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Shock / CPR > Shock - pathophys, general > Flashcards

Shock - pathophys, general Flashcards

1
Q

Draw the VO2 / DO2 curve and oxygen extraction curve

A
  • Supply-dependent
  • Critical DO2 (usually O2 ER of 70%)
  • Supply-independent
  • normally oxygen consumption is only 25%
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2
Q

You have the following patient data:
- SaO2 = 96%
- PaO2 = 99 mmHg
- HR = 160 bpm
- SV = 20 mL
- Hct = 40%
- BW = 30 kg

Calculate DO2

A

DO2 = (HR (beats/min) x SV (mL)) x [(Hb (g/dL) x 1.34 (mL O2/g) x SaO2 (no units)) + (PaO2 (mmHg) x 0.003 (mL O2/mmHg/dL blood)]/100

DO2 = 3200 mL blood / min x 18 mL O2 / dL blood = 3200 mL blood / min x 0.18 mL O2 / dL blood = 576 mL O2 / min

(= 19.2 mL O2 / min / kg)

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3
Q

What is the definition of shock

A

Severe imbalance between O2 supply / use and demand leading to inadequate cellular energy production and causing cellular death and multiorgan failure

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4
Q

Name a few DAMPs released during shock

A

Mitochondrial DNA, histones, heat shock proteins

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5
Q

What are the shock organs in dogs and cats?

A

Dogs: GI
Cats: lungs

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6
Q

What factors contribute to compensation of shock

A
  • Baroreceptor reflex (sympathetic nervous system)
  • Central nervous system ischemic response
  • Reverse stress-relaxation of the circulatory system
  • Secretion of renin by the kidneys ->angiotensin II
  • Secretion of vasopressin by the posterior pituitary gland
  • Secretion of norepi and epi by the adrenal medulla
  • Compensatory mechanisms increasing intravascular volume (reabsorption of fluid from GI, from interstitium, salt and water retention by the kidneys)
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7
Q

What is the 3-stage reduction of oxygen reaction (including enzymes)

A

Reduction of 90-95% of oxygen to water:

2 O2 -> 2 O2- (superoxide anion) -> H2O2 (superoxide dismutase / glutathione peroxidase) -> 2H2O (catalase)

O2- is one of the most reactive ROS

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8
Q

What are the 3 main processes leading to the production of ROS

A
  • Xanthine oxidase system (in phagocytes and hypoxic cells)
  • NADPH oxidase system
  • Mitochrondrial electron transport system
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9
Q

What enzyme catalyzes the conversion of superoxide radical to hydrogen peroxyde?

A

Superoxide dismutase

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10
Q

What is the Fenton or Haber-Weiss reaction

A

** Most cytotoxic of all oxidative pathways –> .OH (hydroxyl free radical) = one of the most toxic ROS

.O2- + H2O2 -> .OH + OH- + 1O2

Requires availability of copper or Fe2+

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11
Q

What is the myeloperoxidase reaction?

A

H2O2 (peroxide) + 2Cl - –> 2HOCl (hypochlorous acid)

HOCl is an ROS and precursor to free radicals

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12
Q

What are the 3 main reactive oxygen species (ROS)

A
  • Superoxide radical .O2-
  • Hydrogen peroxide H2O2
  • Hydroxyl radical .OH
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13
Q

What is the definition of a free radical

A

Reactive atom that has one or more unpaired electron(s)

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14
Q

What is the reaction leading to reactive nitrogen species

A

2.O2- + 2NO. -> 2ONO2- (peroxynitrite)

Peroxynitrite = reactive nitrogen species that can initiate lipid peroxidation

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15
Q

Where in the cell are ROS produced?

A

Within the mitochondria of neutrophils

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16
Q

What are the 2 main free radicals that can initiate lipid peroxidation

A

.OH (hydroxyl radical) and ONO2- (peroxynitrite)

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17
Q

What happens during ischemia that primes more production of free radicals? (3)

A
  • More neutrophils to affected tissues
  • More Fe3+ due to clotting/bleeding
  • Upregulation of xanthine oxidase
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18
Q

What are the 2 amino-acids most susceptible to oxidative injury

A

Cysteine and methionine

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19
Q

What are the reactions of the xanthine oxidoreductase system? What happens during ischemia and what happens during reperfusion

A

Ischemia:
1. ATP -> ADP ->adenosine -> inosine -> hypoxanthine (since ATP cannot be recycled)
2. xanthine dehydrogenase -> xanthine oxidase (reaction catalyzed by increased intracellular calcium)

Reperfusion:
1. hypoxanthine + O2 + NAD+ -> xanthine + O2- + NADH (xanthine oxidase)
2. xanthine + O2 + NAD+ -> uric acid + O2- + NADH (xanthine oxidase)

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20
Q

What is the main metabolic system involved in cellular injury during ischemia-reperfusion injury

A

Xanthine oxidoreductase system

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21
Q

What are some mechanisms of ischemia-reperfusion injury

A
  • Cellular energy depletion during ischemia -> loss of ion channel function and membrane integrity
  • Accumulation of intracellular calcium -> opening of mitochondrial permeability transition pores -> mitochondrial membrane depolarization, cytochrome C release -> apoptosis
  • ROS generation (xanthine oxidase, NADPH oxidase, dysfunctional electron transport chain)
  • Release of DAMPs from injured cells -> inflammation
  • Endothelial damage
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22
Q

What are the cells most susceptible to ischemia reperfusion injury

A
  • Endothelial cells
  • Cells of the GI mucosa

They have the greatest amount of xanthine oxidase

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23
Q

Name a few consequences of hyperoxia on the lungs

A
  • Atelectasis from denitrogenation of alveoli and rapid diffusion of O2 from alveoli to capillaries
  • Atelectasis from down-regulation of surfactant
  • Decreased muco-ciliary clearance
  • Apoptosis and necrosis of cells
  • Pulmonary edema from damaged endothelium
  • Systemic inflammation from release of DAMPs
  • Replacement of pneumocytes I by pneumocytes II –> leads to diffusion impairment
  • Increased production of NO. –> ONO-2. formation –> increased permeability and interstitial edema
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24
Q

What is the main effect of hyperoxia on the cardiovascular system

A

Vasoconstriction secondary to decreased NO availability (with reflex bradycardia with no change in SV –> decreased CO)

ROS (superoxide anion) inhibit NO.

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25
Q

What are 3 major potential indications for hyperbaric oxygen therapy

A
  • Gas embolism
  • Decompression sickness
  • Carbon monoxide toxicity
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26
Q

True or false: with hyperoxia, oxygen delivery is increased.

A

False - it is unchanged

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27
Q

What cellular components are most sensitive to oxidative injury

A

Lipids (causes peroxidation)

DNA and proteins are also sensitive

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28
Q

What are 4 beneficial effects of hyperoxic vasoconstriction?

A
  • Reduction in ICP
  • Counterbalance the vasodilatroy effects of septic shock
  • Preserve perfusion to the sublingual, hepato-splanchnic & pulmonary systems
  • Improve renal circulation
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29
Q

What are the 3 categories of antioxidants? Name examples

A
  • Endogenous enzymes (superoxide dismutase, glutathione peroxidase, catalase)
  • Endogenous non-enzymatic (glutathione, albumin, ferritin, etc.)
  • Exogenous (vitamin C, vitamin E, acetylcysteine, etc.)
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30
Q

Where are the superoxide dismutase and catalase located in the body

A
  • Extracellular
  • Cytoplasmic
  • Mitochondrial
31
Q

What are the definitions of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS)

A

IAH = steady state intra-abdominal pressure > 12 mmHg (grade I & II)
ACS = intra-abdominal pressure > 20 mmHg (grade III & IV)

32
Q

Describe how to measure intra-abdominal pressure

A
  • Insert a Foley catheter in the urinary bladder
  • Attach the Foley to a 3-way stopcock connected to a collection bag and a manometer.
    The patient should be in lateral recumbency and the manometer should be at the level of the patient’s midline at the symphysis pubis.
  • Empty the bladder then instil 1 mL/kg (max 25mL total) of saline
  • Zero the system (closed to the patient)
  • Close the system to the saline syringe and read the pressure on the manometer on end-expiration
  • Convert cmH2O reading into mmHg

Can also be measured in the intra-abdominal vena cava

33
Q

What is the normal intra-abdominal pressure in dogs and cats

A

Dogs: 0-3.7 mmHg (0-5 cmH2O)
Cats: 4.4-8.1 mmHg (6-11 cmH2O) when awake

34
Q

What are negative consequences of increased intra-abdominal pressure

A
  • Decreased venous return -> decreased CO (despite increased CVP)
  • Decreased GFR (due to decreased CO and compression of renal vasculature)
  • Decreased pulmonary compliance
  • Increased intra-cranial pressure (due to increased intra-thoracic pressure and decreased jugular drainage)
  • Decreased hepatic, intestinal, gastric blood flow and lymphatic drainage -> edema worsening intra-abdominal hypertension, bacterial translocation, etc.
  • Increased vasopressin
  • Venous stasis -> thrombosis
  • Wound dehiscence post-op
35
Q

What are therapeutic considerations for intra-abdominal hypertension based on severity

A
  • IAP 7.4-14.7 mmHg (10-20 cmH2O) -> ensure normovolemia and investigate underlying cause
  • IAP 14.7-25.7 mmHg (20-35 cmH2O) -> volume resuscitation, investigations, consider decompression
  • IAP > 25.7 mmHg (35 cmH2O) -> decompression (paracentesis / surgical), consider open abdomen management
36
Q

What is abdominal perfusion pressure?

A

APP = MAP - IAP

Better estimates perfusion pressure to the visceral organs than MAP alone

37
Q

What are parameters to consider in the mechanically ventilated patient with increased IAP?

A
  • These patients may benefit from IAP measurement
  • Volume-controlled ventilation may be preferred due to reduced lung compliance
  • Approximately 60-70% of the IAP is transmitted to the thoracic cavity
  • When considering lung protective strategies, the difference between Pplat and IAP can be used as a pressure goal.
38
Q

Explain why anaerobic conditions lead to hyperlactatemia and acidosis

A
  • Glycolysis produces pyruvate and NADH (and 2 moles of ATP per glucose)
  • Pyruvate normally undergoes decarboxylation to produce acetyl-CoA and joins the tricarboxylic acid cycle in the mitochondria to produce 36 moles of ATP (with the electron transport chain added) but this cannot happen in anaerobic conditions -> pyruvate accumulates as it is not used and the glycolysis runs faster to compensate for ATP deficit
  • Pyruvate gets transformed into lactate by lactate dehydrogenase to convert back NADH to NAD+ and continue to rune the glycolysis
  • H+ is released when ATP is used in the cell, it normally enters the mitochondrion but under anaerobic conditions its accumulates

(The acidosis is not caused by the lactate directly)

39
Q

True or false: Glycolysis requires oxygen to produce ATP?

A

False: requires constant supply of glucose and NAD+ (oxidized nicotinamide adenine dinucleotide), but does not require oxygen

40
Q

Which enzyme complex is involved in pyruvate –> acetyl-CoA

A

Pyruvate dehydrogenase

41
Q

How is lactate metabolized / excreted

A

Metabolized by the liver at 30-60% (used as a substrate) and by the kidneys at 10-30%.
Excreted by the kidneys, but reabsorbed in the proximal convoluted tubule until it reaches 6-10 mmol/L

42
Q

Why is lactate dehydrogenase activity unregulated when oxygen demand exceed supply?

A

Because NAD+ stores become depleted + pyruvate and NADH accumulates in the cytosol. Lactate formation reduces the cytosolic concentrations of pyruvate and H+ while replenishing NAD+.

43
Q

How is lactate transported across cell membranes and why is there a species-dependent variation in lactate concentrations?

A

Predominantly via facilitated passive transport by proton linked MCTs and sodium-coupled MCTs.

MCT expression on erythrocyte membranes varies between species which explains the species-dependant variation.

MCT = monocarboxylate transporters

44
Q

Where is the majority of the lactate produced in the body (3 places)?

A
  • Skeletal muscle
  • Brain
  • Adipose tissue
45
Q

What are the types of hyperlactatemia

A
  1. Type A = tissue oxygen deficiency
    - Increased O2 demand
    - Decreased O2 delivery
  2. Type B1 = associated with underlying disease (sepsis, neoplasia, liver failure, thiamine deficiency)
  3. Type B2 = associated with drugs / toxins (glucocorticoids, ethylene glycol, propylene glycol, catecholamines)
  4. Type B3 = inborn errors in metabolism (pyruvate dehydrogenase deficiency, mitochondrial myopathies)
46
Q

Which lactate isomer is predominant in cats and dogs

A

L-lactate

47
Q

As of what PaO2 value does lactate concentration begin to rise in hypoxemia?

A

PaO2 of 25-40 mmHg

48
Q

What can cause D-lactic acidosis

A
  • Increased bacterial fermentation in GI tract (pancreatic insufficiency, GI disease)
  • Altered carbohydrate metabolism
  • Diabetic ketoacidosis
  • Administration (racemic lactated Ringer’s solution, propylene glycol)
49
Q

Name 4 damaging cellular effects that occur during shock.

A
  1. Active transport of sodium and potassium through the cell membrane is diminished.
  2. Mitochondrial activity in the liver cells, as well as in many other tissues of the body, becomes severely depressed.
  3. Lysosomes in the cells in widespread tissue areas begin to break open, with intracellular release of hydrolases.
  4. Cellular metabolism of nutrients, such as glucose, eventually becomes greatly depressed in the last stages of shock. The actions of some hormones (ex. insulin) are depressed as well.
50
Q

3 causes of neurogenic shock

A
  • General anesthesia
  • Spinal anesthesia
  • Brain damage
51
Q

3 reasons why glucocorticoids are considered in patients with severe shock

A
  • Glucocorticoids increase the strength of the heart in the late stages of shock
  • Glucocorticoids stabilize lysosomes in tissue cells and thereby prevent release of lysosomal enzymes into the cytoplasm of the cells, preventing deterioration from this source
  • Glucocorticoids might aid in the metabolism of glucose by the severely damaged cells.
52
Q

Name 5 free radicals

A
  • Nitric oxide (NO.)
  • Hydroxyl radical (OH.)
  • Superoxide anion (.O2-)
  • Peroxynitrite (ONO-2.)
  • Peroxyl radical (.RO2)
53
Q

What are the consequences of a gas embolism

A
  • Massive gas embolism -> obstruction of blood flow in right heart ->death (with no success of CPR)
  • Gas embolism to lungs -> VQ mismatch, edema, release of vasoactive mediators, alveolar collapse
  • Gas embolism (mostly with nitrogen) will also cause platelet activation, complement response, leukocyte adhesion and endothelial cell damage
  • Gas emboli can also join the systemic circulation and cause impaired blood flow to various organs (worst = brain and coronaries)
54
Q

What inhalant is strictly contra-indicated when gas embolism is present

A

Nitrous oxide: it is vert insoluble and will escape the blood to join the air bubbles

55
Q

What volume of air is required to cause cardiovascular collapse in dogs

A

Around 2 mL/kg

56
Q

What patients are more at risk of negative consequences of air embolism

A

Patients with a right-to-left cardiac shunt

57
Q

What are common causes of gas embolism in cats and dogs

A
  • Intravenous access (highest risk with jugular catheters since usually above the heart so under negative pressure)
  • Laparoscopy (that’s why CO2 is used to inflate since it is more soluble and insufflation rate and pressure are restricted)
  • Surgery (when the surgical site is higher than the heart and a vein is open to room air -> irrigate surgical field!)
  • Intra-cardiac procedures
  • Lung biopsy (can create broncho-venous fistula - also reported with a chest tube mistakenly inserted in the lung)
  • Hyperbaric therapy with too rapid decompression
58
Q

What gas causes the most severe gas embolism

A

Nitrogen (which is very present in room air) ; O2 is better and CO2 the best

59
Q

What is the management of an air embolism

A
  • Stop air entry (clamp catheter, stop insufflation, ligate vessels in surgery, administer fluids to increase CVP and stop air entrainment)
  • Stop any administration of nitrous oxide
  • Administer 100% O2 (unless the gas emboli is made of O2)
  • Position patient to elevate apex
  • Prevent hypotension (which will contribute to bubble entrapment in circulation)
  • Manual aspiration of intracardiac bubble if possible
  • Hyperbaric oxygen therapy if available quickly
60
Q

How can an acute gas embolism be identified in an anesthetize patient

A

Increase in PaCO2 - EtCO2 difference (increases dead space ventilation)

61
Q

What are causes of SQ emphysema

A
  1. Traumatic;
    - Skin puncture
    - Tracheal / esophageal rupture
    - Increased intrathoracic pressure with secondary alveolar rupture (can be from coughing / vomiting)
  2. Iatrogenic
    - Overinflation of ETT cuff
    - Laparoscopy with air leak
    - Positive pressure ventilation
    - Aggressive hydrogen peroxide wound lavage
    - Buccal mucosa disruption with air insufflation during dental procedure (-> in this case antibiotics are recommended)
  3. Infectious
    - Gas producing bacteria: Clostridium, Bacteroides
  4. Spontaneous
    Not really reported
62
Q

Why can administration of 100% FiO2 improve pneumomediastinum and SQ emphysema

A

For patients with a leak in their respiratory system leading to the pneumomediastinum / SQ emphysema, administration of 100% FiO2 will reduce the proportion of nitrogen present in the emphysema and replace it with more soluble O2, which will decrease the amount of gas

63
Q

What are the 3 stages of shock systemically

A
  • Compensated shock: sympathetic response, RAAS response, etc. BP and O2 delivery to tissues overall preserved.
  • Early decompensated shock: tissue hypoperfusion, lactic acidosis, exhaustion of compensatory mechanisms
  • Irreversible decompensated shock: loss of vasomotor tone, irreversible cellular injury, death
64
Q

What are 3 effects of intracellular acidosis?

A
  • Denaturing of proteins
  • Diminished enzyme function
  • Disruption of transport mechanisms
65
Q

Name 6 perfusion parameters that are altered in hypovolemic shock

A
  • MM
  • CRT
  • Pulse quality
  • HR
  • Mentation
  • Extremity temperature
66
Q

A clinical diagnosis of shock is generally associated with what shock index?

A

> 0.9-1

67
Q

Name 2 cytokines released in cardiogentic shock and that cause myocardial depression

A

TNF-alpha
IL-6

68
Q

What role can glucagon play in cardiogenic shock?

A

Positive inotropy

69
Q

Why is dopamine not recommended in management of cardiogenic shock?

A

Has been shown to increase arrhythmias and likely mortality

70
Q

In distributive shock, describe the difference between “cold shock” and “warm shock”

A

Warm shock
- Compensation wth increased CO (increased contractility)
- PE: hyperdynamic pulses, hyperaemic MM with rapid CRT, warm extremities and increased rectal temp

Cold shock:
- Decreased contractility (and CO) from cytokine induced mitochondrial dysfunction, altered cellular substrate provision, desensitization of beta-adrenergic receptors of the myocardium
- PE: reduced pulse quality, pale MM, prolonged CRT, cold extremities and hypothermia

71
Q

What are 2 categories of non-circulatory sock?

A
  • Decreased arterial blood oxygen content (hypoxia, anemia, dyshemoglobinemias)
  • Metabolic (hypoglycemia, mitochondrial dysfunction)
72
Q

What are the 4 elements of the “Lethal Diamond”?

A

Coagulopathy
Acidosis
Hypothermia
Hypocalcemia

(Previously, the lethal triad did not include hypocalcemia)

73
Q

What is the “1.34” in the O2 delivery formula? What are the units?

A

It is the oxygen binding capacity of hemoglobin in mL of O2 / g of Hb

74
Q

What is the point of critical oxygen delivery?

A

The point at which oxygen consumption transitions from delivery independent to delivery dependent

Shock / CPR (5 decks)

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