Shock Flashcards

1
Q

Definition hypoovolaemic?

A

Shock is a life-threatening circulatory disorder leading to tissue hypoxia and disturbance in microcirculation following massive blood or fluid loss.

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2
Q

RF hypovolaemic?

A
  • Trauma
  • GI bleeding
  • Ruptured AAA
  • Burns/heat stroke
  • Diarrhoea and Vomiting
  • Pancreatitis
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3
Q

Ddx hypovolaemic?

A
  • Diff types of shock
  • Simple hypotension
  • syncope
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4
Q

Epidemiology hypovolaemic?

A

Age: Children
Sex:
Ethnicity:

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5
Q

Aetiology hypovolaemic?

A
  • Haemorrhagic
    • Blunt/penetrating trauma
  • Upper GI bleeding
    • Postpartum haemorrhage
    • Ruptured aneurysm or haematoma
    • AV fistula
  • Non-haemorrhagic
    • GI loss-diarrhoea and vomiting
    • Insensible fluid loss
    • Third space fluid loss-bowel obstruction
    • Renal fluid loss-adrenal insufficiency
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6
Q

CP hypovolaemic?

A
  • Weak pulse ,
  • Tachycardia
  • Tachypnoea
  • Hypotension
  • Cold clammy extremities, slow cap refill
  • Less skin turgor
  • Dry mucous membranes
  • Non-distended jugular veins
  • Underlying disease findings
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7
Q

pathophysiology hypovolaemic?

A

Loss of IV fluid vol-less CVP and so SV and CO so compensatory increase in HR and TPR to compensate for low BP and SV
Low pre load, low cardiac output, high afterload, high systemic vascular resistance, low mixed venous oxygen saturation

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8
Q

Investigations first line-H?

A
  • ABCDE
  • Lactate->2 mmol/L (>18 mg/dL)
  • ABG-Metabolic acidosis: pH <7.35, bicarbonate <22.
  • Glucose->7 mmol/L (>126 mg/dL) is abnormal in a non-diabetic patient.
  • FBC-
    • Hb <100 g/L (<10 g/dL) suggests haemorrhage as the cause; however, may be normal in the early stages due to vasoconstriction.
    • WBC count may be >12 x 10³/microlitre if sepsis is present.
  • U and E-
    • Evidence of renal impairment if kidney perfusion is compromised
    • Urea disproportionately raised with upper gastrointestinal bleeding, dehydration, or cardiac failure.
    • Hyperkalaemia in trauma, acute kidney injury, and diabetic ketoacidosis.
    • Hypokalaemia with diarrhoea or vomiting.
    • Hypernatremia in burns and diarrhoea or vomiting.
    • Hyponatraemia in trauma and also sometimes in diarrhoea and vomiting.
  • Coagulation Studies-prolonged in sepsis, depleted in hypovolaemic
  • C-reactive protein-infection and inflammation
  • ECG-Arrhythmias, right heart strain i PE, hypo/hyper kalaemia
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9
Q

Investigations-H second line?

A

• CXR-pleural effusion, PE
• Urinalysis-DKA or infections
US/FAST-underlying cause-left ventricular failure suggests myocardial infarction; right ventricular strain suggests pulmonary embolism; pericardial effusion suggests cardiac tamponade.

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10
Q

Management AB-H?

A
  • ABCDE
  • Secure airway-manoeuvres, suction, OP and NP airway
  • Support breathing-
    • Oxygen-stats of 94% to 98% or 88-92 if COPD
    • Non Invasive Ventilation (NIV)
    • CPAP if hypoxaemic or have LHF
    • Consider bilevel positive airway pressure (BiPAP) if the patient has hypercapnic (type II) respiratory failure (PaCO2>6 kPa or 45 mmHg and acidotic [pH <7.35 or free hydrogen ion {H+} >45 nanomol/L])
  • Treat underlying cause and escalate if more than one type
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11
Q

Management CDE-H?

A

• Haemorrhagic protocol
Use blood products(red blood cells and fresh frozen plasma [FFP])
1:1 ratio of red blood cells to FFP in trauma and at least a 1:2 ratio in non-trauma patients
• Give platelets if platelets <75 x 10⁹/L (or <100 x 10⁹/L in brain and spine injuries)
• Give cryoprecipitate or fibrinogen concentrate if fibrinogen <1.5 g/L (<150 mg/dL) (<2 g/L [<200 mg/dL] if obstetric)
• Give FFP if prothrombin time and/or activated partial thromboplastin time >1.5 times norma
• Target Hb
• Reverse anticoagulation
• IV tranexamic acid if bleeding
• IV fluids
• Crystalloid-Hartmann’s-bolus of 250-500 mL given over less than 15 minutes -adjust
• Fluid challenges- target MAP of 65mmHg
• Vasodilator(GTN)-
• If the patient has pulmonary oedema and systolic blood pressure >90 mmHg, consider a vasodilator (e.g., glyceryl trinitrate, nesiritide) and ensure the patient is transferred to a critical care environment so that blood pressure can be continuously monitored
• Vasopressors agents
• Via CVC/arterial line
• NA, dopamine, vasopressin, adrenaline
• Increases perfusion and reduces mismatch bt tone and volume

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12
Q

Complications H?

A
  • Volume overload induced pulmonary oedema
  • Organ failure
  • Vasopressor induced gangrene
  • DIC
  • Hospital acquired infections
  • IV fluid/blood product associated infection, reactions, thrombosis
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13
Q

Prognosis H?

A
  • High rate of mortality-depends on cause
  • Sepsis highest
  • Cardiogenic deaths in hospital high
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14
Q

Definition-cardiogenic?

A

Shock is a life-threatening circulatory disorder leading to tissue hypoxia and disturbance in microcirculation following acute heart failure.

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15
Q

RF Cardiogenic?

A
• Age
• MI
• Cardiomyopathy
• Heart valve disease
• Arrhythmias
• Myocarditis
• Drugs
Blunt cardiac trauma
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16
Q

ddx cardiogenic?

A
  • Diff types of shock
  • Simple hypotension
  • Syncope
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17
Q

CP cardiogenic?

A
  • Hypotension
  • Tachycardia
  • Weak pulse
  • Cold clammy extremities
  • Slow cap refill
  • Mental status change
  • Presentations of cardiac dysfunction
  • Pulomnary oedema
  • Elevated JVP
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18
Q

Pathophysiology-Cardiogenic?

A
  • Lack of pulmonary circulation and peripheral perfusion
  • Heart failure leads to drop in CO and blood pressure so the SNS increases catecholamines secretion, leading to VC and increased TPR, and HR.
  • This increases myocardial oxygen demand so more compensatory mechanisms like RAAS increase sodium and water retention and VC but less flow to vital organs ,leading to ischaemia.
  • A lack of oxygen leads to less ATP hence more lactic acid-metabolic acidosis-leads to a lower heart rate
  • High/low preload, low CO, high afterload, high TPR, low mixed venous oxygen saturation
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19
Q

Investigations-first line-Cardiogenic?

A
ABCDE
lactate
ABG
Glucose
FBC
U and E
Coagulation Studies
CRP
ECG
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20
Q

lactate cardiogenic?

A

> 2 mmol/L

21
Q

ABG cardiogenic?

A

Metabolic acidosis: pH <7.35, bicarbonate <22.

22
Q

glucose cardiogenic?

A

> 7 mmol/L (>126 mg/dL) is abnormal in a non-diabetic patient.

23
Q

FBC cardiogenic?

A
  • Hb <100 g/L (<10 g/dL) suggests haemorrhage as the cause; however, may be normal in the early stages due to vasoconstriction.
    • WBC count may be >12 x 10³/microlitre if sepsis is present.
24
Q

U and E cardiogenic?

A

• Evidence of renal impairment if kidney perfusion is compromised
• Urea disproportionately raised with upper gastrointestinal bleeding, dehydration, or cardiac failure.
• Hyperkalaemia in trauma, acute kidney injury, and diabetic ketoacidosis.
• Hypokalaemia with diarrhoea or vomiting.
• Hypernatremia in burns and diarrhoea or vomiting.
Hyponatraemia in trauma and also sometimes in diarrhoea and vomiting

25
Q

coagulation studies cardiogenic?

A

prolonged in sepsis, depleted in hypovolaemic

26
Q

CRP cardiogenic?

A

infection and inflammation

27
Q

ECG cardiogenic?

A

Arrhythmias, right heart strain i PE, hypo/hyper kalaemia

28
Q

investigations second line cardiogenic?

A
  • CXR-aortic dissection
  • Urinalysis-DKA or infections
  • US/FAST-underlying cause
  • CT
  • X ray long bones-femur fractures cause blood loss
29
Q

Management cardiogenic AB?

A
  • ABCDE
  • Secure airway-manoeuvres, suction, OP and NP airway
  • Support breathing-
    • Oxygen-stats of 94% to 98% or 88-92 if COPD
    • Non Invasive Ventilation (NIV)
    • CPAP if hypoxaemic or have LHF
    • Consider bilevel positive airway pressure (BiPAP) if the patient has hypercapnic (type II) respiratory failure (PaCO2>6 kPa or 45 mmHg and acidotic [pH <7.35 or free hydrogen ion {H+} >45 nanomol/L])
  • Treat underlying cause and escalate if more than one type
30
Q

Management cardiogenic CDE?

A
  • IV fluids
    • Crystalloid-Hartmann’s-bolus of 250-500 mL given over less than 15 minutes -adjust
    • Fluid challenges- target MAP of 65mmHg
  • Loop diuretic (furosemide)-
    • if Pulmonary oedema or fluid overload
  • Vasodilator(GTN)-
    • If the patient has pulmonary oedema and systolic blood pressure >90 mmHg, consider a vasodilator (e.g., glyceryl trinitrate, nesiritide) and ensure the patient is transferred to a critical care environment so that blood pressure can be continuously monitored
  • Vasopressors/inotropic agents
    • Via CVC/arterial line
    • NA, dopamine, vasopressin, adrenaline
    • Inotropic agents-dobutamine-low CO-increases perfusion
31
Q

Definition obstructive?

A

Shock is a life-threatening circulatory disorder leading to tissue hypoxia and disturbance in microcirculation following impaired diastolic filling of the right ventricle.

32
Q

ddx obs?

A
  • Diff causes of shock
  • Simple hypotension
  • syncope
33
Q

aetiology

A
• Cardiac tamponade
• Constrictive pericarditis
• Restrictive cardiomyopathy
• Obstruction of venous return
• Tension pneumothorax
• Intrathoracic tumour
• Increased ventricular afterload
• PE
• Aortic dissection
• Aortic stenosis
• Systemic emboli
Pulmonary hypertension
34
Q

CP?

A
  • Weak pulse
  • Tachycardia
  • Hypotension
  • Linked to cause
  • Cold clammy extremities
  • Poor cap refill
  • Elevated JVP and distension of veins
35
Q

Pathophysiology?

A
  • Obstruction of heart or great vessels so the heart cannot circulate blood to less venous return and so SV and CO so HR increases as compensation.
  • Hypoxic vasoconstriction in the lungs-dyspnoea
  • Lack of pulmonary perfusion leading to hypoxaemia
  • High/low preload, low CO, high afterload, high TPR, low mixed venous oxygen saturation
36
Q

Investigations first line -obs-?

A
  • ABCDE
  • Lactate->2 mmol/L (>18 mg/dL)
  • ABG-Metabolic acidosis: pH <7.35, bicarbonate <22.
  • Glucose->7 mmol/L (>126 mg/dL) is abnormal in a non-diabetic patient.
  • FBC-
    • Hb <100 g/L (<10 g/dL) suggests haemorrhage as the cause; however, may be normal in the early stages due to vasoconstriction.
    • WBC count may be >12 x 10³/microlitre if sepsis is present.
  • U and E-
    • Evidence of renal impairment if kidney perfusion is compromised
  • Coagulation Studies-TE formation
  • C-reactive protein-infection and inflammation
  • ECG-Arrhythmias, right heart strain in PE, hypo/hyper kalaemia
37
Q

Investigations second line-obs?

A
  • CXR-PE, pneumothorax, aortic dissection
  • US/FAST-underlying cause-renal or biliary tract obstruction, right ventricular strain suggests pulmonary embolism; pericardial effusion suggests cardiac tamponade, pulmonary oedema and pneumothorax
  • CT-tumours, causes of obstructions
  • Echo-Cardiac tamponade
38
Q

Management AB-obs?

A
  • ABCDE
  • Secure airway-manoeuvres, suction, OP and NP airway
  • Support breathing-
    • Oxygen-stats of 94% to 98% or 88-92 if COPD
    • Non Invasive Ventilation (NIV)
    • CPAP if hypoxaemic or have LHF
    • Consider bilevel positive airway pressure (BiPAP) if the patient has hypercapnic (type II) respiratory failure (PaCO2>6 kPa or 45 mmHg and acidotic [pH <7.35 or free hydrogen ion {H+} >45 nanomol/L])
39
Q

management CDE obs?

A
  • Treat underlying cause and escalate if more than one type
  • IV fluids
    • Crystalloid-Hartmann’s-bolus of 250-500 mL given over less than 15 minutes -adjust
    • Fluid challenges- target MAP of 65mmHg
  • Vasopressors/inotropic agents
    • Via CVC/arterial line
    • NA, dopamine, vasopressin, adrenaline
    • Inotropic agents-dobutamine-low CO-increases perfusion
40
Q

definition-distributive?

A

Shock is a life-threatening circulatory disorder leading to tissue hypoxia and disturbance in microcirculation following redistribution of body fluids-can be septic, anaphylactic and neurogenic.

41
Q

ddx distributive?

A

• Diff types of shock
• Simple hypotension
syncope

42
Q

aetiology dis?

A
  • Septic
    • Infection/bacteraemia
  • Anaphylactic
    • Drug reactions
    • Insect bites/stings
    • Food allergies
  • Neurogenic
    • Spinal cord injury
    • Traumatic brain injury
    • Cerebral haemorrhage
43
Q

CP?

A
  • Septic
    • Flushed dry warm
    • Tachycardia
    • Hypotension
    • Fever
  • Anaphylactic
    • Flushed dry warm
    • Tachycardia
    • Hypotension
    • Itchy skin, hives
    • Bronchospasm
    • Laryngeal oedema
    • Swelling of tongue, uvula
    • Angioedema
  • Neurogenic
    • Spinal cord injury
    • Traumatic brain injury
    • Cerebral haemorrhage
    • Flushed dry warm skin
    • Bradycardia
    • Hypotension
    • Neurological deficits
44
Q

pathophysiology of dis?

A

• Septic-dysregulated response to host infection causing acute inflammation, but capillary leakage and systemic vasodilatation reducing blood pressure and perfusion to organs
• Low preload, high CO, low afterload, TPR low, mixed venous oxygen sats high
• immunologicanaphylaxis(type I hypersensitivity reaction;IgE-mediated) or nonimmunologicanaphylaxis(notIgE-mediated) →degranulationofmast cells→massivehistaminerelease →systemicvasodilationandincreasedcapillaryleakage
• Low preload, high CO, low afterload, TPR low, mixed venous oxygen sats high
• Neurogenic-damage of autonomicpathways →loss ofsympatheticvasculartone→unopposedvagaltone→peripheralvasodilation→pooling of peripheral blood
Low preload, low CO, low afterload, TPR low, mixed venous oxygen sats low

45
Q

Investigations-first line dis?

A
  • ABCDE
  • Lactate->2 mmol/L (>18 mg/dL)
  • ABG-Metabolic acidosis: pH <7.35, bicarbonate <22.
  • Glucose->7 mmol/L (>126 mg/dL) is abnormal in a non-diabetic patient.
  • FBC-
    • Hb <100 g/L (<10 g/dL) suggests haemorrhage as the cause; however, may be normal in the early stages due to vasoconstriction.
    • WBC count may be >12 x 10³/microlitre if sepsis is present.
  • U and E-
    • Evidence of renal impairment if kidney perfusion is compromised
    • Urea disproportionately raised with upper gastrointestinal bleeding, dehydration, or cardiac failure.
    • Hyperkalaemia in trauma, acute kidney injury, and diabetic ketoacidosis.
    • Hypokalaemia with diarrhoea or vomiting.
    • Hypernatremia in burns and diarrhoea or vomiting.
    • Hyponatraemia in trauma and also sometimes in diarrhoea and vomiting.
  • Coagulation Studies-prolonged in sepsis, depleted in hypovolaemic
  • C-reactive protein-infection and inflammation
  • ECG-Arrhythmias, right heart strain i PE, hypo/hyperkalaemia
  • Pulmonary artery catheterisation
46
Q

Investigations-second line-dis?

A

• CXR-pleural effusion, PE
• Urinalysis-DKA or infections
• US/FAST-underlying cause-left ventricular failure suggests myocardial infarction; right ventricular strain suggests pulmonary embolism; pericardial effusion suggests cardiac tamponade.
• CT-ruptures or neurological deficits
X ray bones/spine-infection and neurological deficits

47
Q

management AB-dis?

A
  • ABCDE
  • Secure airway-manoeuvres, suction, OP and NP airway
  • Support breathing-
    • Oxygen-stats of 94% to 98% or 88-92 if COPD
    • Non Invasive Ventilation (NIV)
    • CPAP if hypoxaemic or have LHF
    • Consider bilevel positive airway pressure (BiPAP) if the patient has hypercapnic (type II) respiratory failure (PaCO2>6 kPa or 45 mmHg and acidotic [pH <7.35 or free hydrogen ion {H+} >45 nanomol/L])
48
Q

management of underlying cause dis?

A
  • S-Sepsis 6 (oxygen, cultures, IV antibiotics, fluids lactate and urine) and Broad spectrum antibiotics and surgery
    • A-adrenaline Antihistamines and glucocorticoids
    • N-atropine or pacing for bradycardia and vasopressors
49
Q

Management of CDE dis?

A
  • IV fluids
    • Crystalloid-Hartmann’s-bolus of 250-500 mL given over less than 15 minutes -adjust
    • Fluid challenges- target MAP of 65mmHg
  • Vasopressors/inotropic agents
    • Via CVC/arterial line
    • NA, dopamine, vasopressin, adrenaline
    • Inotropic agents-dobutamine-low CO-increases perfusion