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Critical Care > Final Exam > Flashcards

Final Exam Flashcards

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
Q

Preventing delirium in progressive shock

A

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]).

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26
Q

Irreversible stage of shock

A

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)

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27
Q

Nursing management of irreversible shock

A

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

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28
Q

General management strategies of shock

A

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

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29
Q

Insufficient fluid replacement in shock

A

higher incidence of morbidity and mortality from lack of tissue perfusion

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30
Q

Excessive fluid replacement in shock

A

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
Q

Crystalloid solutions in shock

A

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
Q

Colloid solutions in shock

A

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
Q

Colloid solutions in shock

A

large-molecule IV solutions
Contain molecules that are too large to pass through capillary membranes, remain within the intravascular compartment longer
Albumin: expensive

34
Q

Vasoactive meds

A

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
Q

Inotropic meds and examples

A

dobutamine, dopamine, epinephrine, milrinone

36
Q

Inotropic meds pros and cons

A

(+) Increase contractility
(-) Increase oxygen demand of the heart

37
Q

Vasodilator examples

A

Nitroglycerin, nitroprusside

38
Q

Vasodilator pros and cons

A

(+) Reduce preload and afterload (makes pumping easier)
(-) cause hypotension

39
Q

Vasopressor examples

A

norepinephrine, dopamine, epinephrine, vasopressin

40
Q

Vasopressor pros and cons

A

(+) increase blood pressure
(-) increase cardiac workload

41
Q

Nutritional support in shock

A

May require more than 3000 calories daily
Skeletal muscle mass broken down first
Enteral feeding is preferred

42
Q

Hypovolemic shock

A

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
Q

Management of hypovolemic shock

A

fluid replacement
two IV lines (alternative: intraosseous catheter)
Blood products
Modified Trendelenburg position–fluid redistribution (Knee straight, trunk horizontal, head slightly elevated)

44
Q

Nursing management of hypovolemic shock

A

temperature should be monitored to ensure rapid fluid resuscitation does not cause hypothermia

45
Q

Pharm therapy in hypovolemic shock indications

A

If fluid fails to reverse hypovolemic shock, then vasoactive medications that prevent cardiac failure are given
Also given to reverse cause of dehydration

46
Q

Pharm therapy in hypovolemic shock

A

Insulin for hyperglycemia (hyperglycemia can lead to dehydration)
Desmopressin (DDAVP) for diabetes insipidus
Antidiarrheal for diarrhea
Antiemetic for vomiting

47
Q

Cardiogenic shock

A

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
Q

Coronary and noncoronary causes of cardiogenic shock

A

MI
Stress to myocardium (hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax)
Cardiomyopathies
Valvular damage
Cardiac tamponade
Dysrhythmias

49
Q

Patho of cardiogenic shock

A

Impaired tissue perfusion weakens the heart and impairs its ability to pump
Reduced ejection fraction
Fluid accumulates in the lungs

50
Q

Clinical manifestations of cardiogenic shock

A

angina
dysrhythmias
fatigue
express feelings of doom
show signs of hemodynamic instability

51
Q

Medical management of cardiogenic shock

A

increasing cardiac contractility
decreasing ventricular afterload
correction of underlying causes

52
Q

First line treatment of cardiogenic shock

A

O2 (NC 2-6 L/min Sats > 90%)
Pain control–IV morphine
hemodynamic monitoring
laboratory marker monitoring (BNP, cardiac enzymes, ECG)
fluid therapy

53
Q

Dobutamine for cardiogenic shock

A

Inotropic: increasing the strength of contractility
Decrease pulmonary and systemic vascular resistance

54
Q

Nitro for cardiogenic shock

A

Low dose: venous vasodilation–reduce preload
Higher dose: arterial vasodilation–reduce afterload and improve blood flow to the myocardium

55
Q

Dopamine for cardiogenic shock

A

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
Q

Other vasoactive meds for cardiogenic shock

A

Norepinephrine, epinephrine, milrinone, vasopressin, and phenylephrine
They stimulate different receptors of the sympathetic nervous system.

57
Q

Antiarrhythmic meds for cardiogenic shock

A

Used to stabilize HR

58
Q

Mechanical assistive devices for cardiogenic shock

A

Intra-aortic balloon pump
Left and right ventricular assist devices
Total temporary artificial hearts
Cardiopulmonary bypass system

59
Q

Circulatory shock

A

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
Q

Lack of vascular tone in circulatory shock

A

central regulatory mechanisms (sympathetic tone, constriction)
local regulatory mechanisms (cellular biochemical mediators)
Massive arterial and venous dilation

61
Q

Septic shock

A

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
Q

Risk factors of septic shock

A

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
Q

Patho of septic shock

A

immune and inflammatory response cause increased capillary permeability and poor tissue perfusion
Systemic inflammatory response syndrome (SIRS): Clots formation

64
Q

Early stage septic shock

A

hyperthermia and fever, with warm and flushed skin and bounding pulses; elevated RR
Cloudy urine (e. coli)
Warm phase

65
Q

Late phase (true septic shock)

A

BP drops and skin becomes cool, pale, and mottled.
Pulse ox!
Ventilator/intubation possible
Cold phase

66
Q

Medical management of septic shock

A

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
Q

Neurogenic shock

A

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
Q

S/S of neurogenic shock

A

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
Q

Management of neurogenic shock

A

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
Q

Anaphylactic shock

A

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
Q

Medical management of anaphylactic shock

A

Fluid management
IM epinephrine
IV diphenhydramine
Albuterol

72
Q

Multiple organ dysfunction syndrome (MODS)

A

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
Q

Progression of MODS

A

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
Q

Medical management of MODS

A

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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