Week Five Flashcards

1
Q

What is shock?

A
  • A syndrome
  • Characterised by tissue ischemia from decreased perfusion and impaired cellular metabolism
  • Causes imbalance between supply and demand for 02 and nutrients to tissues
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2
Q

What is the pathophysiology of cardiogenic shock (systolic)?

A

Either primary ventricular ischaemia, structural problems or arrhythmias cause systoiloc dysfunction, lowering stroke volume, and decreasing cardiac output. This decreases oxygen supply, lowering tissue perfusion and impaired cellular metabolism.

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3
Q

What is cardiogenic shock?

A

When systolic or diastole dysfunction of the hearts ability to function

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4
Q

What is the pathophysiology of cardiogenic shock (diastolic)?

A
  • When diastolic dysfunction occurs there is ineffective filling causing lowered stroke volume, and decreasing cardiac output.
  • This dysfunction also causes increased pulmonary pressures, resulting in pulmonary oedema and decreased oxygenation.
  • These changes decrease cellular oxygen supply, lowering tissue perfusion and causing impaired cellular metabolism
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5
Q

What is the clinical presentations of cardiogenic shock?

A
  • Tachycardia, decreased BP, decreased capillary refill, chest pain
  • Tachypnoea, crackles, cyanosis, rhonchi
  • Increased Na and h20 retention, decreased renal blood flow, decreased urine output
  • Pallor, cool clammy
  • Decreased cerebral perfusion – anxiety, confusion, agitation
  • Decreased bowel sounds, nausea, vomiting
  • Increased cardiac markers, increased BGL, increased BUN
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6
Q

What is the pathophysiology of hypovolaemic shock?

A

Relative or absolute hypovolaemia causes decreased circulating volume, lowering venous return, then stroke volume. This decreased cardiac output, decreasing cellular oxygen supply and then decreasing tissue perfusion, ultimately causing impaired cellular metabolism.

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7
Q

What is the clinical presentations of hypovolemic shock?

A
  • Decreased preload, decreased stroke volume, decreased capillary refill
  • Tachypnoea causing bradypnoea (late)
  • Decreased urine output
  • Pallor, cool clammy
  • Decreased cerebral perfusion – anxiety, confusion, agitation
  • Absent bowel sounds
  • Decreased haematocrit,
    decreased haemoglobin, decreased lactate
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8
Q

What is the pathophysiology of neurogenic shock?

A
  • Disruption of the sympathetic nervous system causes loss of sympathetic tone, causing a parasympathetic response lowering the heart rate and cardiac output. Loss of sympathetic tone also cause venous and arterial vasodilation, causing decreased venous return, decreasing stroke volume and also lowering cardiac output. This decreased cellular oxygen supply, lowering tissue perfusion and causing impaired cellular metabolism
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9
Q

What is the clinical presentations of neurogenic shock?

A
  • Bradycardia, hypotension
  • Dysfunction related to level of injury
  • Bladder dysfunction
  • Initially warm due to massive dilation, later cool dependent on room temperature
  • Decreased cerebral perfusion – anxiety, confusion, agitation
  • Absent bowel sounds
  • Decreased haematocrit, decreased haemoglobin, increased lactate
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10
Q

What is the pathophysiology of anaphylactic shock?

A
  • Allergens elicit an inflammatory response, with histamine causing vasodilation. This can cause maldistribution of blood, lowering venous return, decreasing cardiac output, then decreasing tissue perfusion, then decreasing BP, and causes LOC.
  • Vasodialation causes increased capillary permeability which causes cell fluid to shift causing oedema, then inflammation, causing decreased oxygen and a LOC.
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11
Q

What is the clinical presentations of anaphylactic shock?

A
  • Chest pain, third spacing of fluid
  • Shortness of breath, oedema of larynx and epiglottis, wheezing, stridor, rhinitis
  • Incontinence
  • Flushing, pruritus, urticaria, angio-oedema
  • Anxiety, feeling of impending doom, confusion, decreased LOC, metallic taste
  • Cramping, abdominal pain, nausea, vomiting, diarrhoea
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12
Q

What is the pathophysiology of septic shock?

A

Invading microorgansims cause damage to endothelial lining, causes release of tumour necrosis factors, interleukin-1 and other proinflammatory cytokines. This causes myocardial depression and cells to increase capillary membrane. This causes maldistribution of circulating blood volume, decreasing cellular oxygen supply, decreasing tissue perfusion and impairing cellular metabolism

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13
Q

What is the pathophysiology of obstructive shock?

A

Structural compression causes decreased venous return, lowering stroke volume, then lowering cardiac output,. This lowers cellular oxygen supply, lowering tissue perfusion and impaired cellular metabolism

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14
Q

What is MDT care for shock?

A
  • Identification of patients at risk
  • Integration of patient history, physical exam and clinical findings
  • Interventions to control or eliminate cause of the decreased perfusion
  • Protection of target and distal organs from dysfunction
  • Provision of multisystem supportive care
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15
Q

What is MDT care for shock?

A
  • Identification of patients at risk
  • Integration of patient history, physical exam and clinical findings
  • Interventions to control or eliminate cause of the decreased perfusion
  • Protection of target and distal organs from dysfunction
  • Provision of multi-system supportive care
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16
Q

What is nursing management for shock?

A
  • Nursing assessment (ABCs)
  • Critical thinking
  • Inter-professional communication
17
Q

What are the stages of shock?

A
  • Initial stage
  • Compensatory stage
  • Progressive stage
  • Irreversible stage
18
Q

What are changes in the respiratory system due to shock?

A
  • Respirations in acute setting should be counted for 1 minute when patient has rested
  • Normal respirations 11- 17 bpm
  • Note increased work of breathing, use of accessory muscles, lung expansion, colour of patient
  • Problems highlight: Need to increased O2, decrease Co2, important role in regulation of acid-base balance; Acidosis or alkalosis; CNS
19
Q

What are changes in heart rate due to shock?

A
  • Should be counted for 1 minute, ideally in radial
  • If deteriorated central pulse may be required
  • Pulse estimations must never be taken from pulse oximeter
  • Tachycardia usually occurs in response to compensatory mechanism
  • Tachycardia is a later sign than changes in respiration and changes may be subtle first
20
Q

What are changes in blood pressure due to shock?

A
  • Track and trigger generally try to identify hypotension
  • Hypotension occurs as a late sign of shock
  • Initial stage: Very little noticeable change, increase in RR
  • Compensatory stage: Slight increased BP, increased diastolic pressure, tachycardia, increased RR, cool peripheries
  • Progressive stage: Hypotension, tachycardia, increased RR, pallor, seating, decreased LOC
  • Refractory stage: Organ dysfunction, death if untreated
21
Q

What are changes in LOC due to shock?

A
  • Progression through AVPU

- If unconscious think of airway

22
Q

What are changes in oxygen saturations due to shock?

A
  • Not simplistic, dependence of amount of oxygen the patient is receiving
  • Factors that affect Sa02
23
Q

How to assess deteriorating patient?

A

Look, listen and feel approach

  • Airway - Look, listen and feel (signs of airway obstruction)
  • Breathing - Look, listen and feel (distress/suppression)
  • Circulation - Look, listen and feel
  • Disability - AVPU
  • Exposure, everything else, escalation
  • Full history
  • Reviewing notes and observations
  • Identifying trends from observation charts
  • Administering medications
  • Review of laboratory results/12 lead ECG recordings
  • Reviewing anything that may impact on the patients condition