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Chapter 19 Shock.

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1 Chapter 19 Shock

2 Learning Objectives List the types of shock.
Describe the pathophysiology of each type of shock. List the signs and symptoms of each stage of shock. Explain the first aid emergency treatment of shock outside the medical facility. Identify general medical and nursing interventions for shock. Explain the rationale for the medical/surgical treatment of shock. Assist in developing care plans for patients in each type of shock.

3 Definition of Shock Inadequate tissue perfusion resulting in impaired cellular metabolism Deprives cells of essential oxygen and nutrients, forcing cells to rely on anaerobic (without oxygen) metabolism Less energy is produced and lactic acid, a by-product of anaerobic metabolism, causes tissue acidosis and subsequent organ dysfunction Shock begins when the cardiovascular system fails to function adequately because of an alteration in at least one of four vital components. What are the four vital components?

4 Hypovolemic Shock Inadequate blood volume to maintain the supply of oxygen and nutrients to body tissues Intravascular or circulating volume deficits can occur from external or internal losses Blood volume falls with excessive blood or fluid loss, inadequate fluid intake, or a shift of plasma from the blood vessels into body tissues/organs Causes of blood/fluid loss: hemorrhage, severe diarrhea or vomiting, excessive perspiration Excessive shift of plasma with pathologic states (burns, peritonitis, and intestinal obstruction)

5 Cardiogenic Shock Occurs when heart fails as a pump
Decreased myocardial contractility causes decreased cardiac output and impaired tissue perfusion Difficult to treat and usually results when diseased coronary arteries cannot meet the demand of the working myocardial cells Causes include conditions that result in ineffective myocardial cell function, such as dysrhythmias, cardiomyopathy, myocarditis, valvular disease, and structural disorders

6 Obstructive Shock Physical impairment of adequate circulating blood flow Obstruction of the heart or great vessels either blocks venous return to the right side of the heart or prevents effective pumping action Causes: tension pneumothorax, pericardial tamponade, pulmonary embolus, abdominal distention, and aortic dissection

7 Distributive Shock The problem is not loss of blood, but excessive dilation of blood vessels or decreased vascular resistance causing the blood to be improperly distributed Fluid pools in dependent areas of body and is not returned to the arterial circulation to supply critical cellular metabolic needs Complicated by increased capillary permeability; plasma leaks into interstitial compartment, decreasing intravascular blood volume

8 Distributive Shock Anaphylactic shock
A severe allergic reaction that results in the release of chemicals that dilate blood vessels and increase capillary permeability Fluid leaks out of capillaries into the tissues Pooling of blood in peripheral tissues and the shift of fluid out of the capillaries cause venous return and cardiac output to fall Allergic reaction also causes constriction of the bronchi and airway obstruction What are some substances that people can be allergic to? The onset of anaphylaxis is typically sudden and dramatic following exposure to a substance to which the patient has developed antibodies.

9 Distributive Shock Septic shock
Hypotension unresponsive to fluid resuscitation along with metabolic acidosis, acute encephalopathy, oliguria, and/or coagulation disorders Pathogenic organisms (bacteria, fungi, viruses, rickettsiae) release toxic substances that cause blood vessels to dilate and decrease vascular resistance and increase capillary permeability Increased permeability: leakage of plasma proteins and reduced intravascular volume, preload, and cardiac output that contributes to inadequate tissue perfusion and oxygenation Sepsis is a systemic inflammatory response to a documented or suspected infection; sepsis can progress to septic shock.

10 Distributive Shock Neurogenic shock
Disruption in the nervous system affects the vasomotor center in the medulla Disrupted sympathetic nerve impulses result in vasodilation or loss of vascular resistance Signs and symptoms: pooling of blood in peripheral tissues with subsequent decreased venous return and cardiac output; bradycardia with hypotension Causes: injury or disease of the upper spinal cord, spinal anesthesia, depression of the vasomotor center from certain drugs In neurogenic shock, what is the result of disturbances that disrupt sympathetic nerve impulses?

11 Effects of Shock on Body Systems and Functions
Respiratory system Tissue hypoxia and anoxia, respiratory failure, acute respiratory distress syndrome (ARDS) Acid-base balance Metabolic acidosis Cardiovascular system Myocardial depression, disseminated intravascular coagulation (widespread clotting caused by sluggish flow of acidic blood combined with bacterial endotoxins or clotting factors released by destruction of red blood cells)

12 Effects of Shock on Body Systems and Functions
Neuroendocrine system Release of catecholamines (epinephrine and norepinephrine), mineralocorticoids (aldosterone and desoxycorticosterone), glucocorticoids (hydrocortisone), and antidiuretic hormone; decreased level of consciousness when cerebral blood flow falls Immune system Depressed immune response

13 Effects of Shock on Body Systems and Functions
Gastrointestinal system Decreased peristalsis, ischemia of intestinal submucosa, impaired liver function Renal system Reduced glomerular filtration, inadequate renal perfusion, tubular necrosis, renal ischemia

14 Stages of Shock

15 Early, Reversible, and Compensatory Stages
Continued reduction in cardiac output triggers set of neural, endocrine, and chemical compensatory mechanisms in an effort to overcome the consequences of anaerobic metabolism and maintain blood flow to vital organs During this stage the following may occur: Activation of baroreceptors in the carotid arteries and the aorta stimulate the sympathetic nervous system Sympathetic stimulation: increased heart rate, constriction of peripheral blood vessels, and reduced blood flow to the kidneys, lungs, muscles, skin, and gastrointestinal (GI) tract

16 Early, Reversible, and Compensatory Stages
Events Decreased renal blood flow triggers the release of renin and a sequence of events that produces angiotensin II Adrenal cortex secretes aldosterone, which promotes sodium retention by the kidneys Antidiuretic hormone released by posterior pituitary, resulting in additional retention of water by the kidneys Falling blood pH and increasing arterial carbon dioxide detected by chemoreceptors in the carotid arteries, which stimulate the respiratory center Increased respiratory rate and depth help to eliminate excess carbon dioxide and normalize the blood pH

17 Early, Reversible, and Compensatory Stages
Symptoms Mental status Irritability, restlessness Blood pressure Normal or slightly decreased, decreasing pulse pressure, orthostatic hypotension Pulse Increased rate; may be thready (as a result of vasoconstriction) or bounding (caused by vasodilation) decreased rate (bradycardia) may be present in neurogenic shock due to loss of sympathetic stimulation Respirations Increased rate and depth

18 Early, Reversible, and Compensatory Stages
Urine output Decreased Skin Cool and pale Exception: warm and dry with septic shock Abdomen Decreased bowel sounds Blood glucose Increased Other Thirst

19 Intermediate (Progressive) Stage
Cause of shock is not corrected or if compensatory mechanisms continue without reversing the shock Neural, endocrine, chemical compensatory mechanisms begin to function independently and in opposition Systemic circulation continues to vasoconstrict in the attempt to maintain blood flow to vital organs Decrease in peripheral blood flow leads to weak or absent pulses and ischemia of the extremities Blood becomes more viscous or thick, causing clumping of red blood cells, platelets, and proteins Deprived of oxygen, cells resort to anaerobic metabolism and produce lactic acid, resulting in metabolic acidosis Depressant effect on myocardial cells

20 Intermediate (Progressive) Stage
Symptoms Mental status Listlessness, confusion Blood pressure Decreased; narrow pulse pressure Pulse Weak and thready, tachycardia, dysrhythmias Respirations Increased, deep, crackles present on auscultation

21 Intermediate (Progressive) Stage
Temperature Subnormal, except with septic shock Urine output Decreased; possible renal failure Skin Cold, pale, clammy, slow capillary refill, cyanosis Other Dry mouth, thirst, sluggish pupillary response, peripheral edema, and muscle weakness What is MODS?

22 Irreversible (Refractory) Stage
Irreversible changes in vital organs as compensatory mechanisms fail Tissue perfusion deteriorates, as blood remains pooled in the capillary bed where sluggish flow is further compromised by clumping and the formation of clots Coronary artery perfusion is reduced causing ischemia and dysrhythmias Cerebral ischemia occurs as a result of the decrease in cerebral blood flow Death is imminent Even patients who are resuscitated during this stage often die within a week or two

23 Irreversible (Refractory) Stage
Symptoms Mental status Loss of consciousness Blood pressure Systolic continues to fall; diastolic approaches zero Pulse Progressive slowing, irregular Respirations Slow, shallow, irregular Urine output Minimal Skin Cold, clammy, cyanosis

24 Diagnosis Based on history and physical examination
Tests and procedures that help establish type of shock, stage, and the cause Blood and urine studies, measurement of hemodynamic pressures, chest radiograph, ECG and continuous cardiac monitoring, pulse oximetry and arterial blood gases, and urine output

25 First Aid for Shock Outside the Medical Facility
Treatment provided before medical care is available can have a significant effect on the chances of survival Healthy People 2010 objectives (2000): the necessity for increasing public awareness of how and whom to call for emergency assistance in addition to providing education concerning initial lifesaving procedures to be followed until arrival of emergency responders What first aid interventions should be performed for the patient in shock?

26 Oxygenation Brain cells begin to die after 4 minutes without oxygen, and oxygen consumption increases as delivery decreases in shock: poor prognosis Oxygen delivery such as increasing arterial oxygen saturation, hemoglobin, and cardiac output Supplemental oxygen may be used or mechanical ventilation may be necessary Paralytics, sedatives, and analgesics may be ordered to decrease oxygen requirements

27 Fluid Replacement Normal saline is usually administered initially
Subsequent fluids may include various crystalloids and colloids depending on situation Crystalloids provide replacement water and electrolytes for all fluid compartments Colloids remain in the vascular system and draw fluid into the bloodstream Especially important when large amounts of plasma proteins have been lost Except for cardiogenic shock, all types of shock require significant fluid volume replacement. The hemorrhaging patient will require blood to replace deficient hemoglobin. The patient’s response must be closely monitored during fluid replacement to ensure adequate, but not excessive, replacement. How is adequate fluid replacement best determined?

28 Pharmacologic Therapy
Based on manipulation of the cardiac dynamics: contractility, preload, afterload, and heart rate No one drug will provide nutrients and oxygen to the cells; several agents assist in manipulation of the four circulatory components See the Drug Therapy table on pp

29 Mechanical Management
Management of shock may include the use of mechanical devices that assist in the restoration of cellular perfusion What mechanical devices may be used to manage shock?

30 Figure 19-1

31 Figure 19-2

32 Nursing Care of the Patient in Shock

33 Assessment Continuous monitoring of cardiac rate and rhythm; blood pressure; body temperature; hemodynamic values; respiratory rate, rhythm, and depth; and arterial blood gases Observe skin color; palpate for warmth and moisture Note pupil size, equality, and response to light Describe patient’s level of consciousness and response to commands, and assess reflexes Auscultate heart, lung, and bowel sounds

34 Assessment Observe movement of the chest wall with respirations; inspect and palpate abdomen for distention Palpate for bladder distention, and note the appearance of urine and the hourly output Inspect the extremities for color, and palpate for peripheral pulses and edema Inspect IV infusion sites for pallor, swelling, or coolness that suggests extravasation

35 Interventions

36 Nursing Diagnosis The primary nursing diagnosis for all patients in shock is Altered Tissue Perfusion May be related to alteration(s) in circulating blood volume, myocardial contractility, blood flow, or vascular resistance

37 Ineffective Tissue Perfusion
Assessment must include all body systems If not corrected, shock eventually results in failure of all major organs

38 Decreased Cardiac Output
Administer intravenous fluids as ordered Assess for fluid volume deficit and excess Administer inotropic and antidysrhythmic agents as ordered; continuous cardiac monitoring Maintain adequate body heat Fever may be treated with acetaminophen or nonsteroidal anti-inflammatory drugs Continuous cardiac monitoring enables you to assess the effectiveness of the drugs. How can you reduce oxygen requirements?

39 Disturbed Thought Processes and Anxiety
May be anxious, then confused and disoriented, and finally unconscious Remain calm; give simple explanations of what is being done Protect patient from constant, excessive noise and light Repeat orientation, instructions, and reassurance often In the presence of unconscious patients, remember that they may hear even when they cannot respond Continue to speak to the patient and beware of negative comments

40 Deficient Fluid Volume
Monitor for hypovolemia Tachycardia, hypotension, tachypnea, decreased urine output, and decreased central venous pressure and pulmonary artery pressure Administer intravenous fluids cautiously while assessing output of urine Assess for fluid overload Full, bounding pulse; dilute urine, increased respiratory rate; abnormal lung sounds; dyspnea; and edema When should the physician be notified about a decreasing urine output?

41 Risk for Injury Related to changes in consciousness
Related to therapeutic measures Antidysrhythmics can depress cardiac activity Anticoagulants can permit excessive bleeding Extravasation of vasopressors (drugs that raise blood pressure by vasoconstriction) can cause local tissue necrosis High risk for complications of immobility Personal hygiene may be limited by the patient’s tolerance of such activity Closely monitor the patient for both therapeutic and adverse effects of drugs used to treat the patient in shock. What measures should be instituted to prevent pressure ulcers?

42 Risk for Infection IV lines, indwelling urinary catheters, chest tubes, airways, ventricular assist devices, and other equipment provide avenues for infection in patient in shock Wash your hands thoroughly between patients Follow agency guidelines for care of IV and urinary catheters Use aseptic technique when inserting these devices, caring for insertion sites, and providing wound care Monitor for signs of infection When antibiotics are ordered, administer them on schedule to maintain a therapeutic blood level Which patients have the greatest risk for infection? What are the signs of infection?

43 Ineffective Family Coping
Be sensitive to the needs of the family for information and support Explain the nursing care and encourage them to ask questions Offer the services of a counselor or patient representative

44 Systemic Inflammatory Response Syndrome (SIRS)
Generalized inflammation that threatens vital organs Conditions that can lead to SIRS are shock, multiple transfusions, massive tissue injury, burns, and pancreatitis Effects are damage to the endothelium of blood vessels and a hypermetabolic state Increases capillary permeability; allows fluid to leak into body tissues Hypotension, microemboli, and shunting of blood flow compromise organ perfusion The hypermetabolic state is characterized by increased serum glucose, which eventually depletes carbohydrate, fat, and protein stores

45 Diagnosis Diagnosis of SIRS is made when a patient manifests two or more of the following: Temperature less than 97° F (36° C) or more than 100.4° F (38° C) Heart rate more than 90 bpm Respiratory rate more than 20/min, or Paco2 less than 32 mm Hg WBC count less than 4000 cells/mm3 or more than 12,000 cells/mm3, or more than 10% immature (band) neutrophils

46 SIRS Manifestations Range from mild to severe Sepsis
A patient has SIRS with a confirmed infection Advanced SIRS and failure of more than one organ Deterioration of cardiac, pulmonary, renal, and central nervous systems, liver, pancreas, and GI tract Thrombocytopenia may develop and progress to disseminated intravascular coagulation If three or more organs fail, the prognosis is very poor Multiple organ dysfunction syndrome (MODS) More than one organ begins to fail

47 Medical Treatment and Nursing Interventions
Prevent and treat infection Monitor potential sites; assess for signs and symptoms Maintain strict asepsis with invasive procedures and equipment Exercise scrupulous hand washing Administer antimicrobials as ordered Administer enteral feedings as ordered to enhance perfusion of the GI tract

48 Medical Treatment and Nursing Interventions
Maintain tissue oxygenation Administer sedatives and analgesics as ordered to reduce oxygen requirements Monitor the patient on mechanical ventilation Administer drugs to improve cardiac output and tissue perfusion as ordered Plan care to minimize physical demands on patient Provide nutritional and metabolic support Provide enteral or parenteral nutrition as ordered Monitor blood glucose and weight

49 Medical Treatment and Nursing Interventions
Support failing organs Mechanical ventilation for respiratory distress syndrome Replacement therapy for renal failure

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