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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)

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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

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3
Q

aerobic metabolism

A

Efficient production of ATP
ATP maintains cellular metabolic function

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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

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5
Q

oxygen delivery and demand causes

A

oxygen delivery
cardiac output, Hgb, O2 saturation

Oxygen demand
metabolic needs, illness, physiologic stress

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6
Q

initial insult of shock

A

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

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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

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8
Q

late sign of shock

A

hypotension

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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.

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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.

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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)

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12
Q

3 stages of shock

A

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

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13
Q

Stage 1 of shock (nonprogressive)

A

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

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14
Q

Stage 2 of shock (progressive)

A

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

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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.

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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

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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.

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18
Q

Why does the pulse become bounding in the compensatory stage?

A

The pulse may be bounding due to catecholamine release.

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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

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20
Q

assessment findings of irreversible shock

A

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

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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

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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

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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

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24
Q

uncompensated shock: Myocardial dysfunction results in

A

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

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25
Movement of fluid from pulmonary vasculature to interstitial space
Pulmonary edema Bronchoconstriction Decreased functional residual capacity
26
uncompensated Mucosal barrier of GI system becomes ischemic
Ulcers GI bleeding Risk of migration of bacteria Decreased ability to absorb nutrients
27
Liver fails to metabolize drugs and waste
Jaundice Elevated enzymes Loss of immune function Risk for DIC and significant bleeding
28
Hypoperfusion leads to renal tubular ischemia
May result in acute kidney injury Worsened by nephrotoxic drugs Decreased urine output Elevated BUN and serum creatinine Metabolic acidosis
29
End-Organ Dysfunction (Irreversible or Refractory stage)
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
causes of obstructive shock:
compression/obstruction Cardiac tamponade Tension pneumothorax
31
cardiogenic shock causes
Pump failure Blunt cardiac injury Dysrhythmia Myocardial infarction
32
hypovolemic shock causes
Reservoir depletion Hemorrhage Hypovolemia
33
distributive shock causes
Vasodilation (pipe problem) Anaphylaxis Sepsis Spinal cord injury (neurogenic shock)
34
What is meant by a pump problem?
Cardiac function impaired
35
What is meant by a tank problem?
Loss of volume
36
What is meant by a pipe problem?
Vasodilation (hypovolemia relative to size of the vasculature)
37
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?
Inadequate tissue perfusion and cellular oxygenation
38
types of shock
Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic
39
hypovolemic shock
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
manifestations of hypovolemic shock
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
assessment of hypovolemic shock
* 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
lab studies for hypovolemic shock
* Lactate * ABG * CBC * Electrolytes * H&H * Coagulation panels
43
management of hypovolemic shock
* 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
cardiogenic shock
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
manifestations of cardiogenic shock
 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
management of cardiogenic shock
* 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
neurogenic shock
* 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
anaphylactic shock
* 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
manifestations of anaphylactic shock
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
management of anaphylactic shock
* 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
Systemic Inflammatory Response Syndrome (SIRS) - understand only the concept
* 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
physiologic changes with sepsis
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
management and tx for sepsis
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
multiple organ dysfunction syndrome
* 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
management of multiple organ dysfunction syndrome
* 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
nursing assessment for MODS
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
care goals
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
management of circulatory system
* Pulse pressure * Mean arterial pressure Administration of intravenous fluid in shock * Limit use * Damage control resuscitation * Permissive hypotension * Hemostatic resuscitation
59
neurologic status
 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
cardiovascular status
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
respiratory status
Monitor:  Respiratory rate, depth, and rhythm; Breath sounds  Continuous pulse oximetry  Arterial blood gases Many patients will be intubated and on mechanical ventilation
62
renal status
Urine output, Serum creatinine
63
body temperature and skin changes
 Core temperature  Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
64
GI status
 Auscultate bowel sounds  NG drainage/stools for occult blood
65
personal hygiene
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
emotional support and interventions
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
signs of decreased oxygen to the brain
confusion LOC agitation

Acute Care Exam 3 (4 decks)

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