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Emergency Critical Care VTS > Shock and Stabilization > Flashcards

Shock and Stabilization Flashcards

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1
Q

Describe the compensatory mechanism of hypovolemic shock

A

Baroreceptors in the carotid sinus and aortic arch detect drop in blood pressure because of reduced stretch. This enables sympathetic activation and inhibits parasympathetic activations.

Sympathetic activation activates alpha 1 and beta 1 adrenergic receptors
Increase vasoconstriction
increase heart rate
increase cardiac contractility
increase systemic vascular resistance
increase cardiac output

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2
Q

What does the Medulla Oblongata regulate?

A

The medulla oblongata is comprised of the cardiovascular and respiratory regulation system.

Descending motor tracts, ascending sensory tracts and origin of cranial nerves IX, X, XI, XII

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3
Q

Describe compensatory mechanism in response to changes in CO2, Hydrogen ions or partial pressure of O2

A

peripheral chemoreceptors in aortic and carotid bodies respond to changes in CO2, pH, and Partial pressure of O2.

Stimulation of chemoreceptors result in vasoconstriction and increase in minute ventilation.
Central chemoreceptors in respiratory center of medulla oblongata sense increase in CO2 or decrease in pH in CSF causing increase in respiratory rate and tidal volume

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4
Q

What is one complication of Oxygen therapy?

A

Hypercapnia is primary stimulus for respirations.
Patients with chronic hypercapnia may be dependent on hypoxia as respiratory stimulant because their hypercapnic drive can be diminished.

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5
Q

Definition of Shock:

A

Severe imbalance between oxygen supply and demand, leading to inadequate cellular energy production, cellular death and multiorgan failure.

When oxygen consumption (VO2) exceeds oxygen delivery (DO2)

VO2>DO2

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6
Q

What are 4 consequences of inadequate cellular energy production at the cellular level?

A
  1. Cell membrane pump dysfunction (Na+/K+ ATPase)
  2. Intracellular edema
  3. Leakage of intracellular contents extracellularly
  4. inability to regulate intracellular pH
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7
Q

Tree of Life

A
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8
Q

Define Cardiac Output and what factors influence cardiac output? Define the relationship as an equation.

A

Cardiac Output is the blood volume ejected with each cardiac contraction multiplied by number of contractions per minute.
CO=Stroke Volume x Heart Rate

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9
Q

What are the determinants of Stroke Volume

A

Preload: end diastolic volume, volume entering ventricles during diastole
Afterload: resistance ventricles must overcome to circulate blood.
Contractility: How hard the myocardium contracts for a given preload.

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10
Q

What factors influence preload?

A
  1. venous return
  2. fluid volume
  3. Atrial Contraction
  4. Intrathoracic Pressure
  5. Pericardial Pressure
  6. Venous tone
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11
Q

Causes for reduction in preload.

A

Hypovolemia: eg. hemorrhage, severe dehydration, edema, cavitary effusion

Obstructive: eg. GDV, severe pleural space disease, mesenteric volvulus, PTE, caval/portal venous occlusion, pericardial effusion

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12
Q

What factors influence Afterload?

A
  1. Pulmonic and systemic vascular resistance
  2. function and integrity of cardiac values
  3. ventricular chamber size.
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13
Q

Causes for increase in afterload

A

Peripheral vasoconstriction
systemic hypertension
aortic stenosis
aortic regurgitation

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14
Q

Causes for reduction in cardiac function (contractility)

A

Primary:
Cardiomyopathy
Valvular disease
tachy or bradyarrhythmia

Secondary:
Systemic inflammatory response syndrome
sepsis
electrolyte abnormalities
severehypoxia
severe acidosis or alkalosis

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15
Q

Correlation between:
mean arterial pressure
central venous pressure
cardiac output
systemic vascular resistance

A

SVR=(MAP-CVP)/CO

Decrease in SVR with Increase in CO is suggestive that vasopressors are indicated.

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16
Q

Expected changes in cardiac output, contractility, and systemic vascular resistance with different causes of shock: Hypovolemic

A

decrease cardiac output, increase contractility, increase systemic vascular resistance

Therapy: fluid resuscitation

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17
Q

Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Obstructive

A

Decrease cardiac output, normal to increased contractility, increased systemic vascular resistance

Therapy: Relieve obstruction and fluid resuscitation

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18
Q

Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Cardiogenic

A

Decreased cardiac output, decreased contractility, increased systemic vascular resistance

Therapy: Positive inotrope

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19
Q

Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Maldistributive

A

increased or decreased cardiac output
increased or decreased contractility
decreased systemic vascular resistance

Therapy: vasopressors

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20
Q

Methods of measuring cardiac output

A
  1. Fick’s oxygen consumption
  2. Fick-based carbon dioxide rebreathing method
  3. indicator dilution method: Thermodilution vs transpulmonary dilution vs lithium dilution
  4. Pulse contour/pulse pressure analysis
  5. Echocardiography
  6. Transthoracic ultrasound
  7. Pulse wave transit time
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21
Q

Define Hypoxia

Give 4 causes of hypoxia

A

Inadequate oxygen delivery (DO2) to meet tissue metabolic demand (VO2)
Caused by:
1. inadequate tissue perfusion
2. metabolic disturbances
3. lack of oxygen supply
4. inability of cells to extract O2

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22
Q

What two factors impact oxygen delivery? Define the relationship.

A
  1. Cardiac output
  2. arterial oxygen content

DaO2=CO x CaO2

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23
Q

Arterial oxygen content (CaO2)
Depends on what two factors?
What is the equation?

A
  • Depends on hemoglobin concentration
  • Binding affinity or degree of oxygen saturation (SaO2) of the hemoglobin present:

most of arterial O2 is delivered by hemoglobin
small fraction of O2 is dissolved in plasma

CaO2(ml/L)=[1.34(mO2/g) x SaO2% x hemoglobin (g/dL)] + [PaO2(mmHg) x 0.003(ml O2/dl/mmHg]

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24
Q

Define: Sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection

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25
Q

Define: Septic Shock

A

subset of sepsis when underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality

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26
Q

What are three definitions of massive transfusion

A
  1. Entire blood volume in 24 hours
  2. 50% of blood volume in 3-4 hours
  3. Administration of blood at 1.5ml/kg/min for 20 minutes
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27
Q

What are the consequences of hypocalcemia? What can cause hypocalcemia?

A

Clinical signs:
* Hypocalcemia can impair coagulation and decrease myocardial contractility and vascular tone.
* muscle tremors
* fasciculations
* seizures
* muscle cramping
* facial rubbing
* panting
* pyrexia
* PU/PD
* rare: hypotension and death
Causes:

  • Massive transfusion can cause hypocalcemia.
  • AKI/CKD
  • eclampsia
  • hypoparathyroism
  • ethylene glycol toxicity
  • GI disease from PLE
  • acute tumor lysis syndrome
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28
Q

What are two complications of massive transfusion?

A
  1. Ionized hypocalcemia
  2. hypomagnesemia due to chelation by citrate anticoagulant
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29
Q

What are the endpoints for hypotensive resuscitation?

A

MAP: 60 mmHg
Systolic: 90 mmHg

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30
Q

What is delayed resuscitation? When is it indicated?

A

Withholding all fluid therapy until definitive control of hemorrhage

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31
Q

When can post-surgical patients begin to hemorrhage from surgical site? Why?

A

1-3 hours post-op because hypotension and hypothermia is resolving upon recovery and vasoconstrictive drugs are wearing off.

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32
Q

What is neurogenic shock?

A

Usually from trauma to the brain or spinal cord resulting in abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscle.

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33
Q

Define: Hypoxemia

A

arterial partial pressure of oxygen is below 80 mmHg at sea level

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34
Q

5 causes of hypoxemia

A
  1. hypoventilation
  2. ventilation/perfusion mismatch
  3. Diffusion impairment
  4. Decrease [O2] in inspired air
  5. intrapulmonary shunting
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35
Q

What are PAMPs?

A

Pathogen-associated molecular patterns

The immune system uses PAMPs to identify pathogens.

PAMPs recognized by Pattern Recognition Receptors (PRR)

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36
Q

DAMPs

A

Damage associated molecular patterns

37
Q

What do DAMPs activate?

A

DAMPs interact with pattern recognition receptors (PRR), activating innate immune system and triggering pathologic response

38
Q

What are PRRs?

A

Pattern Recognition Receptors
Function: Trigger innate immune response by recognizing PAMPs and DAMPs
Activates cytokines, leukocytes, coagulation system and complements

39
Q

What is Cryptic Shock?

A

The disconnect between microcirculatory perfusion and systemic hemodynamics

Microcirculatory disturbances can occur prior to changes in macrohemodynamic variables (e.g. blood pressure)

40
Q

What are pathogen factors that can affect the extent and direction of the inflammatory response?

A
  1. Pathogen load
  2. pathogen virulence
  3. PAMPs
41
Q

What are host factors that can affect the extent and direction of the inflammatory process?

A

genetic characteristics
age
coexisting illnesses
medications

42
Q

What are septic shock risk factors?

A

S uppressed Immune system
E xtreme Age (infant/elderly)
P eople who have received organ transplant
S urgical procedure (anything invasive)
I ndwelling devices
S ickness

43
Q

Why is cytopathic hypoxia? What does it contribute to?

A

Dysfunctional mitochondria
Diminishes ability to produce ATP despite adequate PO2

44
Q

What is Nitric Oxide and its role in sepsis or septic shock?

A

Nitric Oxide is produced from the endothelium
NO is a powerful vascular smooth muscle relaxant that contributes to the vasodilatory state of patients with septic shock.

clinical signs (in dogs and people): hyperemic mucous membranes
short capillary refill times
tachycardia

45
Q

Define: Anaphylaxis

A

Type 1 hypersensitivity reaction that may occur secondary to a variety of antigens.

Mast cell degranulation releasing:
histamine
tryptase
heparin
cytokines

46
Q

2 types of Anaphylactic Reactions

A

Immune-mediated
non-immune mediated

47
Q

What is atopy?

A

Genetic predisposition to produce IgE following exposure to antigen.

These individuals are at risk for hypersensitivity response

48
Q

Function of Histamine Receptor H1
Pathophysiology during anaphylaxis?

A

Activates smooth muscle contraction and endothelial changes resulting in vasodilation and increased vascular permeability.

Anaphylaxis: vasodilatory shock.

49
Q

Function of Histamine Receptor H2
Pathophysiology during anaphylaxis?

A

Modulating gastric acid secretions and regulation of cardiac myocytes.

Anaphylaxis: cardiogenic shock, dysrhythmia, evidence of cardiac ischemia

50
Q

Function of Histamine Receptor H3 and H4
Pathophysiology during anaphylaxis?

A

H3: peripheral neurotransmitter release
H4: central neurotransmitter release

Release vasoactive substances such as dopamine and epinephrine is compromised

51
Q

What are the clinical signs of dogs in anaphylaxis?

A

GI compromise
hepatic congestion -> coagulation, increase ALT
portal hypertension

Can also exhibit cutaneous manifestations:
urticaria
pruritus
angioedema

52
Q

What are the clinical signs of cats in anaphylaxis?

A

Acute respiratory distress, airway edema, and bronchial secretions may be more prominent.
Cutaneous manifestations:
urticaria
pruritus
angioedema

53
Q

Role of prostaglandins in anaphylaxis

A

constriction of coronary and bronchial smooth muscles

54
Q

Role of leukotrienes in anaphylaxis?

A

Slow-acting substance of anaphylaxis. Longer time to onset, longer duration of action.

55
Q

What is Biphasic Anaphylaxis?

A

Initial improvement then relapse. Generally not associated with mortality in humans.

56
Q

Biomarks of Anaphylaxis

A
  • increase ALT 85-98% sensitive
  • POCUS for free fluid (excluding pericardial effusion) + Gallbladder wall edema 93%-98% sensitive
  • +/- Increase in PT/PTT
57
Q

Treatment for anaphylaxis

what are the mechanism of action on adrenergic receptors?

A

Epinephrine
alpha-1 –> vasoconstriction
beta-1 –> positive inotropy/chronotropy and improved cardiac output
beta-2 –> bronchodilation; stabilization of mast cells, preventing further degranulation and relase of anaphylaxis mediators
Dose: 0.01mg/kg IM +/- CRI 0.05 mg/kg/min

58
Q

Which receptor does diphenhydramine act on?

A

H1 receptor

Can be used in acute stabilization period of anaphylaxis

59
Q

Indicators for glucocorticosteroid use in anaphylaxis

A
  • Onset of action is hours after administration
  • works to down regulate late phase eosinophilic response and block the arachadonic cascade tempering delayed inflammatory cascade
  • if used, administer anti-inflammatory dose (not immunosupressive dose)
  • 0.1mg/kg IV of dexamethasone
60
Q

Normal values: Blood pressure

A

Dogs: Systolic 150 +/- 20mmHg
Mean 105 +/- 10mmHg
Diastolic 85+/- 10mmHg
Cats: systolic 125 +/- 10mmHg
Mean 105 +/- 10mmHg
Diastolic 90 +/- 10mmHg

61
Q

Calculating Mean Arterial Pressure

A

MAP = diastolic + [(systolic + diastolic)/3]

62
Q

When can arterial blood pressure monitoring produce erroneous readings?

A
  1. compliant tubing is used
  2. catheter lodged against arterial wall
  3. a clot at the tip of the catheter
  4. air bubbles present in catheter tubing
  5. catheter tubing kinked
63
Q

CENTRAL VENOUS PRESSURE
1. What is it monitoring?
2. How is it monitoring it?
3. When is it indicated?

A
  1. measuring hydrostatic pressure in the intrathoracic vena cava.
  2. used to estimate right ventricular end diastolic volume and the relationship between blood volume and blood volume capacity
  3. low central venous pressure (<0cm H2O) can indicate hypovolemia, fluid loss or vasodilation secondary to decrease in venous resistence.
63
Q

CENTRAL VENOUS PRESSURE
What are the normal values?

A

0-5 cm H2) but that can vary from animal to animal

64
Q

Indications of high vs low central venous pressure

A

LOW CVP (<0 cm H2O)
may indicate hypovolemia
- fluid loss
- vasodilation secondary to decrese peripheral venous resistence
~~~

```HIGH CVP (>10cm H2O)
may indicate volume overload, right-sided heart dysfunction or failure
pericardial effusion or restrictive disease
blood flow obstruction, significant pleural effusion

65
Q

Conditions taht promote thrombosis

A
  • multiple catheter attempts
  • catheter site irritation
  • phlebitis
  • hypovolemia
  • hypotension
  • immobilization of patient
  • hypercoagulable state
  • endothelial injury
  • blood sampling
  • excessive manipulation of catheter
  • inexperienced operators
  • infusate type
  • antibiotic and long corticosteroid administration
66
Q

What are 7 terms for catheter complications?

A
  1. catheter site irritation
  2. catheter site inflammation/phlebitis
  3. catheter coloization
  4. catheter site infection
  5. catheter related blood stream infection (CRBSI)
  6. catheter site sepsis
  7. catheter associated blood stream infections
67
Q

Catheter site irritation

A

localized catheter entrance site reaction with visible signs of bruising or erythema only

Culture negative

68
Q

Catheter site inflammation/phlebitis

A

localized catheter entrance site reaction with visible signs of erythema and at least one other physical anormality (swelling, induration, discomfort, warmth, purulence)

  1. sterile inflammation: culture negative
  2. catheter site contamination: culture positive or cytology positive for organisms
68
Q

Cather site infection

A

Visualized catheter site inflammation and confirmed organism identification.
1. microbioloical: exudate at catheter site yields an organism with or without concomitant bloodstream infection.
2. clinical: phlebitis noted within 2cm of catheter entrance site. Maybe associated with fever or mucopurulent exudate emerging from the site with or without concomitant bloodstream infection.

69
Q

Catheter colonization

A

Significant growth of microorganisms in a quantitative or semiquantitative culture of the catheter tip, subcutaneous catheter segment, or catheter hub.

Includes false-positive cultures (skin contaminant during catheter removal secondary to inadequate sterile skin preparation)

70
Q

Catheter-related bloodstream infection (CRBSI)

A

Catheter site infection or unexplained fever in a patient with identical organisms found on both catheter and blood culture.

Patient exhibiting clinical symptoms of bloodstream infection without any other apparent source of infection.

71
Q

Catheter-related sepsis

A

Patient exhibiting signs of systemic inflammatory response syndrome and confirmed CRBSI.

72
Q

Catheter associated bloodstream infection

A

An identified blood stream infection, patient exhibiting signs of systemic inflammatory response syndrome or unexplained fever, in light of having an intravenous catheter in place with no confirmed or suspected organism identified from the catheter tip.

  • unable to remove catheter, undiagnostic culture
  • unable to rule out another cause being the source of bloodstream infection.
73
Q

____________________ has been associated with increased incidences of CRBSI

A

Thrombosis
likely secondary to the clinically silent fibrin sheath that forms 24 hours after catheter insertion. The sheath is similar to biofilm matrix, increasing bacterial and fungal adherence and promoting coagulase enzyme to escalate thrombogenesis. The sheath/thrombus promotes repeat circulating organismal innoculation and potential for persistent bacteremia.

74
Q

Cardiac Index

A

Cardiac output (ml/min) refereced against body weight (ml/min/kg)
or surface area (ml/min/m^2)

Cardiac index for dogs and cats 120-200mls/min/kg

75
Q

Methodologies to determine cardiac output (6)

A

Fick Method
indicator dilution
pulse contour dialysis
echocardiography
transthoracic doppler
pulse wave transit time

76
Q

Fick’s Oxygen Consumption

A
  • Tissue oxygen consumption is dictated by cardiac output and the difference between arterial and venous content
  • cardiac output can be calculated in oxygen consumption and oxygen extraction ratio:

Cardiac Output = VO2/(CaO2 - CvO2)

CaO2 = (1.36 x [Hb] x SO2) + [0.003 x PaO2]

Oxygen consumption is determined by measuring difference in oxygen concentration between inhaled and exhaled air over time. –> requires the patient be intubated

77
Q

Define: Hypoxemic hypoxia

A

Inadequate oxygen delivery because of inadequate oxygen carrying capacity

78
Q

Define: Hypemic hypoxia

AKA: Anemic hypoxia

A

When anemia causes decreased circulating hemoglobin thus reducing oxygen carrying capacity and oxygen delivery

79
Q

Deifne: Hemoglobinopathy

A

Adequate amount of hemoglobin however the avaialble hemoglobin is dysfunctional and unable to transport oxygen.

e.g. Carbon monoxide toxicity
methemoglobinemia

80
Q

Define: Stagnant hypoxia

AKA Circulatory hypoxia

A

Caused by low cardiac output and low blood flow

therefore low oxygen delivery to tissue (AKA circulatory shock)

81
Q

Define: Histiotoxic hypoxia

A

Adequate delivery of oxygen to tissues but tissues are unable to extract and utilize the oxygen.

e.g. Cyanide poisoning
Carbon monoxide toxicity
mitochondrial dysfunction of sepsis

82
Q

Define: Metabolic hypoxia

A

Occurs when there is an increased intracellular consumptionof oxygen.
e.g. sepsis

83
Q

Oxygen extraction ratio

A

oxygen extraction (O2ER)

O2ER = oxygen consumption / oxygen delivery

O2ER = VO2/DO2

84
Q

Normal O2ER

A

Most tissue: 0.3
Brain: 0.6

85
Q

VO2 is __________________ of DO2 under normal circumstances

A

Independent

86
Q

VO2 is ____.
Body responds by ____ oxygen extraction and ____ cardiac output.

A
  1. constant
  2. increasing
  3. increasing
87
Q

Critical oxygen delivery

A

The point at which oxygen consumption declines because oxygen delivery is unable to keep up with demand.

Emergency Critical Care VTS (21 decks)

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