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Final Exam Flashcards

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1
Q

Shock

A

inadequate tissue perfusion; if untreated, results in cell death
a condition in which widespread perfusion to the cells is inadequate to deliver oxygen and nutrients to support vital organs and cellular function
ANY insult to the body can create a cascade of events resulting in poor tissue perfusion
Requires ongoing assessment
Hydration and oxygenation!
Cell death then tissue death then organ failure

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2
Q

physiologic responses common to all types of shock

A

hypoperfusion of tissues
hypermetabolism
activation of the inflammatory response (cascading event)
Vitals at least every 2 hours

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3
Q

Cellular function in cells (aerobic vs anaerobic)

A

Aerobic metabolism: yields more ATP–more efficient and effective in producing energy
Anaerobic metabolism: less ATP and accumulation of the toxic end product lactic acid (also seen with not enough perfusion, acidic pH and hyperventilation to compensate)

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4
Q

Cellular changes in shock

A

Anaerobic metabolism→ acid accumulation → increase permeability
Electrolytes and fluids seep out of and into the cell.
The sodium-potassium pump becomes impaired; cell structures, primarily the mitochondria, are damaged, and death of the cell results
Glucose is the primary substrate required for the production of cellular energy in the form of ATP.
SELF-PERPETUATING NEGATIVE SITUATION

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5
Q

Stress and cellular changes in shock

A

In stress statues, catecholamines, cortisol, glucagon, and inflammatory cytokines are released, causing hyperglycemia and insulin resistance to mobilize glucose for cellular metabolism→ more glucose is needed→ gluconeogenesis→ Need more energy → gluconeogenesis → hypermetabolic state → use proteins and fats to produce glucose (used up all the glucose) → proteolysis (breakdown of protein) → organ failure
Inflammatory process activates clotting cascade

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6
Q

3 major components of circulatory system

A

blood volume
cardiac pump
vasculature (need good tone)
they must work together to maintain adequate BP to perfuse body tissues

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7
Q

What is a good MAP

A

must exceed 65 mmHg for cells to receive the oxygen and nutrients needed to metabolize energy in amounts sufficient to sustain life

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8
Q

Stages of shock

A

(initial)
compensatory (stage 1)
progressive (stage 2)
irreversible (stage 3)
Better outcome when aggressive therapy begins within 3 hours of identifying a shock state, especially septic shock (gram + up, - down)
Fluids, treat underlying cause

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9
Q

Compensatory shock

A

normal BP
vasoconstriction
increased heart rate (usually 10% of baseline is a good indicator of possible shock)
blood shunts from skin, kidneys, and GI tract to brain, heart, and lungs
Cool pale skin, hypoactive bowel, low urine output
Met acid and resp alk

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10
Q

What to monitor and report in compensatory shock

A

Pt feel anxious or confused
vital signs–key indicators of hemodynamic status
BP: indirect measure of tissue hypoxia
report SBP< 100 mm Hg or drop in SBP of 40 mm Hg from the baseline or MAP less than 65 mmHg
AND
Notify MD promptly if two of the three following signs detected if the patient is concurrently diagnosed with an infection or if an infection is suspected:
Respiratory rate >=22/min
Altered mentation
Systolic BP<=100 mmHg

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11
Q

Pulse pressure

A

Correlates well with stroke volume
Pulse pressure=SBP-DBP
Normal pulse pressure: 40mmHg
Narrowing of pulse pressure: indicates decreased stroke volume
Systolic can keep dropping, diastolic stays around the same, causing narrow pp

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12
Q

Continuous central venous oximetry (ScvO2)

A

Normal 70%
With shock, more oxygen is consumed, ScvO2 will be lower
Obtained through a central catheter in the superior vena cava

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13
Q

Early interventions for compensatory shock

A

Identifying the cause of shock
IV fluids
oxygenation
Obtaining lab tests
pain control
sedating agents when needed
reducing anxiety
promoting safety

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14
Q

Progressive stage of shock

A

BP can no longer compensate: hypotensive (systolic less than 100 mmHg or a decrease of systolic BP of 40 mmHg from baseline)

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15
Q

Cardio effects of progressive shock

A

faster heart rate>150 bpm
failure of the cardiac pump
Possible MI
Levels of cardiac biomarkers increase

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16
Q

Respiratory effects of progressive shock

A

Respirations are rapid and shallow
Crackles are heard over the lung fields
Decreased pulmonary blood flow causes arterial oxygen levels to decrease and CO2 levels to increase
Hypoperfused alveoli stop producing surfactant and subsequently collapse
Pulmonary capillaries begin to leak, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse→ acute lung injury
ARDS

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17
Q

Neuro effects of progressive shock

A

Subtle changes in behavior→ become agitated→ confused→ signs of delirium→ lethargy increases→ lose consciousness

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18
Q

Renal effects of progressive shock

A

AKI from not enough perfusion to kidneys

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19
Q

Liver effects of progressive shock

A

Not able to metabolize medications and metabolic waste products (ammonia and lactic acid)
More susceptible to infection (liver fails to filter bacteria from the blood)
Elevated liver enzymes and bilirubin levels elevated (jaundice)

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20
Q

GI effects of progressive shock

A

stress ulcers–risk for GI bleeding.
Bacteria translocation (due to GI ischemia)

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21
Q

Hematologic effects of progressive shock

A

Disseminated intravascular coagulation DIC: inflammatory cytokines activate the clotting cascade–widespread clotting and bleeding occur simultaneously

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22
Q

Management of progressive shock

A

IV fluids and medications to restore tissue perfusion
mechanical ventilation
Optimizing intravascular volume
Supporting the pumping action of the heart (IABP)
Improving the competence of the vascular system
Early enteral nutritional support (like burns)
Glycemic control, medications to reduce the risk of GI ulceration and bleeding

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23
Q

Preventing complications of progressive shock

A

monitor s/s of infection
aseptic techniques
frequent oral care
aseptic suction technique
turning and elevating the HOB at least 30 degrees

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24
Q

Promoting rest and comfort in progressive shock

A

priority
conserve the patient’s energy
not be warmed too quickly (vasodilation–leads to drop in BP)
Protect the patient from temperature extremes (excessive warmth or cold, shivering)

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25
Preventing delirium in progressive shock
Assess once a shift Frequent orientation activities Assessing and treating pain Promoting sleep Providing early mobilization activities Limiting sedation (especially sedation with benzodiazepines, e.g, lorazepam [Ativan]).
26
Irreversible stage of shock
organ damage is so severe that the patient does not respond to treatment and cannot survive BP remains low renal and liver failure (release of necrotic tissue toxins, metabolic acidosis)
27
Nursing management of irreversible shock
offer brief explanations to the patient about what is happening is essential even if there is no certainty that the patient hears or understands what is being said
28
General management strategies of shock
support of the respiratory system with supplemental oxygen and/or mechanical ventilation to provide optimal oxygenation fluid replacement to restore intravascular volume vasoactive medications to restore vasomotor tone and improve cardiac function nutritional support to address the metabolic requirements that are often dramatically increased in shock--skeletal muscle mass will be broken down first
29
Insufficient fluid replacement in shock
higher incidence of morbidity and mortality from lack of tissue perfusion
30
Excessive fluid replacement in shock
systemic and pulmonary edema--ARDS abdominal compartment syndrome (ACS): too much pressure in the abdomen and the abdominal wall cannot expand anymore can make breathing difficult, check liver function to differentiate from ascites, also we’re giving so much fluid and it’s everywhere in the abdomen now whereas ascites you can just take the fluid out
31
Crystalloid solutions in shock
electrolyte solutions Commonly used: 0.9% sodium chloride solution (NS) and lactated Ringer’s solution. Isotonic solutions disadvantage: diffuse into the interstitial space Hypertonic solution: 3% NaCl--for TBI patient (brings down ICP, also used in TB) These don't stay in vasculature for long
32
Colloid solutions in shock
electrolyte solutions Commonly used: 0.9% sodium chloride solution (NS) and lactated Ringer’s solution. Isotonic solutions disadvantage: diffuse into the interstitial space Hypertonic solution: 3% NaCl--for TBI patient
33
Colloid solutions in shock
large-molecule IV solutions Contain molecules that are too large to pass through capillary membranes, remain within the intravascular compartment longer Albumin: expensive
34
Vasoactive meds
Inotropic vasodilators vasopressors when given must monitor vital signs frequently (every 15 minutes until stable, or more often if indicated) must be given through a central line--tissue necrosis and sloughing should be tapered and weaned--should not stop abruptly (titrated the dosage) When patients are on this for long, fingers and toes can be necrotic
35
Inotropic meds and examples
dobutamine, dopamine, epinephrine, milrinone
36
Inotropic meds pros and cons
(+) Increase contractility (-) Increase oxygen demand of the heart
37
Vasodilator examples
Nitroglycerin, nitroprusside
38
Vasodilator pros and cons
(+) Reduce preload and afterload (makes pumping easier) (-) cause hypotension
39
Vasopressor examples
norepinephrine, dopamine, epinephrine, vasopressin
40
Vasopressor pros and cons
(+) increase blood pressure (-) increase cardiac workload
41
Nutritional support in shock
May require more than 3000 calories daily Skeletal muscle mass broken down first Enteral feeding is preferred
42
Hypovolemic shock
decreased intravascular volume reduction of 15-30% of intravascular fluid 750-1500 mL of blood loss in a 70-kg person due to either fluid loss or shifting (dehydration, edema, ascites...)
43
Management of hypovolemic shock
fluid replacement two IV lines (alternative: intraosseous catheter) Blood products Modified Trendelenburg position--fluid redistribution (Knee straight, trunk horizontal, head slightly elevated)
44
Nursing management of hypovolemic shock
temperature should be monitored to ensure rapid fluid resuscitation does not cause hypothermia
45
Pharm therapy in hypovolemic shock indications
If fluid fails to reverse hypovolemic shock, then vasoactive medications that prevent cardiac failure are given Also given to reverse cause of dehydration
46
Pharm therapy in hypovolemic shock
Insulin for hyperglycemia (hyperglycemia can lead to dehydration) Desmopressin (DDAVP) for diabetes insipidus Antidiarrheal for diarrhea Antiemetic for vomiting
47
Cardiogenic shock
when the heart's ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues
48
Coronary and noncoronary causes of cardiogenic shock
MI Stress to myocardium (hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax) Cardiomyopathies Valvular damage Cardiac tamponade Dysrhythmias
49
Patho of cardiogenic shock
Impaired tissue perfusion weakens the heart and impairs its ability to pump Reduced ejection fraction Fluid accumulates in the lungs
50
Clinical manifestations of cardiogenic shock
angina dysrhythmias fatigue express feelings of doom show signs of hemodynamic instability
51
Medical management of cardiogenic shock
increasing cardiac contractility decreasing ventricular afterload correction of underlying causes
52
First line treatment of cardiogenic shock
O2 (NC 2-6 L/min Sats > 90%) Pain control--IV morphine hemodynamic monitoring laboratory marker monitoring (BNP, cardiac enzymes, ECG) fluid therapy
53
Dobutamine for cardiogenic shock
Inotropic: increasing the strength of contractility Decrease pulmonary and systemic vascular resistance
54
Nitro for cardiogenic shock
Low dose: venous vasodilation--reduce preload Higher dose: arterial vasodilation--reduce afterload and improve blood flow to the myocardium
55
Dopamine for cardiogenic shock
Use with dobutamine and nitroglycerin to improve tissue perfusion Low dose: Improve contractility (2-8 𝛍g/kg/min) Higher dose: > 8 ưg/kg/min vasoconstriction (not desirable; titrate carefully)
56
Other vasoactive meds for cardiogenic shock
Norepinephrine, epinephrine, milrinone, vasopressin, and phenylephrine They stimulate different receptors of the sympathetic nervous system.
57
Antiarrhythmic meds for cardiogenic shock
Used to stabilize HR
58
Mechanical assistive devices for cardiogenic shock
Intra-aortic balloon pump Left and right ventricular assist devices Total temporary artificial hearts Cardiopulmonary bypass system
59
Circulatory shock
Also known as distributive blood volume pools in peripheral blood vessels (abnormal displacement of blood volume) lack of vascular tone: septic shock neurogenic shock anaphylactic shock
60
Lack of vascular tone in circulatory shock
central regulatory mechanisms (sympathetic tone, constriction) local regulatory mechanisms (cellular biochemical mediators) Massive arterial and venous dilation
61
Septic shock
Most common type of circulatory shock caused by widespread infection most common cause of death in noncoronary ICUs in the U.S. Gram-negative bacteria: most common (e. coli) gram-positive bacteria: Staphylococcus aureus, MRSA Fungal infections, viral infections Site of infection not always identified
62
Risk factors of septic shock
Immunosuppression (cancer, HIV/AIDS, organ transplant) Extremes of age (<1 yr and >65 yr) Malnourishment Chronic illness Invasive procedures Emergent and/or multiple surgeries
63
Patho of septic shock
immune and inflammatory response cause increased capillary permeability and poor tissue perfusion Systemic inflammatory response syndrome (SIRS): Clots formation
64
Early stage septic shock
hyperthermia and fever, with warm and flushed skin and bounding pulses; elevated RR Cloudy urine (e. coli) Warm phase
65
Late phase (true septic shock)
BP drops and skin becomes cool, pale, and mottled. Pulse ox! Ventilator/intubation possible Cold phase
66
Medical management of septic shock
identify and treat patients in early sepsis within 3 hours (sepsis bundle chart, tells us when there’s a major change in vitals from baseline) fluid replacement therapy pharmacological therapy nutritional therapy: initiated within 24 to 48 hours of ICU admission Nursing management: Sepsis-Related Organ Failure Assessment Score (SOFA)
67
Neurogenic shock
vasodilation due to a loss of balance between parasympathetic and sympathetic stimulation--predominant parasympathetic stimulation Caused by spinal cord injury, spinal anesthesia, or other nervous system damage. can be caused by lack of glucose venous pooling in the extremities and peripheral vasodilation (dry warm skin)**
68
S/S of neurogenic shock
Low BP low HR (Low CO) dry, warm skin pt does not perspire in the paralyzed portions of the body (neurogenic shock can also be caused by spinal cord injury)
69
Management of neurogenic shock
closely observe for an abrupt onset of fever elevate and maintain the HOB at least 30 degrees to prevent neurogenic shock when the patient receives spinal or epidural anesthesia (prevent the spreading of medication up through the spinal cord) supportive care Higher risk for VTE, evaluated for DVT Monitor closely for internal bleeding among patients with a spinal cord injury (they may not report pain caused by internal injuries.)
70
Anaphylactic shock
caused by a severe allergic reaction when patients who have already produced antibodies to a foreign reaction an antigen-antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, causing widespread vasodilation and capillary permeability rapid onset of hypotension, neurologic compromise, respiratory distress, and cardiac arrest 1st time exposure antibodies formed 2nd time anaphylactic shock
71
Medical management of anaphylactic shock
Fluid management IM epinephrine IV diphenhydramine Albuterol
72
Multiple organ dysfunction syndrome (MODS)
A complication of any form of shock, but is most commonly seen in patients with sepsis. Rapid assessment with early recognition and response to shock states and sepsis is essential to the patient’s recovery dysfunction of one organ system is associated with 20% mortality, and if more than four organ fail, the mortality is at least 60%.
73
Progression of MODS
usually begins in the lungs, and cardiovascular instability as well as failure of the hepatic, GI, renal, immunologic, and CNS (hearing last to go)
74
Medical management of MODS
prevention is the top priority elderly: early signs are changes in mentation and a gradual rise in temperature (mental status first) Controlling the initiating event Promoting adequate organ perfusion Providing nutritional support Maximizing patient comfort

Critical Care (5 decks)

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