Info To Know Mod6

Question 1

• The whole-body response to poor tissue oxygenation. Any problem that impairs oxygen delivery to tissues and organs can start the syndrome of shock and lead to a life-threatening emergency. Any problem that impairs PERFUSION and GAS EXCHANGE to tissues and organs can start the syndrome of shock and lead to a life-threatening emergency. Shock is often a result of cardiovascular problems.

Answer 1

Shock

Question 2

​- a condition in which fluid and proteins leak out of tiny blood vessels and into surrounding tissues. This can result in severely low blood pressure, low albuminemia, and a decrease in plasma volume.

Answer 2

Capillary leak syndrome

Question 3

​- Acronym for systemic inflammatory response syndrome, an inflammatory state affecting the whole body.
Infectious organisms have entered the bloodstream. As their numbers increase, widespread inflammation, known as

, is triggered as a result of infection escaping local control. With the organisms and their toxins in the bloodstream and entering other body areas, inflammation becomes an enemy, leading to extensive hormonal, tissue, and vascular changes and oxidative stress that further impair GAS EXCHANGE and tissue PERFUSION.

Answer 3

SIRS

systemic inflammatory response syndrome (SIRS)

Question 4

​- The sequence of inadequate blood flow to body tissues, which deprives cells of oxygen and leads to anaerobic metabolism with acidosis, hyperkalemia, and tissue ischemia; this is followed by dramatic changes in vital organs and leads to the release of toxic metabolites and destructive enzymes.
When shock conditions continue for longer periods without help, the resulting increased metabolites cause so much cell damage in vital organs that they are unable to perform their critical functions. When this problem, known as ??), occurs to the extent that vital organs die, recovery from shock is no longer possible

Answer 4

MODS

multiple organ dysfunction syndrome (MODS

Question 5

1. What are the four categories of shock

Answer 5

Shock is classified by the type of impairment causing it into the categories of hypovolemic shock, cardiogenic shock, distributive shock (which includes septic shock, neurogenic shock, and anaphylactic shock), and obstructive shock. Table 37-1 describes this classification and common causes of shock. TABLE 37-1

Question 6

2. Name common causes, signs and symptoms, and treatment for each category of shock.
   - ?? shock occurs when too little circulating blood volume decreases MAP, resulting in inadequate total body PERFUSION and GAS EXCHANGE.

Answer 6

Hypovolemic

Question 7

-Common problems leading to hypovolemic shock

Answer 7

are dehydration and poor CLOTTING with hemorrhage. A complete discussion of the pathophysiology and management of hypovolemic shock begins with the PERFUSION concept exemplar.

Question 8

?? shock occurs when the heart muscle is unhealthy and pumping is impaired.

Answer 8

Cardiogenic shock

Question 9

What is the most common cause of direct pump failure. Other causes are listed in Table 37-1. Any type of pump failure decreases cardiac output and MAP. Chapter 38 discusses the pathophysiology and care for the adult with shock from myocardial infarction.

Answer 9

Myocardial infarction

Question 10

?? shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs.

Answer 10

-Distributive shock

Question 11

Distributive shock cause?

Answer 11

It can be caused by blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak.

All these factors decrease MAP and may be started either by nerve changes (neural-induced) or by the presence of some chemicals (chemical-induced).

Question 12

?? shock is caused by problems that impair the ability of the normal heart to pump effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle.

The most common cause of obstructive shock is what?

Answer 12

Obstructive shock

cardiac tamponade

Question 13

Although the causes and initial signs and symptoms associated with the different types of shock vary, eventually the effects of hypotension and anaerobic cellular metabolism (metabolism without oxygen)

Answer 13

Yes

Question 14

: Loss of sympathetic tone due to trauma or spinal shock.

Answer 14

Neurogenic

Question 15

​? is an extreme type of allergic reaction. It begins within seconds to minutes after exposure to a specific allergen in a susceptible adult. The result is widespread loss of blood vessel tone, with decreased blood pressure and cardiac output.

Answer 15

Anaphylaxis

Question 16

is a widespread infection that triggers whole-body inflammation. It leads to distributive shock when infectious microorganisms are present in the blood and is most commonly called septic shock. A complete discussion of the pathophysiology, prevention, and care for the patient with sepsis and septic shock begins with the IMMUNITY concept exemplar.

Answer 16

Sepsis

Question 17

3. What are the stages of shock? And how is your MAP and compensatory mechanisms effected in each state?
   Stages of Shock:

Answer 17

The syndrome of shock progresses in four stages when the conditions that cause shock remain uncorrected and poor cellular oxygenation continues.

These stages are: 1. Initial stage 2. Nonprogressive stage 3. Progressive stage 4.refractory stage

Question 18

? stage is present when the patient’s baseline MAP is decreased by less than 10 mm Hg.

Compensatory mechanisms are effective at returning systolic pressure to normal at this stage; thus oxygen PERFUSION to vital organs is maintained. Cellular changes include increased anaerobic metabolism in some tissues with production of lactic acid, although overall metabolism is still aerobic. The compensation responses of vascular constriction and increased heart rate are effective, and both cardiac output and MAP are maintained within the normal range. Because vital organ function is not disrupted, the indicators of shock are difficult to detect at this stage.
Nursing Safety Priority Action Alert Be aware that increased heart and respiratory rates or a slight increase in diastolic blood pressure may be the only sign of this stage of shock.

Answer 18

Initial Stage. The initial

Question 19

Stage: The nonprogressive stage of shock occurs when MAP decreases by 10 to 15 mm Hg from baseline.

Kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP and supply oxygen to vital organs. The ongoing decrease in MAP triggers the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine to start kidney compensation. Urine output decreases, sodium reabsorption increases, and widespread blood vessel constriction occurs. ADH increases water reabsorption in the kidney, further reducing urine output, and increases blood vessel constriction in the skin and other less vital tissue areas. Together these actions compensate for shock by maintaining the fluid volume within the central blood vessels. Tissue hypoxia occurs in nonvital organs (e.g., skin, GI tract) and in the kidney, but it is not great enough to cause permanent damage. Buildup of metabolites from anaerobic metabolism causes acidosis (low blood pH) and increased blood potassium levels. Signs and symptoms of this stage include changes resulting from decreased tissue PERFUSION. Subjective changes include thirst and anxiety. Objective changes include restlessness, tachycardia, increased respiratory rate, decreased urine output, falling systolic blood pressure, rising diastolic blood pressure, narrowing pulse pressure, cool extremities, and a 2% to 5% decrease in oxygen saturation. Comparing these changes with the values and observations obtained earlier is critical to identifying this stage of shock. If the patient is stable and compensatory mechanisms are supported by interventions, he or she can remain in this stage for hours without having permanent damage. Stopping the conditions that started shock and providing supportive interventions can prevent the shock from progressing. The effects of this stage are reversible when nurses recognize the problem and coordinate the interprofessional health care team to start appropriate interventions.

Answer 19

Nonprogressive Stage

Question 20

Stage?. The progressive stage of shock occurs when there is a sustained decrease in MAP of more than 20 mm Hg from baseline.

Compensatory mechanisms are functioning but can no longer deliver sufficient oxygen, even to vital organs. Vital organs develop hypoxia, and less vital organs become anoxic (no oxygen) and ischemic (cell dysfunction or death from lack of oxygen). As a result of poor PERFUSION and a buildup of metabolites, some tissues die. Indications of the progressive stage include a worsening of changes resulting from decreased tissue PERFUSION. The patient may express a sense of “something bad” (impending doom) about to happen. He or she may be confused, and thirst increases. Objective changes are a rapid, weak pulse; low blood pressure; pallor to cyanosis of oral mucosa and nail beds; cool and moist skin; anuria; and a 5% to 20% decrease in oxygen saturation. Laboratory data may show a low blood pH, along with rising lactic acid and potassium levels. Nursing Safety Priority Action Alert this stage of shock is a life-threatening emergency. Vital organs tolerate this situation for only a short time before developing multiple organ dysfunction syndrome (MODS) with permanent damage. Immediate interventions are needed to reverse the effects of this stage of shock. The patient’s life usually can be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage. Continuously monitor and compare with earlier findings to assess therapy effectiveness and determine when therapy changes are needed.

Answer 20

Progressive Stage

Question 21

Stage? of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have extensive damage and cannot respond effectively to interventions, and shock continues. So much damage has occurred with release of metabolites and enzymes that damage to vital organs continues despite interventions. The sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead cells open and release metabolites. These trigger small clots (microthrombi) to form, which block tissue PERFUSION and damage more cells, continuing the devastating cycle. Liver, heart, brain, and kidney functions are lost first. The most profound change is damage to the heart muscle. Signs are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. Therapy, including fluid replacement, is not effective in saving the patient’s life, even if the cause of shock is corrected and MAP temporarily returns to normal.

Answer 21

The refractory stage

Question 22

4. Name at least one medication from each med classification and its use
   ?–Improve mean arterial pressure by increasing peripheral resistance, increasing venous return, and increasing myocardial contractility. Dopamine (Intropin, Revimine) Norepinephrine (Levophed) Phenylephrine HC.
   ​
   ??– Directly stimulate beta-adrenergic receptors on the heart muscle, improving contractility Dobutamine (Dobutrex) Milrinone (Primacor)

Answer 22

Vasoconstrictors

Inotropic agents

Question 23

5. What are the signs and symptoms of septic shock

Answer 23

•Patients at higher risk:
Malnutrition • Immunosuppression • Large, open wounds • Mucous membrane fissures in prolonged contact with bloody or drainage-soaked packing • GI ischemia • Exposure to invasive procedures • Cancer • Older than 80 years, • Infection with resistant microorganisms 
• Receiving cancer chemotherapy
• Alcoholism
• Diabetes mellitus
• Chronic kidney disease
• Transplantation recipient
• Hepatitis
• HIV/AIDS
Suspected or identified infection with some of the following: • Temperature of more than 101° F (38.3° C) or less than 96.8° F (36° C) • Heart rate of more than 90 beats/min • Respiratory rate of more than 20 breaths/min • Abnormal WBC count (>12,000/mm3 or <4000/mm3) • Normal WBC count with >10% bands • Plasma C-reactive protein >2 standard deviations above normal • Plasma prolactin >2 standard deviations above normal • Arterial hypotension (SBP <90 mm Hg; MAP <70 mm Hg) • Arterial hypoxemia (PaO2/FiO2 <300) • Urine output <0.5 mL/kg/hr for 2 hours despite adequate fluid resuscitation • Creatinine increase >0.5 mg/dL • INR >1.5 or aPTT >60 • Absent bowel sounds • Platelet count <100,000/mm3 • Total bilirubin >4 mg/dL • Elevated lactic acid (lactate) levels • Decreased capillary refill or presence of mottling • Hyperglycemia (plasma glucose >140 mg/dL or 7.7 mmol/L) in absence of diabetes • Unexplained change in mental status • Significant edema or positive fluid balance

Physical Assessment/Signs and Symptoms.

Signs and symptoms of sepsis and septic shock occur over many hours, and some change during the progression. See Table 37-3 for a listing of specific symptoms and laboratory changes that often occur with sepsis and septic shock.

Cardiovascular changes differ in the stages of sepsis and septic shock. Cardiac output and blood pressure are low in early sepsis and very low in septic shock. In severe sepsis, cardiac output is higher as are heart rate and blood pressure, although this is an indication of a worsening condition rather than an improvement. Increased cardiac output is reflected by tachycardia, increased stroke volume, a normal systolic blood pressure, and a normal central venous pressure (CVP). Increased cardiac output and vasodilation make the skin color appear normal with pink mucous membranes and the skin is warm to the touch. This situation is temporary, and eventually the cardiac output is greatly reduced. With progression, disseminated intravascular coagulation (DIC) occurs as a result of excessive CLOTTING, with formation of thousands of small clots in the tiny capillaries of the liver, kidney, brain, spleen, and heart. DIC reduces PERFUSION and GAS EXCHANGE and decreases oxygen saturation, causing widespread hypoxia and ischemia. The huge number of small clots uses clotting factors and fibrinogen faster than they can be produced, which eventually leads to poor CLOTTING. This leads to hemorrhage, which occurs in the septic shock stage. Coupled with continued capillary leak, bleeding causes hypovolemia and a dramatic decrease in cardiac output, blood pressure, and pulse pressure. The signs and symptoms of this phase are the same as those of the later stages of hypovolemic shock.

Respiratory changes are first caused by compensatory mechanisms that try to maintain oxygenation with a rate increase. The lungs are susceptible to damage, and the complication of acute respiratory distress syndrome (ARDS) may occur in septic shock. ARDS in septic shock is caused by the continued systemic inflammatory response syndrome (SIRS) increasing the formation of oxygen free radicals, which damage lung cells. ARDS in a patient with septic shock has a high mortality rate. Skin changes differ at different stages of sepsis. In the hyperdynamic stage, the skin is warm and no cyanosis is evident. With progression to septic shock and compromised circulation, it is cool and clammy with pallor, mottling, or cyanosis. In DIC, petechiae and ecchymoses can occur anywhere. Blood may ooze from the gums, other mucous membranes, and venipuncture sites and around IV catheters. A kidney/urinary change of low urine output compared with fluid intake indicates shock. When a patient who has no known kidney problems suddenly starts having a low urine output, be suspicious of severe sepsis or septic shock. Reduced output is caused by low circulating volume and hormonal changes.

Kidney function decreases, and serum creatinine levels rise.

Psychosocial Assessment. An indicator that patients may be in the beginning of severe sepsis is often a change in affect or behavior. Compare the patient’s current behavior, verbal responses, and general affect with those assessed earlier in the day or the day before. They may seem just slightly different in their reactions to greetings, comments, or jokes. They may be less patient than usual or act restless or fidgety. Patients may make statements such as, “I feel as if something is wrong, but I don’t know what.” If behavior is changed from prior assessments, consider the possibility of severe sepsis and shock.

Question 24

​What lab values are significant for septic shock?

Answer 24

WBC’s and increased serum lactic acid are significant lab values in septic shock. They may also see abnormal ABG’s, increased cardiac enzymes with cardiogenic shock, decreased Hct/Hgb with hypovolemic shock, positive blood cultures.
No single laboratory test confirms the presence of sepsis and septic shock, although hallmarks of sepsis are a rising serum procalcitonin level, an increasing serum lactate level, a normal or low total white blood cell (WBC) count, and a decreasing segmented neutrophil level with a rising band neutrophil level (left shift, see Chapter 17).
The presence of bacteria in the blood supports the diagnosis of sepsis, although this finding may not be present. Obtain specimens of urine, blood, sputum, and any drainage for culture to identify the causative organisms. Blood cultures should be taken before antibiotic therapy is started, provided that this action does not delay antibiotic therapy by more than 45 minutes (Dellinger et al., 2013).
Other abnormal laboratory findings that occur with septic shock include changes in the white blood cell (WBC) count; the differential leukocyte count may show a left shift. Hematocrit and hemoglobin levels usually do not change until late in septic shock. At that point, the hematocrit and hemoglobin levels, fibrinogen levels, and platelet count are low from disseminated intravascular coagulation (DIC). The serum lactate level is above normal, and the serum bicarbonate levels are lower than normal. Unfortunately these parameters may take time to change and cannot be relied on as sensitive indicators of the patient’s worsening condition. Another indicator of sepsis and septic shock is a low blood level of activated protein C. Protein C is an enzyme that prevents inappropriate clot formation. It is activated when it binds to healthy vascular endothelial cells. In severe sepsis, the injured endothelial cells cannot activate protein C, and thousands of small clots form in the capillaries of vascular organs. Decreasing levels of activated protein C indicate the beginning of severe sepsis even before other symptoms are evident. Other biologic indicators of severe sepsis and septic shock are changes in plasma D-dimer levels, cytokine, and interleukin levels. These indicators have a lag time, and changes may not be present soon enough to identify sepsis with SIRS before severe sepsis or septic shock develops. Because the results of blood cultures may not be available until the patient’s condition has progressed to severe sepsis or septic shock, other biomarkers for sepsis and SIRS are needed to help identify the condition when it can be managed and cured. Two such markers are increasing lactic acid levels and increasing procalcitonin levels

Question 25

What is the treatment for septic shock?

Answer 25

Within the first 3 hours of suspecting severe sepsis: 1. Measure serum lactate levels. 2. Obtain blood cultures before administering antibiotics. 3. Administer broad-spectrum antibiotics. 4. Administer 30 mL/kg crystalloids intravenously for hypotension or lactate ≥4 mmol/L.
Within 6 hours of initial indications of suspected septic shock: 5. Administer prescribed vasopressors for hypotension that does not respond to initial fluid resuscitation measures to maintain MAP ≥65 mm Hg. 6. If arterial hypotension persists despite initial fluid volume resuscitation or lactate remains ≥4 mmol/L (36 mg/dL), reassess volume status and tissue perfusion and document findings (reassessment of volume status and tissue perfusion as outlined below). 7. Remeasure lactate level if initial value was elevated. Document reassessment of volume status and tissue perfusion with EITHER: • Repeat focused examination (after initial fluid resuscitation), including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings OR TWO OF THE THREE FOLLOWING: • Measure of central venous pressure • Measure of central venous oxygen saturation • Bedside cardiovascular ultrasound • Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge.
In accordance with the recommendations of The Joint Commission’s National Patient Safety Goals (NPSGs), IV antibiotics with known activity against gram-negative bacteria are given before organisms are identified, preferably within 1 hour of a sepsis diagnosis.

Question 26

The client is unable to provide adequate delivery of oxygen to the body tissues due to a weakened forward pumping function of the heart.  The nurse realizes the client is experiencing which of the following?
A. Anaphylactic reaction
B. Cardiogenic shock
C. Hypovolemic shock
D. Neurogenic shock

Answer 26

B

Question 27

The client experienced a severe burn with massive fluid loss and hypoproteinemia.  When fluid shifts into the interstitial spaces and prevents gas exchange, the nurse understands this fluid shift to be which of the following?
A. Anaphylaxis
B. Septic shock
C. Flail chest
D. Capillary leak syndrome

Answer 27

D

Question 28

The client is brought to the emergency department after a motor vehicle accident. The patient has internal bleeding from a ruptured spleen. The nurse’s primary concern is to monitor for which of the following?
A. Decrease in mean arterial pressure
B. Smell of alcohol on the breath
C. Abdominal pain radiating to the left shoulder
D. Urinary output of 75 mL/hr

Answer 28

D