fludrocortisone anticoagulant therapy ○ heparin ○ anaphylactic shock antigen antibody reaction histamines and leukotrienes bronchoconstriction peripheral vasodilation treatment airway management bronchodilators ○ albuterol epinephrine to stabilize mast cells and increase BP IV therapy ○ normal saline to increase vascular volume steroids ○ methylprednisolone to decrease inflammation ○ neurogenic shock all three types are characterized with vasodilation