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A U E R S & T > Chapter 1 - Shock: pathophysiology, diagnosis, tx > Flashcards

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

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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

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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

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4
Q

In compensated shock, which of the following mechanisms is NOT involved in restoring homeostasis?*

A) Increased sympathetic tone

B) Decreased heart rate

C) Vasoconstriction

D) Enhanced renal water reabsorptio

A

B) Decreased heart rate

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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

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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

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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

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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

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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

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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

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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

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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

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13
Q

What is cardiac output (CO) determined by?

A

Stroke volume (SV)

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14
Q

What is myocardial contractility?

A

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

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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

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16
Q

What is the primary goal in treating shock?

A

To restore and maintain cardiac output

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17
Q

What is hypovolemic shock primarily caused by?

A

A volume deficit

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18
Q

What is the cause of cardiogenic shock?

A

Pump failure of the heart

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19
Q

What is a common cause of distributive shock?

A

Loss of vasomotor tone

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20
Q

What is the response of baroreceptors to a fall in blood pressure?

A

They increase sympathetic tone

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20
Q

How is obstructive shock primarily caused?

A

By obstruction of ventilation or cardiac output

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21
Q

How does renal perfusion decrease affect the body?

A

It stimulates production of renin

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22
Q

What happens during decompensated shock?

A

Ischemia and failure of compensatory mechanisms

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23
Q

What are the signs of Class I blood loss according to the American College of Surgeons?

A

No change in physical findings

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24
Q

What is the effect of moderate to severe hypovolemia on organ systems?

A

Preferential maintenance of cerebral and cardiac flow

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25
Q

What are clinical signs of Class II blood loss?

A

Tachycardia, tachypnea, and increased CO

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26
Q

What does an increase in renin secretion lead to?

A

Stimulation of angiotensin II production

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27
Q

What are the end results of decompensated shock?

A

Pooling of blood in peripheral tissue beds and organ failure

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28
Q

What is a clinical sign of Class IV shock?

A

Profound hypotension and circulatory collapse

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29
Q

What is the first step in restoring oxygen delivery in shock patients?

A

Fluid therapy

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30
Q

Which factor is most commonly the cause of decreased oxygen delivery in shock?

A

Decreased perfusion

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31
Q

What is the effect of administering large volumes of isotonic crystalloids?

A

Majority of the volume diffuses out of the vascular space

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32
Q

What is a negative impact of high volumes of crystalloids?

A

They trigger an inflammatory response

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33
Q

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

A

Lower-volume bolus crystalloid therapy

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34
Q

What is the recommended approach for administering isotonic crystalloids for hypovolemic shock in equine practice?

A

A balanced fluid therapy approach

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35
Q

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

A

B. Sodium and chloride

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36
Q

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

A

B. Expands it by approximately twice the amount infused

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37
Q

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

A

C. 2-4 mL/kg = 1-2L for 500 kg horse

FOLLOWED by isotonic fluids 20mL/kg = 10 L fluids for 50 kgs horse in 30-60 minutes

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38
Q

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

A

They help retain water in the intravascular space

39
Q

What is the primary disadvantage of administering whole blood?

A

Its viscosity makes rapid infusion difficult

40
Q

What is the dosage of the blood transfusion in the first 10-20 minutes?

A

0.3 mL/kg over 10-20 minutes

If horse HR, Tº, RR ok you can increment to 5mL/kg/hr

41
Q

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

A. The severity of shock

42
Q

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

A

B. 7-9% of total body weight

43
Q

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

A

C. 20 mL/kg

44
Q

Which medication is rarely used in standing adult horses in hypovolemic shock?

A. Vasopressors

B. Antibiotics

C. Antibiotics

D. Anti-inflammatory drugs

A

A. Vasopressors

45
Q

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

A

B. To improve oxygen delivery to tissues

46
Q

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

A

B. It improves arterial pressure and urine output

47
Q

What is the role of vasopressin in shock treatment?

A

It acts as a powerful vasoconstrictor

48
Q

What is an important consideration when using vasopressor therapy?

A

Close monitoring of urine output and blood pressure

49
Q

What is a key sign of improved intravascular volume during fluid therapy?

A

Decreased heart rate and improved capillary refill time

50
Q

What is a sensitive method to assess patients in early compensated shock?

A

Repetitive physical exams

51
Q

What is usually prolonged in hypovolemic shock?

A

Capillary Refill Time (CRT)

52
Q

Central Venous Pressure (CVP) assesses all except:

A. Cardiac function

B. Blood volume

C. Vascular resistance or tone

D. Kidney function

A

D. Kidney function

53
Q

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

A

B. 7-12 mm Hg

54
Q

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

A. Cardiac Output (CO) and total vascular resistance

55
Q

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

A. 0.5 mL/kg/h

56
Q

L-lactate is the end product of:

A. Aerobic metabolism of glucose

B. Anaerobic metabolism of glucose

C. Protein metabolism

D. Fat metabolism

A

B. Anaerobic metabolism of glucose

57
Q

What does increased oxygen extraction ratio (O2ER) indicate?

A. Increased oxygen delivery

B. Decreased oxygen delivery

C. Normal oxygen delivery

D. Excessive oxygen delivery

A

B. Decreased oxygen delivery

58
Q

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

A

B. Low-perfusion states

59
Q

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

A

C. Cases with complex diseases or multiple organ systems involved

60
Q

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

A

C. Deteriorates it

61
Q

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

A. Noninvasive assessment and monitoring of the cardiovascular status

62
Q

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

A. Cases of uncontrolled bleeding

63
Q

What is an important factor in predicting outcome in shock patients?

A

B. Lactate values and clearance

64
Q

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

A

B. Goal-directed therapy in hypovolemic shock

65
Q

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

A

B. Ebb and flow

66
Q

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

A

B. Hypovolemia and low flow

67
Q

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

A

B. Tissue injury, hypovolemia, acidosis, shock, and psychological responses

68
Q

Catecholamines, in response to trauma, increase:

A. Only heart rate

B. Peripheral vascular resistance

C. Blood oxygen levels

D. Immune function

A

B. Peripheral vascular resistance

69
Q

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

A

B. Return to homeostasis

70
Q

Name the classification of shock

A

Cardiogenic
Hypovolemic
Obstructive
Distributive

71
Q

What types of fluids do you know?

A

isotonic crystalloids
hypertonic crystalloids
colloids
whole blood
vasopressors

72
Q

Monitoring

A

CRT
Central Venous Pressure
Urine output
Arterial blood pressure
Lactate
Oxygen extraction
Mixed venous partial pressure of oxygen
cardiac output
regional perfusion

73
Q

where are the baroreceptors located?

A

carotid sinus
right atrium
aortic arch sense falls of pressure

74
Q

what happens when the baroreceptors sense fall of pressure?

A

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
Q

Blood pressure increases with increment of sympathetic tone or decrease sympathetic tone?

A

increase in sympathetic tone and fall in ANP results in vasoconstriction, which increases total peripheral resistance and thereby increases blood pressure.

76
Q

cardiac output (CO) determines the blood flow to tissues and is regulated by STROKE VOLUME (SV). SV is a result of what?

A

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 push 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
Q

in which cases the preload is not good?

A

descrease hypovolemia –> pooling of blood and decreased return to the heart

78
Q

in which cases the myocardial contractibility is decreased?

A

shock spesis endotoxemia and ischemia/reperfusion injury

79
Q

in which cases the ventricular afterload is decreased?

A

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
Q

what factors do you have to work on to treat shock?

A

restaoration and maintenance of cardiac output through manipulation of:
- preload
- afterload
-myocardial contractibility
- HR

81
Q

reasons for hypovolemic shock

A

Bleeding, third space sequestration (large colon volvulus) severe dehydration

82
Q

reasons for cardiogenic shock

A

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
Q

reasons for cardiogenic shock

reasons for distributive shock

A

microcirculatory failure consequence of loss in effective circulating volume TTM is fluidotherapy to restore perfusion - neurogenic shock, septic shock and anaphylatic shock

84
Q

reasons for obstructive shock

A

obstruction of ventilation or of cardiac outpur = tension pneumothorax, pericardial tamponad, diaphragmative hernia, severe abdominal distension

85
Q

what is autonomic traffic?

A

interplay btw parasympathetic and sympathetic nervous systems

86
Q

VASOCONSTRICTION (VS9 how does it vary?

A

between organ system it greatest in integument, kidney, viscera and the smalles vasoconstriction is observed in brain and heart

87
Q

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

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
Q

what are teh clinicak signs of shock?

A

Class I
Class II
Class III
Class IV

89
Q
A

Class I when mild blood loss ocurred of less than 15% total blood volume - the body is capable of restoring via compensatory mechanisms

90
Q
A

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
Q

Describe class III of shock

A

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
Q

Class IV

A

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
Q

Troponin I is important to monitor what?

A

is indicated in critical patients with arrhythmias or unexplained tachycardia

94
Q
A
95
Q
A
96
Q

The content of oxygen per volume of blood is determined by

A

hemoglobin (Hb)
or red cell mass and the saturation of that Hb (SaO2)
this 2 variables will affect the oxygen delivery

A U E R S & T (122 decks)

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