Chapter 1 - Shock: pathophysiology, diagnosis, tx Flashcards
1
Q
Which of the following best describes the fundamental cause of shock?
A) Excessive oxygen in the bloodstream
B) Inadequate tissue perfusion
C) Overactive immune response
D) Excessive nutrient supply to cells
A
B) Inadequate tissue perfusion –> leads to energy and oxygen deprivation, release of cellular enzymes and accumulation of calcium and reactive oxygen species (ROS) (cellular injury and death) - leads to activation of inflammatory, coagulation and complement cascadesc - cellular injury and microvascular thrombosis + increased absorption of endotoxin and bacteria = SIRS
2
Q
Hypovolemic shock is primarily caused by
A) Loss of vasomotor tone
B) Volume deficit due to blood loss or dehydration
C) Cardiac muscle failure
D) Obstruction of blood flow
A
B) Volume deficit due to blood loss or dehydration
3
Q
Which of the following is NOT a common cause of distributive shock?
A) Septic shock
B) Neurogenic shock
C) Cardiogenic shock
D) Anaphylactic shock
A
C) Cardiogenic shock
Distributive shock or vasodilatory shock is a medical emergency where your body can’t get enough blood to your heart, brain and kidneys.
4
Q
In compensated shock, which are mechanisms involved in restoring homeostasis?
A
1) Increased sympathetic tone
2) Vasoconstriction
3) Enhanced renal water reabsorptio
5
Q
The primary goal in treating hypovolemic shock is to:*
A) Increase heart rate
B) Restore tissue perfusion and oxygen delivery C) Decrease blood lactate levels
D) Increase blood viscosity
A
B) Restore tissue perfusion and oxygen delivery
6
Q
What is the main reason for the rapid diffusion of isotonic crystalloids out of the vascular space?
A) High glucose content
B) High oxygen content
C) Low viscosity
D) Low oncotic pressure
A
D) Low oncotic pressure
7
Q
Which of the following is NOT a benefit of hypertonic saline solution (HSS) in shock treatment?
A) Rapid expansion of intravascular volume
B) Prolonged intravascular retention
C) Reduction of endothelial cell volume
D) Blunting neutrophil activation
A
B) Prolonged intravascular retention
8
Q
When assessing shock progression, capillary refill time (CRT) is:
A) Only prolonged in hypovolemic shock
B) Unaffected by vascular permeability
C) Useful if assessed over time
D) Always shortened in septic shock
A
C) Useful if assessed over time
9
Q
Hypotensive resuscitation in shock is primarily aimed at:
A) Maximizing oxygen delivery
B) Preventing further blood loss in uncontrolled bleeding
C) Increasing the blood volume rapidly
D) Restoring blood pressure to normal values immediately
A
B) Preventing further blood loss in uncontrolled bleeding
10
Q
Which of the following is NOT a clinical sign of early, hyperdynamic shock?
A) Tachycardia
B) Decreased pulse pressure
C) Mental agitation
D) Tachypnea
A
B) Decreased pulse pressure
11
Q
What does shock result from?
A. Muscular distress
B. Physical injury
C. Inadequate tissue perfusion
D. Excessive blood loss
A
C. Inadequate tissue perfusion
12
Q
What are the major factors affecting blood flow?
A. Brain function, liver function, kidney function
B. Circulating volume, cardiac pump function, vasomotor tone
C. Respiratory rate, blood pressure, temperature
D. Muscle strength, bone density, skin integrity
A
B.Circulating volume, cardiac pump function, vasomotor tone
13
Q
What is cardiac output (CO) determined by?
A
Stroke volume (SV)
14
Q
What is myocardial contractility?
A
The rate of cross-bridge cycling between actin and myosin filaments within cardiomyocytes
15
Q
Which of the following is a component of stroke volume?
A. Ventricular afterload
B. Blood plasma
C. White blood cell count
D. Platelet aggregatio
A
A. Ventricular afterload
16
Q
What is the primary goal in treating shock?
A
To restore and maintain cardiac output
17
Q
What is hypovolemic shock primarily caused by?
A
A volume deficit
18
Q
What is the cause of cardiogenic shock?
A
Pump failure of the heart
19
Q
What is a common cause of distributive shock?
A
Loss of vasomotor tone
20
Q
What is the response of baroreceptors to a fall in blood pressure?
A
They increase sympathetic tone
20
Q
How is obstructive shock primarily caused?
A
By obstruction of ventilation or cardiac output
21
Q
How does renal perfusion decrease affect the body?
A
It stimulates production of renin
22
Q
What happens during decompensated shock?
A
Ischemia and failure of compensatory mechanisms
23
Q
What are the signs of Class I blood loss according to the American College of Surgeons?
A
No change in physical findings
24
What is the effect of moderate to severe hypovolemia on organ systems?
Preferential maintenance of cerebral and cardiac flow
25
What are clinical signs of Class II blood loss?
Tachycardia, tachypnea, and increased CO
26
What does an increase in renin secretion lead to?
Stimulation of angiotensin II production
27
What are the end results of decompensated shock?
Pooling of blood in peripheral tissue beds and organ failure
28
What is a clinical sign of Class IV shock?
Profound hypotension and circulatory collapse
29
What is the first step in restoring oxygen delivery in shock patients?
Fluid therapy
30
Which factor is most commonly the cause of decreased oxygen delivery in shock?
Decreased perfusion
31
What is the effect of administering large volumes of isotonic crystalloids?
Majority of the volume diffuses out of the vascular space
32
What is a negative impact of high volumes of crystalloids?
They trigger an inflammatory response
33
What does the Surviving Sepsis Campaign recommend for fluid therapy?
A. High-volume bolus crystalloid therapy
B. Lower-volume bolus crystalloid therapy
C. High-volume colloid therapy
D. No fluid therapy
Lower-volume bolus crystalloid therapy
34
What is the recommended approach for administering isotonic crystalloids for hypovolemic shock in equine practice?
A balanced fluid therapy approach
35
What are the primary components of commercially available isotonic crystalloids for horses?
A. Proteins and vitamins
B. Sodium and chloride
C. Calcium and potassium
D. Magnesium and bicarbonate
B. Sodium and chloride
36
What is the effect of hypertonic saline solution (HSS) on intravascular space?
A. Reduces it
B. Expands it by approximately twice the amount infused
C. Has no effect
D. Contracts it
B. Expands it by approximately twice the amount infused
37
What is the dosage for hypertonic saline solution?
A. 10-20 mL/kg
B. 20-30 mL kg
C. 2-4mL/kg
D. 1-2 mL/kg
C. 2-4 mL/kg = 1-2L for 500 kg horse 7.2%
FOLLOWED by isotonic crystalloid fluids 20mL/kg = 10 L fluids for 500 kgs horse in 30-60 minutes
38
What is a key benefit of colloids in fluid therapy?A. They are cheaper than crystalloids
B. They help retain water in the intravascular space
C. They provide necessary vitamins
D. They have no side effects
They help retain water in the intravascular space
39
What is the primary disadvantage of administering whole blood?
Its viscosity makes rapid infusion difficult
40
What is the dosage of the blood transfusion in the first 10-20 minutes?
0.3 mL/kg over 10-20 minutes
If horse HR, Tº, RR ok you can increment to 5mL/kg/hr
41
What should the choice of fluid therapy depend on?
A. The severity of shock
B. The availability of fluids
C. The preference of the veterinarian
D. The age of the horse
A. The severity of shock
42
In adult horses with hypovolemic shock, what is the estimated circulating blood volume?
A. 2-5% of total body weight
B. 7-9% of total body weight
C. 15-20% of total body weight
D. 25-30% of total body weight
B. 7-9% of total body weight
43
What is the initial crystalloid intravenous bolus recommended for an adult horse?
A. 5 mL/kg
B. 10 mL/kg
C. 20 mL/kg
D. 30 mL/kg
C. 20 mL/kg
44
Which medication is rarely used in standing adult horses in hypovolemic shock?
A. Vasopressors
B. Antibiotics
C. Antibiotics
D. Anti-inflammatory drugs
A. Vasopressors
45
What is the primary use of dobutamine in shock treatment?
A. To reduce heart rate
B. To improve oxygen delivery to tissues
C. To increase blood viscosity
D. To decrease blood pressure
B. To improve oxygen delivery to tissues
46
What effect does norepinephrine have in shock treatment?
A. It decreases cardiac contractility
B. It improves arterial pressure and urine outputC. It reduces vasoconstriction
D. It has no effect on shock
B. It improves arterial pressure and urine output
47
What is the role of vasopressin in shock treatment?
It acts as a powerful vasoconstrictor
48
What is an important consideration when using vasopressor therapy?
Close monitoring of urine output and blood pressure
49
What is a key sign of improved intravascular volume during fluid therapy?
Decreased heart rate and improved capillary refill time
50
What is a sensitive method to assess patients in early compensated shock?
Repetitive physical exams
51
What is usually prolonged in hypovolemic shock?
Capillary Refill Time (CRT)
52
Central Venous Pressure (CVP) assesses all except:
A. Cardiac function
B. Blood volume
C. Vascular resistance or tone
D. Kidney function
D. Kidney function
53
Normal CVP in standing horses is typically:
A. 3-6 mm Hg
B. 7-12 mm Hg
C. 13-18 mm Hg
D. 19-24 mm Hg
B. 7-12 mm Hg
54
Arterial blood pressure reflects:
A. Cardiac Output (CO) and total vascular resistance
B. Only CO
C. Only total vascular resistance
D. Neither CO nor total vascular resistance
A. Cardiac Output (CO) and total vascular resistance
55
In hypovolemic shock, urine output less than what suggests significant volume depletion?
A. 0.5 mL/kg/h
B. 1 mL/kg/h
C. 1.5 mL/kg/h
D. 2 mL/kg/h
A. 0.5 mL/kg/h
56
L-lactate is the end product of:
A. Aerobic metabolism of glucose
B. Anaerobic metabolism of glucose
C. Protein metabolism
D. Fat metabolism
B. Anaerobic metabolism of glucose
57
What does increased oxygen extraction ratio (O2ER) indicate?
A. Increased oxygen delivery
B. Decreased oxygen delivery
C. Normal oxygen delivery
D. Excessive oxygen delivery
B. Decreased oxygen delivery
58
Mixed venous partial pressure of oxygen (PvO2) falls in:A. High-perfusion states
B. Low-perfusion states
C. Normal-perfusion states
D. It remains constant regardless of perfusion
B. Low-perfusion states
59
Cardiac Output (CO) monitoring is essential in cases of:
A. Simple injuries
B. Expected response to initial resuscitation
C. Cases with complex diseases or multiple organ systems involved
D. Mild shock cases
C. Cases with complex diseases or multiple organ systems involved
60
What does prolonged or specific types of shock, like septic shock, do to cardiac function?
A. Improves it
B. Does not affect it
C. Deteriorates it
D. Stabilizes it
C. Deteriorates it
61
Transcutaneous 2D echocardiography is used for:
A. Noninvasive assessment and monitoring of the cardiovascular status
B. Invasive monitoring of heart rhythm
C. Direct measurement of arterial blood pressureD. Evaluating kidney function
A. Noninvasive assessment and monitoring of the cardiovascular status
62
Hypotensive resuscitation is recommended in:
A. Cases of uncontrolled bleeding
B. Stable patients without bleeding
C. Mild shock cases
D. All shock cases regardless of bleeding
A. Cases of uncontrolled bleeding
63
What is an important factor in predicting outcome in shock patients?
B. Lactate values and clearance
64
What does a "balanced resuscitation" plan focus on?
A. Aggressive fluid replacement
B. Goal-directed therapy in hypovolemic shock
C. Strictly limiting fluid intake
D. Use of vasopressors only
B. Goal-directed therapy in hypovolemic shock
65
The metabolic response to trauma is divided into which two phases?
A. Catabolic and anabolic
B. Ebb and flow
C. Acute and chronic
D. Initial and final
B. Ebb and flow
66
What is the typical initial response during the ebb phase after injury?
A. Increased blood flow
B. Hypovolemia and low flow
C. Hyperthermia
D. Elevated blood pressure
B. Hypovolemia and low flow
67
What triggers the stress response to trauma?
A. Only psychological responses
B. Tissue injury, hypovolemia, acidosis, shock, and psychological responses
C. Elevated blood sugar levels
D. Only physical injuries
B. Tissue injury, hypovolemia, acidosis, shock, and psychological responses
68
Catecholamines, in response to trauma, increase:
A. Only heart rate
B. Peripheral vascular resistance
C. Blood oxygen levels
D. Immune function
B. Peripheral vascular resistance
69
The anabolic period of the physiologic response to trauma is characterized by:
A. Continued catabolism
B. Return to homeostasis
C. Persistent elevated cortisol levels
D. Ongoing tissue damage
B. Return to homeostasis
70
Name the classification of shock
Cardiogenic
Hypovolemic
Obstructive
Distributive
71
What types of fluids do you know?
isotonic crystalloids
hypertonic crystalloids
colloids
whole blood
vasopressors
72
Monitoring
CRT
Central Venous Pressure
Urine output
Arterial blood pressure
Lactate
Oxygen extraction
Mixed venous partial pressure of oxygen
cardiac output
regional perfusion
73
where are the baroreceptors located?
carotid sinus
right atrium
aortic arch sense falls of pressure
74
what happens when the baroreceptors sense fall of pressure?
act to:
**decrease inhibition** of **sympathetic tone** while
**increasing inhibition of vagal activity**
**decreasing** the release of **atrial natriuretic peptide (ANP)** by cardiac myocyte
**increase in sympathetic tone** and **fall in ANP** results in **vasoconstriction**, which increases **total peripheral resistance**and **thereby increases blood pressure.
increased sympathtetic activity** at the heart= **increment of HR** =**increment of systolic cardiac** function =**increment SV and CO**
75
Blood pressure increases with increment of sympathetic tone or decrease sympathetic tone?
increase in sympathetic tone and fall in ANP results in vasoconstriction, which increases total peripheral resistance and thereby increases blood pressure.
76
cardiac output (CO) determines the blood flow to tissues and is regulated by STROKE VOLUME (SV). SV is a result of what?
SV is the result of
1. **ventricular preload **(amount of **blood returning
from the body **and **entering the heart**),
2. the **myocardial contractility**
(systolic cardiac function),
3. and the **ventricular afterload **(the **force
the heart must overcome** to p**ush blood across the aortic** and **pulmonic valves** into the **peripheral or pulmonary vasculature**).
The interplay between these factors is seen in Figure 1-1.
77
in which cases the preload is not good?
descrease hypovolemia --> pooling of blood and decreased return to the heart
78
in which cases the myocardial contractibility is decreased?
shock spesis endotoxemia and ischemia/reperfusion injury
79
in which cases the ventricular afterload is decreased?
**Ventricular afterload **(force of the heart for the blood to come out) is dependent of:
**-vasomotor tone (VMT)
- peripherial vascular resistance (PVR)**
case of **VMT and PVR increment**= **hypertension** = afterload incremented = **CO and tissue perfusion are low**
- if **VMT and PVR low** = **pooling of blood and low blood pressure, low preload** = diminished perfusion and** shock**
80
what factors do you have to work on to treat shock?
restauration and maintenance of cardiac output through manipulation of:
- preload
- afterload
-myocardial contractibility
- HR
81
reasons for hypovolemic shock
Bleeding, third space sequestration (large colon volvulus) severe dehydration
82
reasons for cardiogenic shock
cardiac muscle cannot pump out adequate stroke volume to maintain perfusion (acidemia and ischemia can lead to a depression of cardiac muscle function) --> giving more fluids or aggressive fluidotherapy can worsen
83
# reasons for cardiogenic shock
reasons for distributive shock
microcirculatory failure consequence of loss in effective circulating volume TTM is fluidotherapy to restore perfusion - neurogenic shock, septic shock and anaphylatic shock
84
reasons for obstructive shock
obstruction of ventilation or of cardiac outpur = tension pneumothorax, pericardial tamponad, diaphragmative hernia, severe abdominal distension
85
what is autonomic traffic?
interplay btw parasympathetic and sympathetic nervous systems
86
VASOCONSTRICTION (VS) how does it vary?
between organ system it greatest in integument, kidney, viscera and the smalles vasoconstriction is observed in brain and heart
87
explain the renin-angiotension-aldosterone system (RAAS) what happens when renal perfusion diminishes what happens to renin secretion and production of angiotensin I and consequently to the sympathetic tone
A decrease in renal perfusion results in secretion of renin from juxtaglomerular cells located in the wall of the afferent arteriole. Renin stimulates production of angiotensin I, which, after conversion to angiotensin II, increases sympathetic tone on peripheral vasculature and promotes aldosterone release from the adrenal cortex. Aldosterone restores circulating volume by increasing renal tubular sodium and water reabsorption. Arginine vasopressin (AVP, previously known as antidiuretic hormone, ADH), released from the posterior pituitary gland in response to decreased plasma volume and increased plasma osmolality, is a potent vasoconstrictor and stimulates increased water reabsorption in the renal collecting ducts. Finally, an increase in thirst and a craving for salt is mediated by both the renin-angiotensin-aldosterone system (RAAS) and a fall in ANP
(Figure 1-2).
88
what are teh clinical signs of shock?
Class I
Class II
Class III
Class IV
89
describe class 1 of shock
Class I when mild blood loss ocurred of less than 15% total blood volume - the body is capable of restoring via compensatory mechanisms
90
describe class II of shock
Class II --> onset hyperdynamic shock - blood loss 15-30% onset of hyperdynamic shock (tachycardia, tachypneia -increased CO and PVR) mental agitation or anxiety is present and sympathetic output resultis in pupil dilation and sweating. Although these compensatory mechanisms can normalize blood pressure, perfusion deficits will persist and can be detected by blood gas analysis (increased lactate and a high anion gap metabolic acidosis).
91
Describe class III of shock
Moderate hypovolemic shock - If blood loss continues, or if hypovolemia persists, compensatory mechanisms can become insufficient
At this time profound** tachycardia and tachypnea**, anxiety, and agitation are present. **Urine output may cease**, **jugular filling** and **CRT** are prolonged, pulse pressure is weak, and extremity temperatures are decreased. If blood gases are collected, a lactic acidosis will be present
92
Class IV
Blood pressure will drop despite increases in heart rate, cardiac contractility, and total peripheral resistance. Without intervention, continued cellular hypoxia and acidosis result in failure of compensatory mechanisms, causing peripheral vasodilation and decreased myocardial contractility. A vicious cycle ensues with decreased coronary artery perfusion causing decreased cardiac function, resulting in decreased CO and a further drop in perfusion (see Figure 1-4). If uncontrolled, clinical signs will progress from tachycardia and anxiety to bradycardia, obtundation, anuria, profound hypotension, circulatory collapse, and death (class IV, uncompensated life-threatening hemorrhagic shock)
93
Troponin I is important to monitor what?
is indicated in critical patients with arrhythmias or unexplained tachycardia
94
95
96
The content of oxygen per volume of blood is determined by
hemoglobin (Hb)
or red cell mass and the saturation of that Hb (SaO2)
this 2 variables will affect the oxygen delivery
97
What is the goal of fluid administration?
restore perfusion and oxygen delivery to the tissues while maintaining CO and BP
98
Regardless the etiology of the shock the need to restore perfusion is defined by a formula nam ethe formula
delivery of oxygen (DO2) is defined by the content of oxygen in the arterial blood (CaO2) as well as the amount of blood perfusing the tissue
99
When you give crystalloids fast and quick approximately 80% of the volume will rapidly diffuse out of the vascular space into the interstitial and intercellular space. So, when using **crystalloids** what are the volumes given comparing to the volume lost?
Consequently, when using **crystalloids**, replacement volumes must be **four to five times** greater than the volume lost
100
Large-volume fluid therapy in patients with underlying SIRS or patients that have a low colloid oncotic pressure can result in
**significant edema**, which can **negatively affect intestinal motility** and **barrier function**, and can also affect the function of other organ systems
101
Name the isotonic crystalloids and what they are designed to remplace
designed to be replacement fluids, not maintenance fluids, meaning that the electrolyte composition is designed to closely approximate the electrolyte composition of the extracellular fluid and not the daily replacement needs.
The common BES available for horses include **lactated Ringer solution, Plasma-Lyte, and Normosol-R**
102
What is the difference btw NaCl 0.9% and the Ringer Lactate/Plasma-lyte and Normosol?
principally composed of sodium and chloride with varying amounts of calcium, potassium, and magnesium. Physiologic saline solution (0.9% NaCl) differs in that it contains only sodium and chloride but no other electrolytes (
103
Should you not give fluids in case of severe blood loss?
In cases of moderate to severe blood loss, infusion of large volumes of crystalloids alone can cause dilutional anemia and hypoproteinemia, although the oxygen-carrying capacity (red blood cell mass) will remain unchanged or become improved intravenous crystalloid fluid therapy should never be withheld, even when the packed cell volume (PCV) and total solids (TS) are reduced
104
Which patients are contra-indicated aggressive high-volume crystalloid therapy?
SIRS and endotoxemia
105
When there is severe blood loss you give crystalloid fluido therapy followed by
These patients may require subsequent plasma or whole blood transfusions to improve coagulation, oncotic pressure, and oxygen content of blood.
106
What is the % most common hypertonic saline solution used?
Hypertonic saline solution (HSS) is available in several concentrations, with 7.2% being the most commonly used formulation (=8 times teh tonacity of plasma)
107
Hypertonic fluids pulls volume from the intracellular space or interstitial space? hy it may be benificial in teh shock state?
HSS principally pulls volume from the intracellular space, not the interstitial space. This is particularly beneficial in the shock state, where endothelial cell volume rises with loss of membrane pump function. The decrease in endothelial cell volume increases capillary diameter and improves perfusion. In addition, HSS appears to blunt neutrophil activation and may alter the balance between inflammatory and antiinflammatory cytokine responses to hemorrhage and ischemia
108
what it the normal colloid oncotic pressure of a horse?
20 mmHG
109
what type of molecules are colloids and name some examples of natural and synthetic
colloids are solutions containing large molecules (size and charge) that retain within the vascular space that will retain and draw water into intravascular space
Natural colloids; plasma, whole blood, bovine albumin
synthetic colloids HES (hetastarch and tetrastarch), dextrans
110
what are the advantages of giving plasma?
albumin, antibodies, critical clotting factors, antithrombin 3, and other plasma constituents
111
what % o horses makes hypersentitivity reaction to plasma?
10%
112
The elimination of HES occurs via two major mechanisms, name them
renal excretion and extravasation.
113
dose of 10 mL/kg will significantly increase oncotic pressure in some patients for longer than
120 hours =5 days
114
Is whole blood necessary in patients with mild to moderate hypovolemia?
No, the use of whole blood is generally unnecessary in patients with mild to **moderate hypovolemia** because **restoration of perfusion often results in adequate oxygen delivery**. Only in severe cases with ongoing bleeding is indicated to provide oxygen-carrying capacity
115
how do you monitor the needs for colloid?
total protein they are not accurate so you neeed to measure COP (colloid oncotic pressure)
116
In an adult horse, the circulating blood volume is estimated to be __% to __% of the total body weight or 35 to ___L for a 500-kg horse.
In an adult horse, the circulating blood volume is estimated to be 7% to 9% of the total body weight or 35 to 45 L for a 500-kg horse.
117
Clinical signs of blood loss will occur after the loss of ___% of circulating blood volume or approximately 6 L, during an acute hemorrhage
Clinical signs of blood loss will occur after the loss of 15% of circulating blood volume or approximately 6 L, during an acute hemorrhage
118
Signs of improved intravascular volume include
decreased heart rate, improved CRT and jugular filling, skin temperature, and mentation
119
In situations where bleeding is uncontrolled, normalization of blood pressure should or should not be the goal ?
In situations where bleeding is uncontrolled, normalization of blood pressure should not be the goal because this may promote continued bleeding (permissive hypotension, i.e., mean arterial blood pressure [MAP] >65 mm Hg, rather than MAP
>90 mm Hg).
120
Vasopressors when are they given?
Vasopressors are rarely used in standing adult horses in hypovolemic shock.
121
What are the most vasopressor used?
Dobutamine
122
What is the molecule of dobutamine?
strong β1-adrenoreceptor agonist with relatively weaker β2- and α-adrenoreceptor affinity
123
Dobutamine dosage
Recommended dosages are 1 to 5 μg/kg/min.
124
Norepinephrine what is it? what dosage?
Norepinephrine has been reported to be useful in restoring adequate organ perfusion. Strong β1- and α-adrenergic affinity resulting in vasoconstriction and increased cardiac contractility
125
Give an example where norepinephrine with dobutamine?
persistently hypotensive foals (increments urine output and arterial pressure)
126
Vasopressin what is it?
powerful vasoconstrictor released from the pituitary gland following periods of hypotension
127
what do you have to monitor when you give vasopressor?
urine output and blood pressure
128
What should you monitor in order to know if you are restoring the hypovolemia?
Heart rate, CRT, jugular venous fill, extremity temperature, pulse pressure, urine output, and mentation are all useful when repeatedly evaluated
129
AVP (arginine vasopressin previously known as ADH) increments in horses with colic why?
compensatory effect for hypotension
130
what is the normal value for urine output?
Normal is 1 mL/kg/hr
131
name a sensitive indicator of hypovolemia
urine output or production 1 mL/kg/hr and this is difficult in adults but very used in neonatal medicine by placing a sterile urinary catheter with a sterile 5L bag
132
Arterial blood pressure is a reflection of CO and total vascular resistance. Can it rule out hypovolemic shock?
NO, because blood pressure doesn't go bloe normal until the blood volume is profoundly descreased 30% or more
133
Central venous pressure (CVP) assesses what?
1) cardiac function
2) blood volume
3) vascular resistance or tone
134
Holding the jugular vein within __ seconds in normal hydrated horse standing with elevated head should have a visible filling which corresponds to a normal central venous pressure (CVP) or with a ___________ ___________(2w) a more accurate estimate can be seen
within 5 seconds holding a a visilbe filling of jugular vein should be seen. A more accurate estimate of CVP can be obtained with water manometer attached to a large bore jugular catheter at the level o the heart base or point of the shoulder.
135
Elevated CVP can be due to
cardiogenic shock,
fluid overload,
pericardial effusion due to increment of inotropine the failure of the cardiac pump results in backup of blood within the venous system.
In this case the jugular veins are distended with the horse standing (rare condition)
136
Low CVP can occur with
hypovolemia or drop in effective circulating volume - occurs with distributive shock
137
Direct invasive blood pressure is measured in _____ __________ artery in adults or neonates ______or____ or___ arteries
IndirecT measurement of MAPS can be done with ___________ and normal values are _____ and _____ mmHG
- transverse facial artery in adult
or in neonates: transverse facial artery
- metatarsal
- radial
- auricular arteries
Indirect can be done with coccygel artery between 105 and 135 mmhg
138
L-lactate is what?
end product of the anaerobic metabolism of glucose
139
Aerobic metabolism of glucose results in the production of ____ moles of adenosine triphosphate (ATP) per molecule of glucose. In the absence of adequate oxygen to meet energy demands, anaerobic metabolism of glucose to lactate results in production of only ___moles of ATP
Aerobic metabolism of glucose results in the production of **36 moles of adenosine triphosphate (ATP)** per **molecule of glucose**. In the absence of adequate oxygen to meet energy demands, anaerobic metabolism of glucose to lactate results in production of only 2 moles of ATP
140
What is a type A hyperlactemia and a type B?
Type A: indaquate oxygen to the tissue - increment blood lactate
Type B: hepatic dysfunction (impaired clearance), pyruvate dehydrogenase inhibition catecholamine surges and sepsis or SIRS but oxygenation ok
141
When should you remeasure the lactate?
In 12 to 24 hours and not short term
142
Arterial blood pressure is a reflection of 2 things, name them
cardiac output CO
total vascular resistance
143
Does arterial pressure reflect the adequate perfusion and oxygen?
No, normal blood pressure does not indicate adequate perfusion and oxygen deivery to peripheral tissue beds --> it only gives signs when blood volume is bellow 30% (profoundly decreased)
144
Arterial pressure if low can indicate what?
A normal low blood pressure cannot exclude hypovolemic shock but a low blood pressure is indicator of significant blood loss
145
What is the value of blood pressure you want to keep above?
Above 65 mmHg to ensure adequate perfusion to the brain
146
The normal response to a decrease in perfusion or CO is the increase _________ extraction ratio of the blood
of oxygen extraction ratio (O2ER) of the blood as it moves through the capillaries
147
Oxygen extraction is determined by the difference between the oxygen saturation of arterial blood (SaO2) and oxygen saturation of venous blood (SvO2) - write the formula
148
Mixed venous partial pressure of oxygen assesses what?
oxygen delivery and a low perfusion means more oxygen is extracted per volume of blood and PvO2 will fall
149
How do you obtain mixed venous partial pressure? you have to cathetirize what?
you have to catheterize the pulmonary artery
150
Normal partial pressure of oxygen ranges from ___ to__- mmHg
40 to 50 mmHg
151
CO or caridac outpur monitores what?
volume return to the heart and cardiac function
152
what are the 2 ways to measure the CO?
1 - gold standard RARe in horses: catheterization of the pulmonary artery
2 - lithium dilution with injection of lithium dye into the venous system taht results in generation of lithium concentration-time curve
153
CO measurement is useful in which cases?
CO measurement has its greatest benefit in cases that fail to respond as expected to initial resuscitation efforts, cases with **complex disease involving multiple organ systems**, or those with cardiac disease.
154
Give a pratical example where hypotensive resuscitation would be beneficial with whole blood
**hypotensive resuscitation** (with whole blood as part of the fluid plan) is indicated in situations such as **bleeding of the uterine artery in a pregnant mare**, where ligation of the vessel is unlikely and of great risk to the mare and fetus
155
In case of bleeding should you go for aggressive large volume therapy and why? name 3 reasons
No,
-results in increased blood loss
- dilution of blood components
- may blow out a clot because of increasing systolic blood pressure
you should prevent or minimize the blood loss until surgical cntrol
156
Metabolc response to trauma has been classified in 2 phases, name them
1. ebb phase (first several hours) hypovolemia + low flow or perfusion to the injured site
2. flow phase (days to weeks) perfusion is restored
- catabolic period triggered by many of same mediators of shock
-anabolic period return to homeostasis + normalization of the physiology with diminishment of cortisol
157
Mediators of the stress response: Ebb phase
The stress response to trauma is initiated by...(name 6 factors)
pain
tissue injury
hypovolemia
acidosis
shock
hypothermia
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direct injury ischemia and inflammation (Ebb phase) will activate the
afferent nerve endigns which exert local and systemic effects via central nervous system (CNS)
159
hypovolemia, acidosis and shock (ebb phase) will activate the..
baroreceptors and chemoreceptors at heart and great vessels
160
Fear and pain happen in the ebb phase and they have efecte in the
cortex! and stimulate cortisol secretion via the hypothalamic-pituitary-adrenal axis (HPA) which increases the sympathetic output so for this reason pain control is important
161
The symphatetic stimulation (ebb phase) is important because it will realase _____ ________ (2w) by the pituitary gland and adrenal glands. what are the effects?
It will release endogenous opioids that has effects in the
-modulation of pain
-catecholamine release
-insulin scretion
-modulate lymphocyte + neutrophil function
-counter cortisol effect pon the immune system
162
Is cortisol release (ebb phase) correlated to the severity of injury?
yes and it will persist until the anabolic phase of healing begins
163
Cortisol secretion (ebb phase) results in
- sodium and water retention (edema)
-insulin resistance
-gluconeogenesis
-lipolysis
-protein catabolism
-affects leukocytes and inflammatory mediator production
164
local mediators are released in response to injury and will trigger multiple cascades name them
**tissue factor exposure** will activate coagulation and inflammatory response
**cell membrane injury** will activate the arachidonic acid cascade and production of cytokines --> that will activate coagulation and platelets alter blood flow via VC and VD and increase chemotactic activity mediating the nflux
**microvascular thrombosis** at the site of endothelial injury
if perfusion is restored it will e**levate the local concetrations ROS** and influx of oxygen
165
In the **catabolic period **there are changes in behavior (fear anxiety and agression) what other signs come with it?
cardiovascular changes: **tachycardia**
hypotension
decreased perfusion
decreased urine output
reduced cardiac contractility
**fever **(early period after injury) is response to injury and inflammation itself (specially in head trauma)
**edema** loss of capillary integrity with protein loss
166
coagulation dysfunction is recognized in which types of situations?
large colon volvulus
severe traumatic injury
SIRS
septic shock
167
why the circulating leukocytes increase in the catabolic phase can increased the ROS?
This accumulation may be exacerbated by vasoconstriction due to hypovolemia and catecholamines and the activated neutrophils are a major sourve of reactive oxygen metabolites
168
The anabolic phase corresponds to destruction or recovery phase?
recovery phase
169
What happens in the anabolic period?
Appetite returns, body protein is synthesized, and weight is restored, resulting in improved organ function and energy stores. Metabolic demands diminish, water balance is restored, and as hormonal levels decrease, a generalized feeling of well-being develops
170
how much length of time it takes the anabolic phase?
The length of this period will depend on the severity of the injury, the number and type of complications, the patient’s condition before injury, and the length of the catabolic period of recovery
