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
Q

Pathophysiology of septic shock x4

A

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
Q

Describe 2 phases of septic shock

A

Warm- early, vasodilation, hyperdynamic response
Cold- late, hypodynamic response, decompensated state