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Eq ACVS Phase 1 > Ch.1 Shock: Pathophysiology, Diagnosis, Treatment and Physiologic Response to Trauma > Flashcards

Ch.1 Shock: Pathophysiology, Diagnosis, Treatment and Physiologic Response to Trauma Flashcards

1
Q

Major factors affecting blood flow

A

1 - Circulating volume
2 - Cardiac pump function
3 - Vasomotor tone/peripheral resistance.

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2
Q

Stroke volume is the result of?

A

1 - Ventricular preload
2 - Myocardial contractility
3 - Ventricular afterload.

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3
Q

Myocardial contractility is defined as

A

The rate of cross-bridge cycling between actin and myosin filaments within cardiomyocytes.

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4
Q

Causes of decreased preload

A

1 - Hypovolemia
2 - Decreased ventricular filling time
3 - Impaired ventricular relaxation
4 - Decrease in vasomotor tone
5 - Vasodilation

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5
Q

Clinically how is myocardial contractility assessed?

A

Echocardiographic measures of global systolic function
like left ventricular ejection fraction
and fraction shortening

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6
Q

The fundamentals of treatment of shock

A

Restoration and maintenance of CO through
1- Manipulation of preload
2 - After load
3 - Myocardial contractility
4 - Heart rate

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7
Q

Ventricular after load is directly affected by what?

A

Vasomotor tone or peripheral vascular resistance

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8
Q

What is the outcome of hypertension on ventricular after load

A

Afterload rises with a resultant fall in CO and tissue perfusion

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9
Q

The three classifications of shock

A

1 - Hypovolemic
2 - Cardiogenic
3 - Distributive

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10
Q

Define cariogenic shock

A

Cardiac m cannot pump out adequate SV to maintain perfusion

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11
Q

Define distributive shock

A

Vasomotor tone is lost resulting in decrease in BP and venous return

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12
Q

Common causes of distributive shock

A

1 - Neurogenic shock
2 - Septic shock
3 - Anaphylactic shock

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13
Q

What is relative hypoxia or dysoxia

A

Increased metabolic demand resulting in relative tissue deficits or
Oxygen uptake is impaired because of mitochondrial failure

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14
Q

What is the mechanism of obstructive shock?

A

Obstruction of ventilation or of CO

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15
Q

Examples of obstructive shock

A

1 - Pneumothorax
2 - Pericardial tamponade
3 - Diaphragmatic hernia
4 - Severe abdominal distension causing vena cava obstruction

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16
Q

Autonomic traffic

A

Interplay btw parasympathetic and sympathetic nervous system

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17
Q

How do the baroreceptors in the carotid sinus, aortic arch and right atrium respond to a fall in pressure within the vessels

A

Decrease inhibition of sympathetic tone
while increasing inhibition of vagal activity
and decreasing the release of atrial natriuretic peptide (ANP) by cardiac myocytes.
Resulting in vasoconstriction and an increase in peripheral resistance and BP

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18
Q

What occurs in hyperdynamic stage of shock

A

Tachycardia
Increased SV
Shortened CRT

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19
Q

What does renin stimulate the production of

A

Angiotensin I (Converts to angiotensin ii - acts directly on blood vessels causing contraction - vasoconstriction)

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20
Q

What results from a decrease in renal perfusion

A

Secretion of renin - stimulates production of angiotensin I which converts to angiotensin II
This increases sympathetic tone on peripheral vasculature and promotes aldosterone release

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21
Q

Effect of aldosterone on BP

A

Restores circulating volume by increasing renal tubular sodium and water reabsorption

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22
Q

How does AVP (ADH) act to augment low BP

A

Potent vasoconstrictor
Stimulates increased water reabsorption in the renal collecting tubules

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23
Q

What is seen clinically in decompensated shock

A

1 - Tachycardia
2 - Tachypnea
3 - Poor peripheral pulses
4 - Cool extremities
5 - Mild anxiety
6 - Sweating

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24
Q

What occurs at a cellular level during decompensated shock

A

Decreased oxygen delivery and accumulation of waste products results in loss of critical energy-dependent functions
ie enzymatic activities, membrane pumps and mitochondrial activity leading to cell swelling and release of intracellular calcium stores.

Cytotoxic lipids, enzymes and ROS released from damaged cells further damage cells, triggering inflammation

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25
Q

Exposure of sub endothelial tissue factor activates what?

A

Coagulation and complement cascades

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26
Q

What are the end results of decompensated shock

A

Pooling of blood in peripheral tissue beds
Decrease in in BP
Decrease in venous return
Decrease in CO
Decrease in perfusion
Resulting in organ failure

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27
Q

Class 1 shock

A

Blood loss of <15% total blood volume

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28
Q

Class 2 shock

A

Blood loss of 15-30% - is the inset of hyper dynamic shock
Clinical signs - tachycardia, tachypnea, increased CO and peripheral resistance, anxiety, sweating.
Increased lactate and high anion gap

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29
Q

Class 3 shock

A

Hypodynamic shock
Profound tachycardia, tachypnea, anxiety, prolonged CRT, decreased urine output, cold extremities, lactic acidosis
Hypotensive

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30
Q

Class 4 uncompensated shock

A

Bradycardai
Obtundation
Anuria
Profound hypotension
Circulatory collapse
Death

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31
Q

Define delivery of oxygen (DO2)

A

DO2 = CO X CAO2
(CAO2 = content of oxygen in the arterial blood)
(CO = amount of blood perfusing the tissue)

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32
Q

The amount of oxygen per volume of blood is determined by

A

The amount of haemoglobin or red cell mass and the saturation of that Hamoglobin

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33
Q

What is the first vital step to restoring oxygen delivery in shock?

A

Fluid therapy

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34
Q

The ideal fluid should produce what?

A

A predictable and lasting increase in intravascular volume
with an electrolyte composition as close as possible to that of extracellular fluid
being metabolised and excreted without any accumulation in the tissues
without producing adverse metabolic or systemic effects
and remain cost effective

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35
Q

What % of rapidly infused crystalloids will diffuse out of the vascular space into the interstitial and intercellular space

A

80%

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36
Q

Why are crystalloids alone not suitable for total volume loss replacement

A

80% will diffuse out, therefore will need to use 4-5 times the vol of fluid lost
results in excess total body water
extreme excess of sodium and chloride
Cellular swelling can occur triggering/potentiating inflammatory responses

Large vol infusions can cause
1 - abdominal compartment syndrome,
2 - acute respiratory distress syndrome,
3 - congestive heart failure,
4 - dilution coagulopathy

37
Q

“A balanced fluid therapy approach of administering crystalloids for hypovolemic shock is currently recommended” - how should this be delivered?

A

Initially a rapid 20ml/kg(10L fro 500kg) bolus over 30-60mins - assessing cardiovascular system regularly

38
Q

BES (Balanced electrolyte solutions) are designed to be what sort of fluids in equine medicine

A

Replacement fluids not maintenance fluids.

39
Q

Most common concentration used of hypertonic saline solution

A

7.2%

40
Q

What is the tonicity of HSS compared to plasma?

A

HSS has 8 times the tonicity of plasma

41
Q

in IV infusion of HSS will expand the intravascular space by how much

A

Approximately twice the volume infused

42
Q

Where does HSS principally pull volume from?

A

Intracellular space

43
Q

Effect of HSS on neutrophils

A

Blunts neutrophil activation and may alter balance btw inflammatory and antiiflammatory cytokine responses

44
Q

Recommended dose of HSS?

A

2-4ml/kg or 1-2L for a 500kg horse

45
Q

How do colloids work?

A

Retained within the vascular space, exert oncotic pressure that helps draw water in

46
Q

Normal equine plasma has a colloid oncotic pressure of?

A

20mmHg

47
Q

What is the oncotic pressure of HES (Hydroxyethyl Starch)?

A

30mmHg

48
Q

Benefits of colloids over HSS?

A

Prolonged action

49
Q

Advantages of natural colloids

A

Provide protein such as albumin, antibodies, clotting factors, antithrombin 3

50
Q

Cons of natural colloids such as plasma

A

Hypersensitivity rxns in up to 10% of horses
Also need to defrost so not good in emergency

51
Q

HES products should be used cautiously in what patients

A

Preexisting renal disease

52
Q

What dose of HES is recommended

A

10ml/kg

53
Q

What % and kDa HES is currently used

A

6% HES,130kDa/0.4:tetrastarch

Higher molecular weight has been associated with coagulopathies in human med

54
Q

A 10ml/kg dose of HES has been shown to increase oncotic pressures for how long?

A

120hours

55
Q

At what dose of HES has evidence of spontaneous bleeding been reported

A

20-40ml/kg

56
Q

Why is whole blood indicate in severe cases of hypovolemia

A

Provide oxygen carrying capacity
Colloid oncotic support
Platelets
Coagulation factors

57
Q

What is the circulating blood volume in an adult horse?

A

7-9% of body weight (35-45L in a 500kg horse)

58
Q

When will clinical signs of blood loss be seen?

A

After the loss of 15% of circulating blood volume or (approx 6L during an acute bleed)

59
Q

What does Dobutamine act on?

A

Strong Beta 1 adrenoreceptor agonist
Weaker Beta2 and Alpha adrenoreceptor affinity

60
Q

Primary use of dobutamine?

A

Deliver oxygen to tissues via its positive inotropic activity

61
Q

Dose of dobutamine

A

1-5ug/kg/min

62
Q

What does norepinephrine act on?

A

Strong B1 and Alpha adrenergic affinity resulting in vasoconstriction and increased cardiac contractility

63
Q

What does CVP asses

A

Cardiac function
Blood volume
Vascular resistance

64
Q

Holding off the jugular vein should result in visible filing within how long

A

5 seconds

65
Q

What is the normal CVP in a standing horse

A

7-12mmHg

66
Q

How is CVP measured in a standing horse

A

Catheter in cranial vena cava/right atrium
If measured in jugular vein with standard ivc will get false elevated CVP but can be used to track changes

67
Q

What is normal urine output

A

1ml/kg/hr

68
Q

Fluid therapy to prevent renal ischemia is indicated when urine output is how much?

A

0.5ml/kg/hr

69
Q

Arterial blood pressure is a reflection of?

A

CO and total vascular resistance

70
Q

Because of the compensatory increase in peripheral resistance, blood pressure does not consistently fall until blood volume has decreased by what %

A

30% or more

71
Q

A MAP of what is necessary to maintain adequate perfusion of the brain

A

65mmHg

72
Q

Normal MAPs in healthy awake horses using indirect coccygeal artery are..

A

105-135mmHg

73
Q

Aerobic metabolism of glucose results in

A

36 moles of ATP per molecule of glucose

74
Q

Anaerobic metabolism of glucose results in

A

2 moles of ATP per molecule of glucose
and L-lactate

75
Q

Type B hyperlactatemia can occur as a result of

A

hepatic dysfunction, pyruvate dehydrogenase inhibition, catecholamine surges, sepsis or SIRS

76
Q

Oxygen extraction is determined by

A

The difference btw the oxygen saturation of arterial blood (SaO2) and oxygen saturation of venous blood (SvO2)

O2ER = (SaO2-SvO2)/SaO2
Can be determined by measuring central venous saturation and arterial oxygen saturation

77
Q

In a healthy horse the O2ER ranges from

A

20-30%

78
Q

The O2ER can be useful in evaluating what

A

Response to resuscitative strategies

79
Q

In low-perfusion states PvO2 will increase or decrease?

A

Decrease

80
Q

Mixed venous blood is obtained from where to asses mixed PvO2

A

Catheterise the pulmonary artery

81
Q

Normal PjvO2 (Jugular venous pressure of oxygen)

A

40-50mmHg

82
Q

Normal SjvO2 (Jugular venous oxygen saturation)

A

65-75%

83
Q

Increased venous partial pressure of oxygen in the presence of significant perfusion or supply deficits can signify what

A

Impaired oxygen consumption caused by mitochondrial or cellular dysfunction

  • recognised in septic shock or after cardiopulmonary resuscitation
84
Q

What is the gold standard for CO monitoring?

A

Pulmonary thermodilution method which requires catheterisation of the pulmonary artery

85
Q

What techniques are used to monitor CO in equine medicine

A

1 - Lithium dilution - lithium injected into venous system - lithium concentration-time curve which is used to calculate CO

Repeated sampling can lead to lithium toxicity

2 - Transcutaneous echocardiography - volumetric better results than Doppler

86
Q

In what cases is measuring CO most beneficial

A

Cases failing to respond to initial resuscitation efforts
Cases with complex disease involving multiple organ systems
Cases with cardia disease

87
Q

What is the MAP and systolic pressure desired in controlled resuscitation

A

MAP 40-60mmHg
Systolic 80-90mHg

88
Q

What is the ebb phase of metabolic response to trauma characterised by?

A

Hypovolemia and low flow or perfusion to the injured sit
Occurs during first several hours after injury

Eq ACVS Phase 1 (72 decks)

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