Shock Flashcards

1
Q

Describe the 4 stages of shock

A
  1. Initial- tissues under perfused, increased metabolic rate and lactic acid accumulation
  2. Compensatory - Sympathetic NS activated
  3. Progressive - failing compensatory mechanisms, metabolic acidosis due to ischemia and lactic acid production
  4. Refractory - cellular necrosis and multiple organ dysfunction syndrome
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2
Q

Pathophysiology of shock x4

A
  1. Decreased myocardial contractility
  2. Systemic lactic acidosis
  3. Decreased vascular tone
  4. Decreased BP, preload and CO
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3
Q

External fluid loss causes of hypovolemic shock x5

A

External fluid loss:
Hemorrhage
Dehydration- Vomiting, diarrhea, burns, massive diuresis

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4
Q

Internal fluid loss causes of hypovolemic shock x3

A

Loss of vascular integrity
Increased capillary membrane permeability
Decreased colloidal osmotic pressure

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5
Q

Hypovolemic shock therapy x5

A

ABC
Stop obvious bleeding
Insert IV lines and take GXM
Give rapid bolus and reassess
Investigations vs surgery

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6
Q

Signs of cardiogenic shock x6

A

Raised JVP
Cold skin
Tachycardia
Engorged liver
Peripheral edema
Added heart sounds S3(V gallop) S4(A gallop)

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7
Q

Causes of cardiac shock x5

A

Acute myocardial infarction
Severe arrhythmias
Severe valve disease
Tension pneumothorax
Tamponade (obstructive too)

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8
Q

Mechanical complications of myocardial infarction that cause CG shock x3

A

Papillary muscle rupture
Ventricular aneurysm
Ventricular septal rupture

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9
Q

Decreased how CG shock can cause pulmonary edema x5

A

Decreased CO> increased LV filling pressure(preload) > increased LA filling pressure> increased capillary pressure> interstitial and intra alveolar edema

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10
Q

Interpretation of MAP- mean arterial pressure x2

A

<70mmHg = compromised coronary perfusion
<60mmHg = compromised renal perfusion

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11
Q

Signs of tension pneumothorax x5

A

Raised JVP
Tracheal deviation
Reduced chest expansion
Hyperresonant percussion
Diminished breath sounds

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12
Q

Treatment aim for CG shock x4

A

Treat reversible causes
Increase myocardial O2 delivery
Maximizing CO
Decreased LV workload

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13
Q

How to reduce myocardial damage during myocardial infarction x5

A

Vasoactive drugs- dopamine
Inotropic agents
Cautious administration of fluids
Intra aortic balloon pump
Transplantation
Short acting B blockers- reduced contractility of heart hence less o2 needed

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14
Q

Function of dobutamine x2

A

B1 receptor agonist - promotes cardiac stimulation
Mild B2 effects- vasodilation

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15
Q

Characteristics of distributive shock x2

A

Leaky blood vessels due to infection
Vasodilation > reduced vascular resistance

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16
Q

Describe how distributive shock results in decreased tissue perfusion

A

Vasodilation > decreased vascular resistance > blood moving too fast > less time to unload oxygen
OR
Decreased bp > less pressure to push out blood from vessels to tissues

17
Q

Causes of distributive shock x3

A

Septic shock
Anaphylactic shock
Neurogenic shock

18
Q

Anaphylactic response x5

A

Vasodilation, increased capillary permeability
Bronchoconstriction, increased mucus production
Increased inflammatory mediators
Recruitment to sites of antigen interaction

19
Q

Management of anaphylactic shock x5

A

Airway support
Epinephrine IV
Antihistamines
Corticosteroids
Positive inotropes
Vasopressors

20
Q

Pathophysiology of neurogenic shock x5

A

Disruption in sympathetic nervous system
Decreased sympathetic tone
Arterial and venous vasodilation
Decreased venous return, SV, CO
Impaired tissue perfusion and cellular metabolism

21
Q

Goals of therapy in neurogenic shock x2

A

Treat and prevent CVS instability
Promote optimal tissue perfusion

22
Q

Define septic shock

A

A life threatening organ dysfunction caused by dysregulated host response to an infection

23
Q

3 Risk factors for sepsis

A

Reduced immunity
Extremes of age limiting communication
Recent surgery, invasive procedure, pregnancy or miscarriage

24
Q

Conditions which increase risk of sepsis x5

A

Diabetes
HIV/AIDS
Liver cirrhosis
SCD, Splenectomy
Autoimmune diseases

25
Pathophysiology of septic shock x4
1.Vasodilation and increased capillary permeability 2.Endotoxins release inflammatory mediators 3.Cell walls of organisms release endotoxins 4. Initiated by gram neg and gram positive
26
Describe 2 phases of septic shock
Warm- early, vasodilation, hyperdynamic response Cold- late, hypodynamic response, decompensated state
27