Chapter 16. Learning Objectives. Learning Objectives 9/11/2012. Shock. Explain difference between compensated and uncompensated shock

Transcription

1 Chapter 16 Shock Learning Objectives Explain difference between compensated and uncompensated shock Differentiate among 5 causes and types of shock: Hypovolemic Cardiogenic Neurogenic Septic Anaphylactic Learning Objectives Define rapid responders, transient responders, and nonresponders List benefits of packed red blood cell transfusion Differentiate among 4 blood types: O, A, B, and AB 1

2 Learning Objectives Demonstrate proper procedure for packed red blood cell administration for hypovolemic shock Learning Objectives Discuss medications used in treatment of cardiogenic shock: Dobutamine (Dobutrex) Dopamine (Intropin) Norepinephrine (Levophed) Milrinone (Primacor) Learning Objectives Discuss use of phenylephrine (Neo- Synephrine) in treatment of neurogenic shock Explain why, in septic shock, the exaggerated response, not the infection, creates shock state 2

3 Introduction Must understand: What shock is Causes Treatments for each particular type Must recognize: Condition and know appropriate drug intervention Presence of condition and determine cause Overview of Shock Abnormality of circulatory system Results in inadequate tissue perfusion and O 2 delivery Impaired O 2 delivery can occur in presence of low, normal, and elevated BP Do not assume only hypotensive patients can be in shock Overview of Shock Decompensated shock Presentation of hypotension and tachycardia occurring in late stages of shock Patient has lost ability to compensate Before becoming unstable, patient s physiologic functioning alters to compensate Normal mentation Slight alterations in vital signs Appear stable 3

4 Overview of Shock Early findings: Skin perfusion Respiratory rate Altered mental status Delayed capillary refill Cold and clammy skin Overview of Shock Respiratory rate can increase to improve minute ventilation Compensates for metabolic acidosis Improves blood return to the heart Improved cardiac output Must maintain high index of suspicion Signs of shock can be subtle Overview of Shock Uncompensated shock Can be determined quickly Indicator is perfusion of BP Can be obtained by palpation of peripheral pulses Bounding radial pulse indicates patient has adequate BP of at least 90 mm Hg Cerebral perfusion can be determined by evaluating patient s mental status 4

5 Causes of Shock Hypotension treatment Administer fluids and vasopressor If cause is blood loss from GI bleed or MI, blood flow to vital organs actually decreases despite normal BP If patient is in septic shock from perforated colon, IV fluids and vasopressors do nothing to control fecal contamination of abdominal cavity If tension pneumothorax, requires rapid decompression of the chest Causes of Shock Types of shock Hypovolemic Cardiogenic Neurogenic Septic Anaphylactic IV resuscitation is required in all types Tachycardic Prolonged capillary refill and cool extremities indicates peripheral vasoconstriction Typically associated with heart rate slower than expected for degree of hypotension Drop in BP from acute hemorrhage requires a loss of approximately 30% of the circulating blood volume 5

6 Must control source of hemorrhage Begin fluid resuscitation Crystalloid, preferably normal saline Ringer lactate solution is used, but it is not compatible with infusion of blood IV lines must be flushed with normal saline before blood administration Route is optimally two large-bore peripheral IV sites Rapid bolus of 1 to 2 L of crystalloid Rapid responders Patients with improved perfusion, heart rate, or BP from crystalloid infusion Do not need further aggressive resuscitation No ongoing hemorrhage Source of bleeding controlled with pressure or patient s normal hemostatic mechanisms Transient responders Improve as their intravascular volume is replenished Ongoing manifestations of poor perfusion return Require blood transfusion and control of hemorrhage Nonresponders Uncontrolled hemorrhage Require blood transfusion and control of bleeding 6

7 Hypotensive resuscitation Goal is not to return vital signs to normal, but to maintain physiologic functioning until source of hemorrhage can be controlled Administration of IV fluids in excessive amount or too rapidly can cause patient to bleed more rapidly Control of hemorrhage for torso trauma requires rapid access to trauma surgeon Saline lacks ability to carry O 2 and unable to form blood clots Can dislodge clot and cause bleeding to resume Platelets and coagulation proteins consumed in clot formations would be lost If fluids are not warmed, possible hypothermia occurs Must restore systolic BP to subnormal levels, not normal levels After control of hemorrhage, standard end points of resuscitation are sought 7

8 Fluid is administered in volumes to achieve one of the following results: Consciousness, as demonstrated by ability to follow commands Palpable radial pulse Systolic BP of 90 mm Hg Mean arterial pressure of 60 mm Hg May require blood transfusion Skill required of air medics, interhospital transport, and military providers Blood product most often used: packed red blood cells (prbcs) prbc transfusion has benefits: O 2 -carrying capability Risk: disease transmission Risk: ABO-incompatible blood transfusions May require blood transfusion Blood types: O: universal donor A: has A antigen on RBC surface B: has B antigen on RBC surface AB: has A and B antigens on RBC surface Natural antibodies occur against cell surface antigen that is not present on RBC surface 8

9 May require blood transfusion Optimal unit of prbcs for field administration if type O Rh Rh status is of minimal consequence unless female patient with possibility of future pregnancy Rh patients who receive Rh + blood develop antibodies against Rh factor in approximately 80% of cases Administering blood transfusion Equipment needed: 1 U prbcs Blood tubing Normal saline PPE Administering blood transfusion Procedure: Observe universal precautions Confirm right patient When possible, explain to patient what procedure you are going to perform and why Examine refrigeration record to ensure proper prbc temperature has been maintained Examine expiration date on the units 9

10 Administering blood transfusion Procedure: Confirm blood type is O Examine blood for evidence of leakage, clumps, or abnormal color Confirm the blood is Rh if the patient is a woman younger than 50 years Record patient vital signs before transfusion and at least every 15 min during transfusion Ensure all tags and labels remain attached to unit of blood Administering blood transfusion Procedure: Ensure tubing to unit of blood is filtered Confirm prbcs will be infused through line flushed with normal saline Attach unit of prbcs to tubing and open valve to begin transfusion Closely observe transfusion during first 15 ml of transfusion Document identifying numbers of unit infused, infusion times, and vital signs Inadequate tissue perfusion caused by pump failure, most commonly from acute MI Myocardium loses its ability to contract effectively Factors other than pump failure can result in cardiogenic shock Mechanical factors that result in inadequate filling of right or left atrium can prevent effective cardiac function Pericardial tamponade Severe cardiac valve dysfunction 10

11 Blood does not maintain an effective, unidirectional flow through the heart Tissue perfusion is negatively affected Clinical findings: Tissue perfusion manifested by: Peripheral vasoconstriction Delayed capillary refill Decreased mental capacity Pulmonary congestion Pulmonary edema In acute left ventricular dysfunction, heart is unable to propel blood to systemic peripheral circulation Lower pressure right ventricle and pulmonary circulation are less affected by pump failure Blood flow through right side of the heart to the lungs continues In left side of the heart, cardiac emptying to peripheral circulation is compromised Left arterial filling pressures increase, resulting in congestion of pulmonary vascular bed In acute left ventricular dysfunction, heart is unable to propel blood to systemic peripheral circulation Tachypnea, shortness of breath, and rales are observed In acute valvular dysfunction, cardiac murmurs can be heard 11

12 Mortality rate is between 50% and 80% Risk factors for death: Age Previous MI Cold and clammy skin Oliguria Best outcomes are in patients when cause of cardiac dysfunction can be quickly reversed Achieved by myocardial revascularization In cardiogenic shock caused by cardiac ischemia: Nitroglycerin is not indicated Hypotension can be exacerbated by its vasodilatory effects Beta adrenergic blockers should be limited Only used after resolution of the state of hypoperfusion Adrenergic agonists can manipulate: Heart rate Force of cardiac contraction Systemic vascular resistance Adrenergic receptor groups: Alpha 1 Alpha 2 Beta 1 Beta 2 12

13 Dobutamine Agent of choice for patients with systolic pressure greater than 80 mm Hg Increases cardiac contractility and output Does not significantly increase heart rate Does not raise systemic vascular resistance Must observe for tachycardia and hypotension Use with caution in atrial fibrillation Dopamine Beta 1 -mediated increase in contractility and heart rate improves cardiac output Downside: increases myocardial O 2 consumption Used for cardiogenic shock associated with hypotension Has beta 1 and alpha 1 effects Can exacerbate myocardial ischemia from tachycardia and increased systemic vascular resistance Norepinephrine Used in patients with cardiogenic shock refractory to dopamine Is an alpha 1, alpha 2, and beta 1 agonist Results in alpha-mediated peripheral vasoconstriction 13

14 Milrinone (Primacor) Stimulates heart to increase cardiac output independently of adrenergic receptors Phosphodiesterase inhibitor Used in patients who are nonresponsive to adrenergic stimulating agents Has positive inotropic effect and peripheral vasodilatory action No significant chronotropic or arrhythmogenic action Closely observe for hypotension When infusing vasoactive medications, monitoring is critical for: Hypoperfusion Cardiac arrhythmias Exacerbation of myocardial ischemia Venous access must be maintained and secured If IV line becomes dislodged and vasoactive drug infiltrates into soft tissue, may cause soft tissue necrosis at site of infiltration Possible soft tissue damage with Sub-Q infusion of adrenergic agonists from an infiltrated site 14

15 Neurogenic shock Possible with spinal cord injury When sympathetic pathways from spinal cord are interrupted, blood vessels dilate Volume of vascular tree has enlarged but amount of blood filling vasculature has remained the same Relative hypovolemia occurs Lesion to spinal cord involves sympathetic innervations of the heart Possible bradycardia Neurogenic shock Patients lose input to blood vessels from the nervous system Blood vessels dilate Without losing single drop of blood, patient is initially hypovolemic Neurogenic shock Fluid infusion to improve preload is initial therapy Must manage bigger vascular container; fluid administration refills that vascular container Do not assume hypotension is from spinal shock and then use a vasopressor Worsens shock 15

16 Neurogenic shock Treatment for hypotensive trauma: IV fluid therapy Use in moderation Hypotension from spinal shock may not exhibit expected tachycardia Neurogenic shock Vasopressor agents Used after the volume status is adequate Dopamine Used if patient has low heart rate Possesses alpha effects Has beta 1 properties that increase heart rate Neurogenic shock Vasopressor agents Phenylephrine (Neo-Synephrine) Stimulates only the alpha receptor Most common choice for neurogenic shock 16

17 Septic shock Poor blood perfusion from systemic effects of infection Infection localized to blood, lungs, urine, or an abscess Body responds to infection by defensive inflammatory response that is exaggerated Exaggerated response, not the infection, creates shock state Septic shock Systemic inflammatory response Massive inflammatory reaction that produces chaos in several of body s vital organ systems Produces toxins within body that result in dilation of blood vessels Blood vessels become leaky Patient can become hypovolemic Septic shock Supportive drug therapy Intravascular volume expansion with IV fluids Vasopressors after fluid resuscitation Norepinephrine Dopamine Anaphylactic shock 17

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