Shock

Question 1

What is the definition of shock?

Answer 1

Shock is defined as - inadequate cellular energy production and most commonly occurs secondary to poor tissue perfusion from low or unevenly distributed blood flow. This leads to a critical decrease in oxygen delivery (DO2) compared with oxygen consumption (VO2) in the tissues.
Source - CCM

Question 2

What are the three mechanisms stated to commonly result in a reduced DO2?

Answer 2

Loss of intravascular volume, maldistribution of vascular volume, failure of the cardiac pump?
Source - CCM

Question 3

What does the term compensated shock denote?

Answer 3

Mild to moderate mental depression, tachycardia with normal or prolonged capillary refill time, cool extremities, tachypnea, and a normal blood pressure. Pulse quality is often normal – when sympathetic stimuli compensates for losses.
Source - CCM

Question 4

What is decompensated shock?

Answer 4

Pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent as the animal progresses to decompensated shock. Ultimately, if left untreated, reduced organ perfusion results in signs of end organ failure (e.g., oliguria) and ultimately death.
Source - CCM

Question 5

What are the classifications of Shock

Answer 5

Hypovolaemic, Cardiogenic, Distributive, Metabolic, Hypoxaemic
Source - CCM

Question 6

What is the initial hyperdynamic phase of SIRS/Sepsis?

Answer 6

tachycardia, fever, bounding peripheral pulses, hyperaemic Mm – secondary to cytokine mediate vasodilation –> if this progresses signs of decreased cardiac output may predominate –> pale mms, tachycardia, prolonged crt, hypothermia
Source - CCM

Question 7

How do feline shock presentations differ to canine?

Answer 7

less predictable – may be brady or tachycardic, pale mms, weak pulses, hypothermic.
Source - CCM

Question 8

What testing is recommended in patients exhibiting shock states?

Answer 8

venous or arterial blood gas with
lactate measurement, a complete blood cell count, blood chemistry
panel, coagulation panel, blood typing, and urine analysis should
be performed. Thoracic and abdominal radiographs, abdominal
ultrasound, and echocardiography may be indicated once the patient
is stabilized
Source - CCM

Question 9

What is a normal pulmonary capillary edge pressure and how is it measured?

Answer 9

10-12mmHG –> swann-Ganz in floated into branch of the pulmonary artery

Question 10

When is mixed venous O2 decreased?

Answer 10

if DO2 decreases or if VO2 increases
Source CMM

Question 11

What is the mainstay of treatment of shock?

Answer 11

Re-establishing DO2 – usually with rapid administration of intravascular volume except in cardiogenic.
Source CCM

Question 12

What volume of crystalloids remains in the intravascular space after 30 mins

Answer 12

25%
Source - CCM

Question 13

In what situation is hypotensive resuscitation advantageous?

Answer 13

Poorly controlled haemorrhage
Source CCM

Question 14

What does the administration of hypertonic saline cause?

Answer 14

A transient shift of fluid into the intravascular space.
May also reduce endothelial swelling, modulate inflammation, increase contractility, produce mild vasodilation.
Source - CCM

Question 15

What are the characteristics of cardiogenic shock?

Answer 15

a systolic or diastolic cardiac dysfunction resulting in hemodynamic abnormalities such as increased heart rate; decreased stroke volume; decreased cardiac output; decreased blood pressure; increased peripheral vascular resistance; and increases in the right atrial, pulmonary arterial, and pulmonary capillary wedge pressures. These pathologic changes result in diminished tissue perfusion and increased pulmonary venous pressures, resulting in pulmonary oedema and dyspnoea.
Source - CCM

Question 16

Next Questions from - Cellular Metabolic Changes in Shock PDF MDR 2020 - Corrin Boyd

Answer 16

Next Questions from - Cellular Metabolic Changes in Shock PDF MDR 2020 - Corrin Boyd

Question 17

List some effects of ATP depletion

Answer 17

intracellular acidosis
ion flux
oxidative stress
adenosine release
altered gene expression

Question 18

How much ATP is produced per molecule of glucose in aerobic metabolism?

Answer 18

36 ATP

Question 19

What happens to glycolysis in shock?

Answer 19

Initially upregulated however ox-phos cannot occur, pyruvate accumulates and NAD is depleted.
Pyruvate is converted to lactate to allow replenishment of NAD –> allowing glycolysis to continue.

Question 20

How does intracellular acidosis occur in shock?

Answer 20

Normally hydrolysis of ATP produces one H+ and oxidative production of ATP consumes H+
In shock ATP continues to be used and hydrolysed however glycolysis does not consume H+ therefore an intracellular acidosis results.
CO2 production from small amounts of remaining oxidative metabolism contributes

Question 21

What is the cellular response to intracellular acidosis

Answer 21

Activation of multiple acid extruders - these often require ATP and therefore fail during shock

Question 22

Discuss the action of Monocarboxylate transporter (MCT) in shock?

Answer 22

An acid extrusion transmembrane protein - carry one H+ and a monocarboxylate out of the cell. The most abundant monocarboxylate in shock is lactate.
Beta-hydroxybutyrate and acetate are also transported out.
Which explains why lactate isn’t solely responsible for base deficit in shock

Question 23

What percentage of ATP in the normal cell is used by Na+/K+ atpase pumps?

Answer 23

25-50%

Question 24

Discuss ion change ion flux in shock?

Answer 24

• No ATP for maintenance of Na+/K+ pumps –> influx of Na and efflux of K+
• As cell depolarises more Na+/K+ channels open - makes it worse
• in an attempt to combat intracellular acidosis Na/H+ pumps result in an even worse accumulation of Na+
• cell depolarisation also opens Ca2+ channels, while Na+/Ca2+ channels cause an increase in Ca2+ while trying to get Na+ out
• This increase in Ca2+ results in activation of ryanodine receptors (calcium-induced-calcium release) worsening intracellular Ca2+

Question 25

List some dysfunction caused by an increase in intracellular Ca2+

Answer 25

Cellular swelling (also caused by Na+)
causes mitochondrial swelling
may activate several atp consuming metabolic pathways - further reducing ATP
upregulates proteolytic enzymes
Key to ROS production via activation of calpain on xanthine-oxidase system

Question 26

Describe the xanthine oxidase process

Answer 26

When ATP is broken down further than ADP the final product is hypoxanthine. In health xanthine dehydrogenase (not requiring O2) metabolises hypoxanthine.
In shock increased calcium activates calpain which converts xanthine dehydrogenase to xanthine oxidase. This pathway needs O2 = hypoxanthine and XO build up until O2 is restored. Then result in an explosive production of hydrogen peroxide and superoxide

Question 27

What is the Haber-Weiss reaction

Answer 27

The reaction in which ferric (Fe3+) irons react with superoxide and hydrogen peroxide to produce the more damaging hydroxyl radical
Fe3+ + superoxide –> Fe2+ + O2
Fe2+ + hydrogen peroxide –> Fe3+ + OH- + OH-

Question 28

Describe the mechanism of irreversible shock and adenosine release?

Answer 28

As ATP is broken down into adenosine in shock it may be released from the cell via equilibration nucleoside transporters (ENT).
This extracellular adenosine may then go on to cause bradycardia and vasodilation (resulting in decompensation)
Additionally, adenosine that leaves the cell can’t re-enter and even if O2 is restored to the cell it can’t remake the purine substrates to replace ATP quick enough.
This often results in cellular death - on a global scale is termed irreversible shock and is fatal

Question 29

What is ‘hypoxia-inducible factor 1 (HIF-1)?

Answer 29

produced constitutively in normal cells but has a short half life in presence of O2. in shock, hypoxia prevents it’s degradation. It inhibits adenosine kinases and therefore results in adenosine accumulation.

Question 30

Questions from TEXTBOOK OF EMERGENCY MEDICINE
Ch 152 - PATHOPHYSIOLOGY OF SHOCK

Answer 30

Questions from TEXTBOOK OF EMERGENCY MEDICINE
Ch 152 - PATHOPHYSIOLOGY OF SHOCK

Question 31

Is oxygen carying capacity determined more by hb saturation or dissolved O2

Answer 31

Hb saturation
(CaO2=1.34×Hb×SO2+0.003 PaO2)

Question 32

In a normal state what percentage of O2 is extracted from arterial blood?

Answer 32

25%
Can increase to 70-80% when needed

Question 33

What are the three stages of shock

Answer 33

1. Compensated
2. Decompensated
3. Irreversible

Question 34

What occurs in compensated shock

Answer 34

Recognition of decreased O2 delivery - baroreceptors, chemoreceptors. Increased CO via sympathetic stimulation. RAAS, ADH release. Self-autotransfusion

Question 35

What occurs in decompensated shock?

Answer 35

Acidosis and hypotension. Worsens cardiovascular performance due to acidosis impairing catecholamine sensistivity and exhaustion of compensatory mediators.

Question 36

How may the complement system be involved in Shock

Answer 36

C3a and C5a are released due to tissue injury. Resulting in increased vascular permeability, they stimulate histamine release and arachidonic acid product release. Induce cytokines and promote neutrophil adherence

Question 37

How may the coagulation system be induced in shock

Answer 37

inflammatory cytokines - IL1, IL6, TNFa, arachadonic acid products
increased tissue factor expression on the endothelium - this then drives thrombin production and platelet and fibrin formation

Question 38

Why is fibrinolysis reduced?

Answer 38

increased activity of plasminogen activator inhibitor and thrombin-activatable fibrinolysis inhibitor

Question 39

Why may mitochondria continue to be dysfunctional following shock resolution

Answer 39

related to cytokines like TNFa leading to uncoupling of ox-phos, increased mitochondial permiability and apoptosis.
As mitochondia are membrane bound they are also predisposed to ROS damage