General Medicine Lecture- Shock

Front 1

What is the definition of shock?

Back 1

Hemodynamic and metabolic abnormalities
Systemic hypoperfusion
-Decreased or uneven blood flow
-Poor tissue perfusion
-Decreased oxygen delivery

Front 2

What is the ultimate result of shock?

Back 2

Decreased cellular energy for metabolism
Decreased ATP production

Front 3

What are 2 reasons that the circulatory system is extremely important?

Back 3

1) Delivery of raw materials to all tissues
2) Waste removal

Front 4

What 4 things is required for adequate circulation?

Back 4

1) Blood maintained in the fluid state
2) Appropriate regulation of fluid balance and oncotic pressure
3) Normal patent blood vessels and appropriate vascular tone, which can be regulated at the tissue level
4) A functional pump

Front 5

What are the 3 sequelae to hypovolemia?

Back 5

1) Decreased CO==> Decreased GFR
2) Increased osmolality
3) Loss of baroreceptor stretch

Front 6

What is the sequel to decreased GFR?

Back 6

Activation of renin-angiotensin system

Front 7

What happens when there's an increase in the osmolality?

Back 7

Signals hypothalamus

Front 8

What are the sequelae to activation of the renin-angiotensin system?

Back 8

-ADH & aldosterone release-->
Kidneys increase sodium and water retention --> increased blood volume and CO

Front 9

What happens when an increased osmolality signals the hypothalamus?

Back 9

Get ACTH release that goes to the adrenal glands and causes release of aldosterone (increase water and Na retention) , cortisol (gluconeogenesis and protein synthesis) and epinephrine and norepinephrine (vasoconstriction)

Front 10

What are the 5 intracellular affects of shock?

Back 10

1) Cell injury
2) Loss of osmotic gradients--> cell swelling
3) Increased intracellular calcium triggers arachidonic acid breakdown
4) Production of inflammatory mediators
5) Free radical damage, reperfusion injury

Front 11

What are 4 ways that cell injury occurs during shock?

Back 11

1) oxygen deprivation
2) anaerobic metabolism
3) Increased lactate
4) Decrease in pH (bc of lactic acid build up)

Front 12

What are the 5 types of shock?

Back 12

1) Hypovolemic shock
2) Cardiogenic shock
3) Distributive shock (vasodilatory shock)
4) Metabolic shock
5) Hypoxemic shock

Front 13

True or false. Shock can usually be traced back to one type.

Back 13

False, usually more than one type simultaneously

Front 14

What is the most common type of shock?

Back 14

Hypovolemic shock

Front 15

What is hypovolemic shock?

Back 15

Life-threatening decrease in blood volume

Front 16

What are 4 causes of hypovolemic shock?

Back 16

1) Hemorrhage: trauma, coagulopathy
2) Severe dehydration
3) Severe burns
4) Third space loss

Front 17

What are the 6 sequelae to hypovolemic shock?

Back 17

1) Inadequate delivery of oxygen and nutrients
2) Accumulation of by-products of cellular metabolism (insufficient circulating blood volume)
3) Heart has decreased fluid to pump to body
4) Tachycardia
5) Decreased ventricular filling
6) Increased myocardial oxygen demand (diastolic impairment)

Front 18

What are 3 ways the body tries to compensate for hypovolemic shock?

Back 18

1) Generalized vasoconstriction
2) Tachycardia
3) Fluid retention

Front 19

What are 4 clinical signs of hypovolemic shock?

Back 19

1) Pale mucous membranes
2) Increased capillary refill time (CRT)
3) Cold extremities
4) Decreased body temperature

Front 20

What is cardiogenic shock?

Back 20

Mainly failure of forward blood flow

Front 21

What are 4 ways that cardiogenic shock can develop?

Back 21

1) Systolic/forward flow failure
2) Diastolic failure
3) Obstruction of blood flow
4) Myocardial pump failure

Front 22

What are 2 abnormalities that can result in systolic/forward flow failure, resulting in cardiogenic shock?

Back 22

1) Overt failure of contractility
2) Severe tachyarrhythmias

Front 23

What causes diastolic failure, resulting in cardiogenic shock?

Back 23

Primary cardiac disease
-Hypertrophic cardiomyopathy
-Restrictive cardiomyopathy

Front 24

What are 5 causes of obstruction of blood flow that results in cardiogenic shock?

Back 24

1) Congestive heart failure
2) Cardiac arrhythmia
3) Cardiac tamponade
4) GDV (3rd space loss--> hypovolemia)
5) Drug overdose (anesthetics, beta blockers, calcium channel blockers)

Front 25

What are 6 clinical signs of congestive heart failure?

Back 25

1) Respiratory distress
2) Collapse
3) Exercise intolerance
4) Pulmonary edema
5) Jugular distension
6) Cyanotic mucous membranes

Front 26

How does the body attempt to compensate for cardiogenic shock?

Back 26

Sympathetic nervous system and renin angiotensin-aldosterone system
-Increased HR, retain fluid
-Too much volume to pump
-Results in hypoperfusion

Front 27

What is distributive shock?

Back 27

AKA vasodilatory shock
Decreased systemic vascular resistance (SVR)
Inappropriate vasodilation

Front 28

What are 6 causes of distributive shock?

Back 28

1) Septic shock*
2) Systemic inflammatory response syndrome
3) Adverse drug reactions or overdose
4) Anaphylaxis
5) Heat stroke
6) Neurogenic shock

Front 29

What is the definition of anaphylaxis?

Back 29

-Generalized IgE mediated hypersensitivity response
-Generalized systemic vasodilation and increased vascular permeability

Front 30

What is the neurogenic cause of distributive shock? What causes it?

Back 30

Loss of vascular tone and get peripheral pooling
-Anesthesia, spinal cord injury

Front 31

What will you find on physical exam during the early stages of distributive shock?

Back 31

Warm well-perfused extremities

Front 32

What cell is primarily involved with anaphylaxis?

Back 32

Eosinophils -release hundreds of granules simultaneously

Front 33

Describe the mortality rate of animals with septic shock.

Back 33

Extremely high mortality rate, complex pathogenesis

Front 34

What are the 5 components of septic shock syndrome?

Back 34

1) systemic vasodilation
2) Diminished myocardial contractility
3) Widespread endothelial injury and activation
4) Activation of coagulation and DIC
5) Multiorgan failure

Front 35

The success of septic shock depends on what 2 things?

Back 35

Early recognition and treatment

Front 36

What are 2 causes septic shock?

Back 36

1) Gram negative species!!!!
-Lipopolysaccharides
2) Staphylococcal antigens
-Polyclonal T cell activation
-Can also trigger septic shock

Front 37

What is the mechanism of action of septic shock?

Back 37

Expression of certain proteins leads to binding of coagulation factors to the surface of bacteria
-Contact system is activated as a result of assembly on bacterial surface ---> formation of BRADYKININ
-Bacterial proteinases can also generate related kinins that produce hypotension and increased vascular permeability

Front 38

What are the 4 effects of bradykinin?

Back 38

1) Profound, refractory hypotension
-via beta2 receptors
2) Pain
-Via beta1 receptors
-induced by damage/trauma
3) Natriuresis
4) Fever

Front 39

What is metabolic shock?

Back 39

Altered cellular metabolism
decreased cellular energy production

Front 40

What are 3 causes of decreased cellular energy production, resulting in metabolic shock?

Back 40

1) Cyanide and bromethalin toxicity
-Direct interference w/ mitochondrial function / ATP production
2) Severe hypoglycemia
3) Severe pH derangements

Front 41

What is hypoxemic shock?

Back 41

Decreased blood oxygen content
-despite normal blood volume and BP, can display cardinal signs of shock

Front 42

What are 5 causes of hypoxemic shock?

Back 42

1) Anemia
2) Methemoglobinemia
3) Carbon monoxide poisoning
4) Hypoventilation
5) Pulmonary parenchymal disease

Front 43

What are the 3 clinical stages of shock?

Back 43

1) Compensated stage
2) Early decompensated stage
3) Late decompensated/ irreversible stage

Front 44

What is the normal physiologic response to shock (3)?

Back 44

1) Increase sympathetic tone
2) Vasoconstriction
3) Increased HR & RR

Front 45

What 3 things does the compensated stage of shock include?

Back 45

1) Baroreceptor mediated release of catecholamines
-Systemic vascular resistance
2) Kidneys conserve water and Na
3) Requires energy

Front 46

True or false. The signs present during the compensated stage of shock are often overlooked.

Back 46

True

Front 47

What are the 4 clinical signs of the compensated stage of shock?

Back 47

1) increased HR & RR
2) Injected mucous membranes
3) CRT <1 sec
4) Normal BP, pulse

Front 48

What is the treatment for the compensated stage of shock?

Back 48

Provide adequate fluid volume

Front 49

The compensated stage is seen as the "_______" phase.

Back 49

Hyperdynamic phase

Front 50

During what clinical stage of shock is there redistribution of blood flow to preferred organs such as the heart and brain?

Back 50

Early decompensated stage

Front 51

Widespread ______and to other organs occurs during the early decompensated stage.

Back 51

Tissue hypoxia

Front 52

Why does acidosis develop during the early decompensated stage of shock?

Back 52

Aerobic respiration----> anaerobic glycolysis ----> lactic acidosis

Front 53

What are the sequelae to acidosis developing during the early decompensated stage of shock?

Back 53

Acidosis blunts the vasomotor response---> arteriolar dilation, pooling of blood ---> further decrease in CO

Front 54

Why does DIC develop during the early decompensated stage of shock?

Back 54

Persistent blood pooling injures endothelial cells, exposing collagen and causing clot formation --> DIC

Front 55

Why does the early decompensated stage of shock cause a decrease in urine output?

Back 55

Because organ failure begins

Front 56

What are the 6 clinical signs that allow doctors to diagnose the early decompensated stage of shock?

Back 56

1) Increased HR & RR
2) Pale MM
3) Prolonged CRT
4) Decreased BP & pulse quality
5) Decrease temp, mentation
6) Increased lactate

Front 57

What is the treatment for an animal in the early decompensated stage of shock?

Back 57

Aggressive fluid therapy
-Cats may not have tachycardia in this stage

Front 58

What is the "autoregulatory escape" phenomenon that occurs during the late decompensated stage of shock?

Back 58

-Prolonged tissue hypoxia results in overriding of vasoconstriction and massive vasodilation occurs in all organs (including heart & brain)
-Chronotropic and ionotropic effects lost, brain non-responsive to sympathetic stimulation
-Complete circulatory collapse

Front 59

What is the prognosis of an animal in the late decompensated stage of shock? Why?

Back 59

Poor, because at this point can get reperfusion injury

Front 60

When does the late decompensated stage of shock begin?

Back 60

When have hypoxia for 8-10 minutes

Front 61

What type of shock usually occurs during the late decompensated stage of shock?

Back 61

Often culmination of all categories of shock
-e.g. ischemia of bowel allows superimposition of endotoxic/ septic shock
-Renal shutdown due to acute tubular necrosis

Front 62

What are the 10 clinical signs of the late decompensated stage of shock?

Back 62

1) Low HR
2) Low CO
3) Severe hypotension
4) Pale/ cyanotic mm
5) Absent CRT
6) Cardiopulmonary arrest imminent
7) Weak/absent pulses
8) Low temp
9) No urine roduction
10) Stupor/coma

Front 63

What is the main goal of shock treatment?

Back 63

Restore PERFUSION

Front 64

In order to determine a treatment plan, what type of shock should you try to differentiate from the others?

Back 64

Cardiogenic- treatment is different

Front 65

What are the 6 components of differentiating cardiogenic shock?

Back 65

1) FLUIDS
2) Murmur
3) Jugular pulses
4) Ascites
5) Echo
6) History

Front 66

What are the 4 components for the treatment of cardiogenic shock?

Back 66

1) Address perfusion
2) Identify/address underlying problem
3) Interrupt harmful processes
-Inflammation, endotoxemia
4) Organ support

Front 67

What are the 6 components of treating non-cardiogenic shock?

Back 67

1) Volume resuscitation/ fluid therapy
-Electrolyte deficits
2) Cardiovascular support
-Dobutamine
-Dopamine
-Antiarrhythmic therapy
3) Analgesia
4) Antibiotics
5) Prevention of DIC
6) Monitoring

Front 68

What type of fluids should be initially used for treatment of non-cardiogenic shock?

Back 68

Crystalloids w/ colloids or hypertonic saline for rapid intravascular expansion
-Support the vascular space at the expense of the interstitium
-Hetastarch
-Dextran
-3%, 5%, 5% NaCl

Front 69

What type of fluids should be used for the ongoing treatment of non-cardiogenic shock?

Back 69

Crystalloids +/- continued colloids

Front 70

Why should sympathomimetics and positive inotropes be given for cardiovascular support for patients in shock?

Back 70

-Maintain/ increase CO (oxygen demands must be considered)
-Restore vascular tone (this may be one of the most difficult goals)

Front 71

When should antiarrhythmics be given to patients in shock?

Back 71

Only if the arrhythmia is contributing to hypoperfusion or is inherently life-threatening
-Arrhythmias are usually secondary phenomena

Front 72

Why is it important to provide analgesia to patients in shock?

Back 72

Pain may feed back positively on inflammatory cascades
-May contribute a "neurogenic" component
-Improves ability to monitor

Front 73

When should antibiotics be administered to a patient in shock?

Back 73

Patients in septic or toxic shock

Front 74

What are some indications for antibiotics in forms of shock other than septic or toxic shock?

Back 74

-Visceral hypoperfusion --> compromised GI mucosal barrier ---> bacterial translocation
-Visceral hypoperfusion --> compromised reticuloendothelial system---> reduced bacterial removal from blood stream