Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Acute Care Exam 3 > Shock > Flashcards

Shock Flashcards

1
Q

what is shock

A

Typically, as oxygen demand increases, compensatory mechanisms balance oxygen delivery
Shock results from a failure to meet cellular
oxygen demands (cellular hypoperfusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

shock oxygen supply and oxygen demand

A

Increased metabolic oxygen demand

Decreased oxygen supply, inadequate tissue perfusion, cellular hypoxia

this triggers compensatory mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

aerobic metabolism

A

Efficient production of ATP
ATP maintains cellular metabolic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

anaerobic metabolism

A

Inefficient production of ATP
Lactic acid is a byproduct of production
– Lactate and ABGs
Leads to metabolic acidosis
Cellular dysfunction leads to cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

oxygen delivery and demand causes

A

oxygen delivery
cardiac output, Hgb, O2 saturation

Oxygen demand
metabolic needs, illness, physiologic stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

initial insult of shock

A

Activation of the sympathetic nervous system, inflammatory response, and the immune system
state of hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

compensatory mechanisms of shock

A

increased HR
increased systemic vascular resistance(SVR)- increase BP
increased preload
increased cardiac contractibility

peds and gero do not compensate well

Oxygen is consumed at a much greater rate than it is delivered.
Derangement of compensatory mechanisms that results in further circulatory and respiratory dysfunction with subsequent multiple organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

late sign of shock

A

hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

All shock states are affected by the components of cardiac output

A

Cardiac output is the product of stroke volume multiplied by the heart rate. Stroke volume is the volume of blood in the ventricles that is ejected with each contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What affects stroke volume?

A

Preload: the volume of venous blood returning to the heart. This represents circulatory volume. Dehydration, blood loss, and vasodilation result in loss of preload. Increased preload can also cause problems such as heart failure or fluid overload.
Afterload: the pressure the heart must overcome in order to pump blood. This is represented by the diastolic blood pressure. Hypertension makes it harder to pump blood and is an example of increased afterload. Decreased afterload can be a result of hypovolemia or vasodilation.
Contractility: the strength of contraction of the cardiac muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Shock is categorized into 4 overlapping stages:

A

Initial
Pre-shock (Nonprogressive or Compensated stage)
Shock (Progressive or Uncompensated stage)
End-Organ Dysfunction (Irreversible or Refractory stage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 stages of shock

A

Stage 1: compensated shock
Stage 2: Decompensated
Stage 3: Irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Stage 1 of shock (nonprogressive)

A

Compensatory mechanisms are effective in maintaining relatively normal vital signs and tissue perfusion. Commonly goes unrecognized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stage 2 of shock (progressive)

A

Compensatory mechanisms begin to fail; metabolic and circulatory derangements become more pronounced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

stage 3 of shock (irreversible)

A

Cellular and tissue injury is so severe that correction of metabolic, circulatory, and inflammatory derangements is difficult or impossible, and cellular hypoxia and death ensue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Assessment Findings of compensated shock

A

OFTEN VERY SUBTLE
Anxiety, confusion, restlessness
Narrowing pulse pressure
- Rising diastolic BP
- Minimal change in systolic BP
Tachycardia with bounding pulse
Decreasing urinary output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In compensated shock, vasoconstriction and nervous system responses are selective and are evidenced by the following:

A

Blood is shunted away from the skin and gut to the heart, brain, and lungs.
The patient may experience subtle changes in mental status including anxiety, confusion, and restlessness.
The pulse rate increases and becomes bounding.
The respiratory rate increases.
Diastolic BP rises, causing a slight narrowing of the pulse pressure (minimal or no changes to the systolic BP).
Urine output decreases due to decreased renal blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does the pulse become bounding in the compensatory stage?

A

The pulse may be bounding due to catecholamine release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

assessment findings for decompensated/hypotensive shock

A

Decreased level of consciousness
Hypotension
Narrowed pulse pressure
Tachycardia with weak pulses
Tachypnea
Cool, clammy, cyanotic skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

assessment findings of irreversible shock

A

Obtunded or comatose
Profound hypotension
Bradycardia
Dysrhythmias
Slow, shallow respirations
Petechiae or purpura
worsening acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

changes with initial stage

A

Usually not clinically apparent
Metabolism changes at cellular level from aerobic to anaerobic
Lactic acid builds up and must be removed by liver
Process requires O2, unavailable due to decreased tissue perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

pre-shock (compensated) cempensatory mechanisms

A

Compensatory mechanisms (neural, hormonal, biochemical)
- attempt to overcome consequences of anaerobic metabolism and maintain homeostasis
BP often normal and helps maintain adequate CO and SVR
The body initiates a “fight-or-flight” response (stimulation of SNS)
- Anxiety and confusion
- Tachycardia
- Peripheral vasoconstriction, Pallor
Impaired GI motility
- Slowed peristalsis
- Risk for paralytic ileus
Cool, clammy skin
- Except septic patient who is warm and flushed
Decreased blood to kidneys activates renin–angiotensin system
- Angiotensin I converted to angiotensin II
– Vasoconstriction
– Increased venous return to heart
– Stimulates release of aldosterone
– Increased sodium reabsorption stimulates ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Shock (Progressive or Uncompensated stage)

A

Begins when compensatory mechanisms fail
Patient moved to ICU for advanced monitoring and treatment
Cardiac output begins to decrease, resulting in a decrease in BP
Common manifestations:
- Hypotension, Tachycardia
- Tachypnea, Dyspnea
- Diaphoresis
- Renal hypoperfusion
- Metabolic acidosis
- Lethargy and/or restlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

uncompensated shock: Myocardial dysfunction results in

A

Dysrhythmias
Myocardial ischemia
Possible myocardial infarction
End result: complete deterioration of cardiovascular system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Movement of fluid from pulmonary vasculature to interstitial space

A

Pulmonary edema
Bronchoconstriction
Decreased functional residual capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

uncompensated
Mucosal barrier of GI system becomes ischemic

A

Ulcers
GI bleeding
Risk of migration of bacteria
Decreased ability to absorb nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Liver fails to metabolize drugs and waste

A

Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding

28
Q

Hypoperfusion leads to renal tubular ischemia

A

May result in acute kidney injury
Worsened by nephrotoxic drugs
Decreased urine output
Elevated BUN and serum creatinine
Metabolic acidosis

29
Q

End-Organ Dysfunction (Irreversible or Refractory stage)

A

Exacerbation of anaerobic metabolism
Accumulation of lactic acid and waste products → Increased capillary permeability
Profound hypotension and hypoxemia
Tachycardia worsens → Heart rate erratic or asystole
Failure of one organ system affects others
Recovery unlikely

30
Q

causes of obstructive shock:

A

compression/obstruction

Cardiac tamponade
Tension pneumothorax

31
Q

cardiogenic shock causes

A

Pump failure

Blunt cardiac injury
Dysrhythmia
Myocardial infarction

32
Q

hypovolemic shock causes

A

Reservoir depletion

Hemorrhage
Hypovolemia

33
Q

distributive shock causes

A

Vasodilation (pipe problem)

Anaphylaxis
Sepsis
Spinal cord injury
(neurogenic shock)

34
Q

What is meant by a pump problem?

A

Cardiac function impaired

35
Q

What is meant by a tank problem?

A

Loss of volume

36
Q

What is meant by a pipe problem?

A

Vasodilation (hypovolemia relative to size of the vasculature)

37
Q

Obstructive shock can be thought of as a mechanical problem with the pump or pipes. The blood in the pericardial sac compresses the heart with a tamponade, a tension pneumothorax compresses the heart and great vessels, a fetus compresses the vena cava.
What do they all have in common?

A

Inadequate tissue perfusion and cellular oxygenation

38
Q

types of shock

A

Hypovolemic
Cardiogenic
Neurogenic
Anaphylactic
Septic

39
Q

hypovolemic shock

A

Inadequate circulating volume
Caused by sudden blood loss or severe
dehydration, burns
Hypotension, electrolyte, and acid–base
disturbances, and organ dysfunction
resulting from hypoperfusion
Failed compensatory mechanisms, which
were initiated to restore cardiac output,
eventually cause the myocardium to fatigue.

40
Q

manifestations of hypovolemic shock

A

Tachypnea
Increase in heart rate, CO
Decrease in stroke volume, CVP, PAWP, urinary output
Anxiety
Patient may compensate for up to 15% loss
Loss of 15-30% results in SNS-mediated response
If loss is greater than 30%, blood volume should be replaced
immediately

41
Q

assessment of hypovolemic shock

A
  • Tachycardia
  • Decreased LOC
  • Rapid and deep respirations, which
    gradually become labored and shallower
    as the patient’s condition deteriorates
  • Hypotension
  • Decreased urine output
  • Cool and clammy skin
42
Q

lab studies for hypovolemic shock

A
  • Lactate
  • ABG
  • CBC
  • Electrolytes
  • H&H
  • Coagulation panels
43
Q

management of hypovolemic shock

A
  • Restore circulating volume with crystalloids first (isotonic preferred over hypotonic)
  • Blood products (can be with only NS)
  • STILL HAVE TO REMEMBER TRANSFUSION REACTIONS
  • Oxygen, monitor VS, Labs, respiratory status, mentation, urine output, GCS with VS
44
Q

cardiogenic shock

A

Loss of critical contractile function of the heart
Extensive left ventricular myocardial
infarction
Assessment findings are similar to HF but are more severe.
Chest pain, hypotension, cool skin, oliguria,
decreased mentation, dyspnea, crackles
Labs: elevated myocardial tissue markers, BNP

45
Q

manifestations of cardiogenic shock

A

 Tachycardia, Hypotension
 Narrowed pulse pressure
 Increased systemic vascular resistance (SVR)
 Increased myocardial O2 consumption
 Tachypnea, pulmonary congestion
 Pallor and cool, clammy skin
 Decreased capillary refill time
 Decreased renal perfusion and urinary output
 Anxiety, confusion, agitation

46
Q

management of cardiogenic shock

A
  • Increase myocardial oxygen delivery, maximize
    cardiac output, decrease left ventricular
    workload.
  • Correct reversible problems.
  • Fluids, diuresis, or nitrates
  • Electrolyte repletion
  • Analgesia, sedatives
  • Monitor for dysrhythmias and hemodynamic
    status.
  • Monitor respiratory status.
47
Q

neurogenic shock

A
  • Loss or disruption of sympathetic tone causes peripheral
    vasodilation and subsequent decreased tissue perfusion.
  • SCI above T6, spinal analgesia, emotional stress, pain,
    drugs, CNS problems
  • Circulating volume is decreased because of venous
    pooling.
  • Characterized by hypotension, bradycardia, and
    hypothermia.
  • Manage with fluids and vasopressors.
48
Q

anaphylactic shock

A
  • Allergic reaction to a specific antigen (food, insect stings, medications) that evokes a life-threatening
    hypersensitivity reaction.
  • Underlying mechanism is decreased venous return
    resulting from displacement of blood volume away from the heart because of enlargement of the vascular compartment and loss of blood vessel tone.
  • Assess for known allergens, obtain a thorough history.
  • Generalized erythema, urticaria, and pruritus, anxiety and restlessness, dyspnea, wheezing, chest tightness, a warm feeling, nausea and vomiting, angioedema, and abdominal pain, laryngeal edema, and severe bronchoconstriction.
49
Q

manifestations of anaphylactic shock

A

Dizziness
Chest pain
Incontinence
Swelling of lips and tongue, angioedema
Flushing, pruritus, urticaria
Anxiety, Confusion, Sense of impending doom
Wheezing, stridor due to laryngeal edema
Respiratory distress and circulatory failure

50
Q

management of anaphylactic shock

A
  • Early recognition
  • Remove offending antigen.
  • Mild symptoms: oxygen, subcutaneous or IV
    diphenhydramine
  • Life threatening: epinephrine (not the same as cardiac arrest/never IV, do IM), fluids, steroids,
    bronchodilators, vasopressors
  • Airway management, VS, and hemodynamic
    status
51
Q

Systemic Inflammatory Response Syndrome (SIRS) - understand only the concept

A
  • May be caused by any type of shock or other insults such as massive blood transfusion, traumatic injury, brain injury, surgery, burns, and pancreatitis and typically precedes septic shock
  • Local inflammatory response becomes a
    systemic response that results in an
    unregulated inflammatory response with
    widespread involvement of endothelial cells
    and a generalized activation of inflammation
    and coagulation.
52
Q

physiologic changes with sepsis

A

Vascular alterations
* Increased capillary permeability
* Microthrombi form throughout microvasculature
Cardiovascular alterations
* Vasodilation, maldistribution of blood flow, and
myocardial depression
Pulmonary alterations
* capillary leak in the pulmonary interstitium, ARDS
Hematologic alterations
* DIC
Metabolic alterations
* severe metabolic dysfunction

53
Q

management and tx for sepsis

A

Screening and Early Treatment
*Severe Sepsis Screening Tool
*SIRS, NEWS, or MEWS score recommended
Fluid Resuscitation
*Early treatment is key
*30 mL/kg IV balanced crystalloid fluid in first 3 hours
Mean arterial pressure
*Target mean arterial pressure (MAP) of 65 mm
Infection
*Administering antimicrobials immediately, ideally within 1 hour of
recognition
Hemodynamics
*Using norepinephrine as the first-line agent over other vasopressors
Ventilation- For adults with sepsis-induced ARDS
*low tidal volume ventilation strategy (6 mL/kg)
*Limit plateau pressures to below 30 cm H2O
*Higher PEEP
*Proning for greater than 12 hours daily

54
Q

multiple organ dysfunction syndrome

A
  • Release of systemic inflammatory mediators
    found in SIRS may play a role in the etiology
    of MODS.
  • Loss of integrity of mucosal barrier function
    may liberate bacterial toxins from the gut
    causing damage to multiple organs.
  • Tissue hypoxia caused by microvascular
    thromboses
  • Hypotension, tachycardia, tachypnea,
    hypothermia, and hyperthermia
55
Q

management of multiple organ dysfunction syndrome

A
  • Prevent nosocomial infections.
  • Treat hemodynamic and metabolic derangements.
  • Supportive measures for organ systems
  • CRRT, low tidal volume ventilation
  • Normalize ScvO2, arterial lactate, base deficit, and
    pH.
56
Q

nursing assessment for MODS

A

ABCs (Airway, Breathing, Circulation)
Focused assessment of tissue
perfusion
 Vital signs
 Peripheral pulses
 Level of consciousness
 Capillary refill
 Skin (e.g., temperature, color,
moisture)
 Urine output
Brief history
 Events leading to shock
 Onset and duration of symptoms
Health history
 Medications
 Allergies
 Vaccinations, recent travel

57
Q

care goals

A

Adequate tissue perfusion
Restoration of normal or baseline BP
Recovery of organ function
Avoiding complications from prolonged states of hypoperfusion
Preventing health care-associated complications

58
Q

management of circulatory system

A
  • Pulse pressure
  • Mean arterial pressure
    Administration of intravenous fluid in shock
  • Limit use
  • Damage control resuscitation
  • Permissive hypotension
  • Hemostatic resuscitation
59
Q

neurologic status

A

 Assess orientation and level of consciousness, every 1 to 2 hours
 Orient to person, place, time, events
 Reduce noise and light levels in ICU
 Keep a day-night cycle

60
Q

cardiovascular status

A

Monitor:
 HR and continuous ECG, BP, CVP, PA pressures, CO, SVR, SVV
 Dysrhythmias
 Heart sounds: murmurs, S3, S4
Give prescribed fluid and drug therapy

61
Q

respiratory status

A

Monitor:
 Respiratory rate, depth, and rhythm; Breath sounds
 Continuous pulse oximetry
 Arterial blood gases
Many patients will be intubated and on mechanical ventilation

62
Q

renal status

A

Urine output, Serum creatinine

63
Q

body temperature and skin changes

A

 Core temperature
 Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection

64
Q

GI status

A

 Auscultate bowel sounds
 NG drainage/stools for occult blood

65
Q

personal hygiene

A

Perform bathing, nursing measures carefully
Turn every 1 to 2 hours
Passive/active range of motion
Oral care
 Apply a water-soluble lubricant to the lips to prevent drying and cracking.
 Brush the patient’s teeth or gums with a soft toothbrush every 12 hours.
 Swab the lips and oral mucosa with a moisturizing solution every 2 to 4 hours.

66
Q

emotional support and interventions

A

Assess level of anxiety, fear, pain
Interventions:
 Drugs as needed
 Address spiritual needs
 Involve caregivers
 Give simple explanations of all procedures
 Privacy
 Call light within reach

67
Q

signs of decreased oxygen to the brain

A

confusion
LOC
agitation

Acute Care Exam 3 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions